ketamine Search Results


ketamine hydrochloride  (LGC Standards)
94
LGC Standards ketamine hydrochloride
Ketamine Hydrochloride, supplied by LGC Standards, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/ketamine hydrochloride/product/LGC Standards
Average 94 stars, based on 1 article reviews
ketamine hydrochloride - by Bioz Stars, 2026-04
94/100 stars
  Buy from Supplier
ketamine  (Tocris)
95
Tocris ketamine
( a ). Schematic illustrating viral transduction strategy and two-photon Ca 2+ imaging of VTA DA neurons in acute brain slices. ( b ). Example 2PLSM image of VTA DA neurons expressing GCaMP6f. Scale bar, 20 µm. ( c ). Spontaneous Ca 2+ oscillations in one neuron with and without <t>ketamine</t> bath application (50 µM). <t>Black,</t> <t>ACSF;</t> blue, with ketamine. ( d ). Power spectral density of Ca 2+ transients for the neuron in ( c ). ( e ). Left, quantification of max power with and without ketamine treatment (n = 410 neurons). Right, quantification of frequency at max power. Paired two-tailed t test, ACSF vs KET, Max power, p = 0.8865, Frequency at max power, p = 0.3779. ( f ). Left, histogram showing the distribution of changes in max power with ketamine application. Right, same but for frequency at max power. n = 410 neurons. ( g ). Schematic illustrating viral transduction strategy and electrophysiological recording of VTA DA neurons in acute brain slices. ( h ). Spontaneous action potentials recorded in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. ( i ). Quantification of neuronal firing rate with and without ketamine treatment (n = 9 neurons from three animals). Paired two-tailed t test, ACSF vs KET, p = 0.2561. ( j ). Spontaneous EPSCs recorded in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. Holding membrane potential at –70 mV, 10 µM Gabazine in ASCF for both conditions. ( k ). Left, cumulative frequency distribution of sEPSCs amplitudes. Right, quantification of sEPSC amplitude in recorded neurons. Paired two-tailed t test, ACSF vs KET, p = 0.1958. n = 17 neurons from three animals. ( l ). Same as ( k ), but for sEPSCs inter-event intervals (IEI). Paired two-tailed t test, ACSF vs KET, p = 0.8413. ( m ). Spontaneous IPSCs recorded in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. Holding membrane potential at –70 mV with high chloride internal solution, 10 µM CNQX in ASCF for both conditions. ( n ). Left, cumulative frequency distribution of sIPSCs amplitudes. Right, quantification of sIPSC amplitude in recorded neurons. Paired two-tailed t test, ACSF vs KET, p = 0.9164. n = 12 neurons from two animals. ( o ). Same as ( n ), but for sIPSCs inter-event intervals (IEI). Paired two-tailed t test, ACSF vs KET, p = 0.5675. Figure 4—source data 1. Numerical data for the graphs in .
Ketamine, supplied by Tocris, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/ketamine/product/Tocris
Average 95 stars, based on 1 article reviews
ketamine - by Bioz Stars, 2026-04
95/100 stars
  Buy from Supplier
ketamine  (Cayman Chemical)
93
Cayman Chemical ketamine
( a ). Schematic illustrating viral transduction strategy and two-photon Ca 2+ imaging of VTA DA neurons in acute brain slices. ( b ). Example 2PLSM image of VTA DA neurons expressing GCaMP6f. Scale bar, 20 µm. ( c ). Spontaneous Ca 2+ oscillations in one neuron with and without <t>ketamine</t> bath application (50 µM). <t>Black,</t> <t>ACSF;</t> blue, with ketamine. ( d ). Power spectral density of Ca 2+ transients for the neuron in ( c ). ( e ). Left, quantification of max power with and without ketamine treatment (n = 410 neurons). Right, quantification of frequency at max power. Paired two-tailed t test, ACSF vs KET, Max power, p = 0.8865, Frequency at max power, p = 0.3779. ( f ). Left, histogram showing the distribution of changes in max power with ketamine application. Right, same but for frequency at max power. n = 410 neurons. ( g ). Schematic illustrating viral transduction strategy and electrophysiological recording of VTA DA neurons in acute brain slices. ( h ). Spontaneous action potentials recorded in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. ( i ). Quantification of neuronal firing rate with and without ketamine treatment (n = 9 neurons from three animals). Paired two-tailed t test, ACSF vs KET, p = 0.2561. ( j ). Spontaneous EPSCs recorded in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. Holding membrane potential at –70 mV, 10 µM Gabazine in ASCF for both conditions. ( k ). Left, cumulative frequency distribution of sEPSCs amplitudes. Right, quantification of sEPSC amplitude in recorded neurons. Paired two-tailed t test, ACSF vs KET, p = 0.1958. n = 17 neurons from three animals. ( l ). Same as ( k ), but for sEPSCs inter-event intervals (IEI). Paired two-tailed t test, ACSF vs KET, p = 0.8413. ( m ). Spontaneous IPSCs recorded in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. Holding membrane potential at –70 mV with high chloride internal solution, 10 µM CNQX in ASCF for both conditions. ( n ). Left, cumulative frequency distribution of sIPSCs amplitudes. Right, quantification of sIPSC amplitude in recorded neurons. Paired two-tailed t test, ACSF vs KET, p = 0.9164. n = 12 neurons from two animals. ( o ). Same as ( n ), but for sIPSCs inter-event intervals (IEI). Paired two-tailed t test, ACSF vs KET, p = 0.5675. Figure 4—source data 1. Numerical data for the graphs in .
Ketamine, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/ketamine/product/Cayman Chemical
Average 93 stars, based on 1 article reviews
ketamine - by Bioz Stars, 2026-04
93/100 stars
  Buy from Supplier
ketamine  (Biosynth Carbosynth)
93
Biosynth Carbosynth ketamine
( a ). Schematic illustrating viral transduction strategy and two-photon Ca 2+ imaging of VTA DA neurons in acute brain slices. ( b ). Example 2PLSM image of VTA DA neurons expressing GCaMP6f. Scale bar, 20 µm. ( c ). Spontaneous Ca 2+ oscillations in one neuron with and without <t>ketamine</t> bath application (50 µM). <t>Black,</t> <t>ACSF;</t> blue, with ketamine. ( d ). Power spectral density of Ca 2+ transients for the neuron in ( c ). ( e ). Left, quantification of max power with and without ketamine treatment (n = 410 neurons). Right, quantification of frequency at max power. Paired two-tailed t test, ACSF vs KET, Max power, p = 0.8865, Frequency at max power, p = 0.3779. ( f ). Left, histogram showing the distribution of changes in max power with ketamine application. Right, same but for frequency at max power. n = 410 neurons. ( g ). Schematic illustrating viral transduction strategy and electrophysiological recording of VTA DA neurons in acute brain slices. ( h ). Spontaneous action potentials recorded in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. ( i ). Quantification of neuronal firing rate with and without ketamine treatment (n = 9 neurons from three animals). Paired two-tailed t test, ACSF vs KET, p = 0.2561. ( j ). Spontaneous EPSCs recorded in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. Holding membrane potential at –70 mV, 10 µM Gabazine in ASCF for both conditions. ( k ). Left, cumulative frequency distribution of sEPSCs amplitudes. Right, quantification of sEPSC amplitude in recorded neurons. Paired two-tailed t test, ACSF vs KET, p = 0.1958. n = 17 neurons from three animals. ( l ). Same as ( k ), but for sEPSCs inter-event intervals (IEI). Paired two-tailed t test, ACSF vs KET, p = 0.8413. ( m ). Spontaneous IPSCs recorded in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. Holding membrane potential at –70 mV with high chloride internal solution, 10 µM CNQX in ASCF for both conditions. ( n ). Left, cumulative frequency distribution of sIPSCs amplitudes. Right, quantification of sIPSC amplitude in recorded neurons. Paired two-tailed t test, ACSF vs KET, p = 0.9164. n = 12 neurons from two animals. ( o ). Same as ( n ), but for sIPSCs inter-event intervals (IEI). Paired two-tailed t test, ACSF vs KET, p = 0.5675. Figure 4—source data 1. Numerical data for the graphs in .
Ketamine, supplied by Biosynth Carbosynth, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/ketamine/product/Biosynth Carbosynth
Average 93 stars, based on 1 article reviews
ketamine - by Bioz Stars, 2026-04
93/100 stars
  Buy from Supplier
s ketamine  (Tocris)
94
Tocris s ketamine
( a ). Schematic illustrating viral transduction strategy and two-photon Ca 2+ imaging of VTA DA neurons in acute brain slices. ( b ). Example 2PLSM image of VTA DA neurons expressing GCaMP6f. Scale bar, 20 µm. ( c ). Spontaneous Ca 2+ oscillations in one neuron with and without <t>ketamine</t> bath application (50 µM). <t>Black,</t> <t>ACSF;</t> blue, with ketamine. ( d ). Power spectral density of Ca 2+ transients for the neuron in ( c ). ( e ). Left, quantification of max power with and without ketamine treatment (n = 410 neurons). Right, quantification of frequency at max power. Paired two-tailed t test, ACSF vs KET, Max power, p = 0.8865, Frequency at max power, p = 0.3779. ( f ). Left, histogram showing the distribution of changes in max power with ketamine application. Right, same but for frequency at max power. n = 410 neurons. ( g ). Schematic illustrating viral transduction strategy and electrophysiological recording of VTA DA neurons in acute brain slices. ( h ). Spontaneous action potentials recorded in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. ( i ). Quantification of neuronal firing rate with and without ketamine treatment (n = 9 neurons from three animals). Paired two-tailed t test, ACSF vs KET, p = 0.2561. ( j ). Spontaneous EPSCs recorded in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. Holding membrane potential at –70 mV, 10 µM Gabazine in ASCF for both conditions. ( k ). Left, cumulative frequency distribution of sEPSCs amplitudes. Right, quantification of sEPSC amplitude in recorded neurons. Paired two-tailed t test, ACSF vs KET, p = 0.1958. n = 17 neurons from three animals. ( l ). Same as ( k ), but for sEPSCs inter-event intervals (IEI). Paired two-tailed t test, ACSF vs KET, p = 0.8413. ( m ). Spontaneous IPSCs recorded in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. Holding membrane potential at –70 mV with high chloride internal solution, 10 µM CNQX in ASCF for both conditions. ( n ). Left, cumulative frequency distribution of sIPSCs amplitudes. Right, quantification of sIPSC amplitude in recorded neurons. Paired two-tailed t test, ACSF vs KET, p = 0.9164. n = 12 neurons from two animals. ( o ). Same as ( n ), but for sIPSCs inter-event intervals (IEI). Paired two-tailed t test, ACSF vs KET, p = 0.5675. Figure 4—source data 1. Numerical data for the graphs in .
S Ketamine, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/s ketamine/product/Tocris
Average 94 stars, based on 1 article reviews
s ketamine - by Bioz Stars, 2026-04
94/100 stars
  Buy from Supplier
ketamine hydrochloride  (Randox)
94
Randox ketamine hydrochloride
( a ). Schematic illustrating viral transduction strategy and two-photon Ca 2+ imaging of VTA DA neurons in acute brain slices. ( b ). Example 2PLSM image of VTA DA neurons expressing GCaMP6f. Scale bar, 20 µm. ( c ). Spontaneous Ca 2+ oscillations in one neuron with and without <t>ketamine</t> bath application (50 µM). <t>Black,</t> <t>ACSF;</t> blue, with ketamine. ( d ). Power spectral density of Ca 2+ transients for the neuron in ( c ). ( e ). Left, quantification of max power with and without ketamine treatment (n = 410 neurons). Right, quantification of frequency at max power. Paired two-tailed t test, ACSF vs KET, Max power, p = 0.8865, Frequency at max power, p = 0.3779. ( f ). Left, histogram showing the distribution of changes in max power with ketamine application. Right, same but for frequency at max power. n = 410 neurons. ( g ). Schematic illustrating viral transduction strategy and electrophysiological recording of VTA DA neurons in acute brain slices. ( h ). Spontaneous action potentials recorded in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. ( i ). Quantification of neuronal firing rate with and without ketamine treatment (n = 9 neurons from three animals). Paired two-tailed t test, ACSF vs KET, p = 0.2561. ( j ). Spontaneous EPSCs recorded in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. Holding membrane potential at –70 mV, 10 µM Gabazine in ASCF for both conditions. ( k ). Left, cumulative frequency distribution of sEPSCs amplitudes. Right, quantification of sEPSC amplitude in recorded neurons. Paired two-tailed t test, ACSF vs KET, p = 0.1958. n = 17 neurons from three animals. ( l ). Same as ( k ), but for sEPSCs inter-event intervals (IEI). Paired two-tailed t test, ACSF vs KET, p = 0.8413. ( m ). Spontaneous IPSCs recorded in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. Holding membrane potential at –70 mV with high chloride internal solution, 10 µM CNQX in ASCF for both conditions. ( n ). Left, cumulative frequency distribution of sIPSCs amplitudes. Right, quantification of sIPSC amplitude in recorded neurons. Paired two-tailed t test, ACSF vs KET, p = 0.9164. n = 12 neurons from two animals. ( o ). Same as ( n ), but for sIPSCs inter-event intervals (IEI). Paired two-tailed t test, ACSF vs KET, p = 0.5675. Figure 4—source data 1. Numerical data for the graphs in .
Ketamine Hydrochloride, supplied by Randox, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/ketamine hydrochloride/product/Randox
Average 94 stars, based on 1 article reviews
ketamine hydrochloride - by Bioz Stars, 2026-04
94/100 stars
  Buy from Supplier
ketamine hydrochloride  (Cerilliant Corporation)
90
Cerilliant Corporation ketamine hydrochloride
Enrichment recoveries obtained with the different extraction solvents evaluated for the extraction of drugs by dispersive liquid–liquid microextraction (DLLME).
Ketamine Hydrochloride, supplied by Cerilliant Corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/ketamine hydrochloride/product/Cerilliant Corporation
Average 90 stars, based on 1 article reviews
ketamine hydrochloride - by Bioz Stars, 2026-04
90/100 stars
  Buy from Supplier
ketamine hydrochloride  (Biosynth Carbosynth)
94
Biosynth Carbosynth ketamine hydrochloride
Enrichment recoveries obtained with the different extraction solvents evaluated for the extraction of drugs by dispersive liquid–liquid microextraction (DLLME).
Ketamine Hydrochloride, supplied by Biosynth Carbosynth, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/ketamine hydrochloride/product/Biosynth Carbosynth
Average 94 stars, based on 1 article reviews
ketamine hydrochloride - by Bioz Stars, 2026-04
94/100 stars
  Buy from Supplier
r ketamine  (Tocris)
94
Tocris r ketamine
Enrichment recoveries obtained with the different extraction solvents evaluated for the extraction of drugs by dispersive liquid–liquid microextraction (DLLME).
R Ketamine, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/r ketamine/product/Tocris
Average 94 stars, based on 1 article reviews
r ketamine - by Bioz Stars, 2026-04
94/100 stars
  Buy from Supplier
r ketamine  (Cayman Chemical)
93
Cayman Chemical r ketamine
Schemes for Experiments and post hoc analyses. (A) Scheme of the <t>ketamine</t> injection paradigm for Experiment 1 during development of LID <t>(daily</t> <t>L-DOPA</t> injections). FAS = Forelimb adjusting steps test. (B) Scheme of the injection paradigm in PD rats for Experiment 2 . AR = amphetamine-rotation test; RR = RotaRod test. (C) Scheme of the injection paradigm for Experiment 3 during development of LID (daily L-DOPA injections). (D) Verification of unilateral 6-OHDA lesion and evaluation of striatal dopamine (DA) levels after ketamine in the rats from the study shown in (A). Electrochemical detection of striatal DA content (mean ± SEM) is reduced by>95% in the lesioned side. Striatal DA content was unchanged by a 10-h-treatment of either ketamine (K; n =9), R -ketamine ( R -K; n =9) vs. vehicle (V; n = 9) 1-h before rats were euthanized, showing no effect on overall striatal DA levels by ketamine or R -ketamine-treatment compared to vehicle in either the lesioned (Lx) or the intact hemisphere. (E) Verification of unilateral 6-OHDA lesion from the study shown in (B) using semi-quantitative TH western analysis in striatal tissue plotting % loss (mean ± SEM) in Lx vs. intact (In) hemisphere ( n =9). Two-tailed t -test, *** p < .001. (F) Verification of unilateral 6-OHDA lesions in the rats from the study depicted in (C). The graph shows the quantification of the TH-ir plotting the % loss (mean ± SEM) in the Lx vs. intact SN hemispheres ( n =10/group; V =vehicle, K =ketamine, K +A = ketamine+ ANA-12). (G) Example photomicrograph of a SN in Experiment 3 shows the unilateral reduction in TH-ir post-lesion. Two-way ANOVAs, Bonferroni post hoc tests, *** p < .001. (H) Verification of unilateral 6-OHDA lesion from the ANA-12-only control study, the negative control for Experiment 3 , using semi-quantitative TH western analysis in striatal tissue, plotting % loss (mean ± SEM) in Lx vs. intact hemisphere ( n = 10). Two-tailed t -test, *** p < .001.
R Ketamine, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/r ketamine/product/Cayman Chemical
Average 93 stars, based on 1 article reviews
r ketamine - by Bioz Stars, 2026-04
93/100 stars
  Buy from Supplier
m 5mpep  (Tocris)
93
Tocris m 5mpep
Schemes for Experiments and post hoc analyses. (A) Scheme of the <t>ketamine</t> injection paradigm for Experiment 1 during development of LID <t>(daily</t> <t>L-DOPA</t> injections). FAS = Forelimb adjusting steps test. (B) Scheme of the injection paradigm in PD rats for Experiment 2 . AR = amphetamine-rotation test; RR = RotaRod test. (C) Scheme of the injection paradigm for Experiment 3 during development of LID (daily L-DOPA injections). (D) Verification of unilateral 6-OHDA lesion and evaluation of striatal dopamine (DA) levels after ketamine in the rats from the study shown in (A). Electrochemical detection of striatal DA content (mean ± SEM) is reduced by>95% in the lesioned side. Striatal DA content was unchanged by a 10-h-treatment of either ketamine (K; n =9), R -ketamine ( R -K; n =9) vs. vehicle (V; n = 9) 1-h before rats were euthanized, showing no effect on overall striatal DA levels by ketamine or R -ketamine-treatment compared to vehicle in either the lesioned (Lx) or the intact hemisphere. (E) Verification of unilateral 6-OHDA lesion from the study shown in (B) using semi-quantitative TH western analysis in striatal tissue plotting % loss (mean ± SEM) in Lx vs. intact (In) hemisphere ( n =9). Two-tailed t -test, *** p < .001. (F) Verification of unilateral 6-OHDA lesions in the rats from the study depicted in (C). The graph shows the quantification of the TH-ir plotting the % loss (mean ± SEM) in the Lx vs. intact SN hemispheres ( n =10/group; V =vehicle, K =ketamine, K +A = ketamine+ ANA-12). (G) Example photomicrograph of a SN in Experiment 3 shows the unilateral reduction in TH-ir post-lesion. Two-way ANOVAs, Bonferroni post hoc tests, *** p < .001. (H) Verification of unilateral 6-OHDA lesion from the ANA-12-only control study, the negative control for Experiment 3 , using semi-quantitative TH western analysis in striatal tissue, plotting % loss (mean ± SEM) in Lx vs. intact hemisphere ( n = 10). Two-tailed t -test, *** p < .001.
M 5mpep, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/m 5mpep/product/Tocris
Average 93 stars, based on 1 article reviews
m 5mpep - by Bioz Stars, 2026-04
93/100 stars
  Buy from Supplier

Image Search Results


( a ). Schematic illustrating viral transduction strategy and two-photon Ca 2+ imaging of VTA DA neurons in acute brain slices. ( b ). Example 2PLSM image of VTA DA neurons expressing GCaMP6f. Scale bar, 20 µm. ( c ). Spontaneous Ca 2+ oscillations in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. ( d ). Power spectral density of Ca 2+ transients for the neuron in ( c ). ( e ). Left, quantification of max power with and without ketamine treatment (n = 410 neurons). Right, quantification of frequency at max power. Paired two-tailed t test, ACSF vs KET, Max power, p = 0.8865, Frequency at max power, p = 0.3779. ( f ). Left, histogram showing the distribution of changes in max power with ketamine application. Right, same but for frequency at max power. n = 410 neurons. ( g ). Schematic illustrating viral transduction strategy and electrophysiological recording of VTA DA neurons in acute brain slices. ( h ). Spontaneous action potentials recorded in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. ( i ). Quantification of neuronal firing rate with and without ketamine treatment (n = 9 neurons from three animals). Paired two-tailed t test, ACSF vs KET, p = 0.2561. ( j ). Spontaneous EPSCs recorded in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. Holding membrane potential at –70 mV, 10 µM Gabazine in ASCF for both conditions. ( k ). Left, cumulative frequency distribution of sEPSCs amplitudes. Right, quantification of sEPSC amplitude in recorded neurons. Paired two-tailed t test, ACSF vs KET, p = 0.1958. n = 17 neurons from three animals. ( l ). Same as ( k ), but for sEPSCs inter-event intervals (IEI). Paired two-tailed t test, ACSF vs KET, p = 0.8413. ( m ). Spontaneous IPSCs recorded in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. Holding membrane potential at –70 mV with high chloride internal solution, 10 µM CNQX in ASCF for both conditions. ( n ). Left, cumulative frequency distribution of sIPSCs amplitudes. Right, quantification of sIPSC amplitude in recorded neurons. Paired two-tailed t test, ACSF vs KET, p = 0.9164. n = 12 neurons from two animals. ( o ). Same as ( n ), but for sIPSCs inter-event intervals (IEI). Paired two-tailed t test, ACSF vs KET, p = 0.5675. Figure 4—source data 1. Numerical data for the graphs in .

Journal: eLife

Article Title: Attenuated dopamine signaling after aversive learning is restored by ketamine to rescue escape actions

doi: 10.7554/eLife.64041

Figure Lengend Snippet: ( a ). Schematic illustrating viral transduction strategy and two-photon Ca 2+ imaging of VTA DA neurons in acute brain slices. ( b ). Example 2PLSM image of VTA DA neurons expressing GCaMP6f. Scale bar, 20 µm. ( c ). Spontaneous Ca 2+ oscillations in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. ( d ). Power spectral density of Ca 2+ transients for the neuron in ( c ). ( e ). Left, quantification of max power with and without ketamine treatment (n = 410 neurons). Right, quantification of frequency at max power. Paired two-tailed t test, ACSF vs KET, Max power, p = 0.8865, Frequency at max power, p = 0.3779. ( f ). Left, histogram showing the distribution of changes in max power with ketamine application. Right, same but for frequency at max power. n = 410 neurons. ( g ). Schematic illustrating viral transduction strategy and electrophysiological recording of VTA DA neurons in acute brain slices. ( h ). Spontaneous action potentials recorded in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. ( i ). Quantification of neuronal firing rate with and without ketamine treatment (n = 9 neurons from three animals). Paired two-tailed t test, ACSF vs KET, p = 0.2561. ( j ). Spontaneous EPSCs recorded in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. Holding membrane potential at –70 mV, 10 µM Gabazine in ASCF for both conditions. ( k ). Left, cumulative frequency distribution of sEPSCs amplitudes. Right, quantification of sEPSC amplitude in recorded neurons. Paired two-tailed t test, ACSF vs KET, p = 0.1958. n = 17 neurons from three animals. ( l ). Same as ( k ), but for sEPSCs inter-event intervals (IEI). Paired two-tailed t test, ACSF vs KET, p = 0.8413. ( m ). Spontaneous IPSCs recorded in one neuron with and without ketamine bath application (50 µM). Black, ACSF; blue, with ketamine. Holding membrane potential at –70 mV with high chloride internal solution, 10 µM CNQX in ASCF for both conditions. ( n ). Left, cumulative frequency distribution of sIPSCs amplitudes. Right, quantification of sIPSC amplitude in recorded neurons. Paired two-tailed t test, ACSF vs KET, p = 0.9164. n = 12 neurons from two animals. ( o ). Same as ( n ), but for sIPSCs inter-event intervals (IEI). Paired two-tailed t test, ACSF vs KET, p = 0.5675. Figure 4—source data 1. Numerical data for the graphs in .

Article Snippet: In vivo injections included intraperitoneal and subcutaneous injections of ketamine (10 mg/kg, Vedco, St. Joseph, MO) and Clozapine N-oxide (3 mg/kg in vivo, 1 μM in vitro, Sigma-Aldrich); intracranial injections of ketamine (12.5 μg in 500 nl ACSF) and Chicago Sky Blue 6B (50 μg in 500 nl ACSF, Tocris, Bristol, United Kingdom).

Techniques: Transduction, Imaging, Expressing, Two Tailed Test, Membrane

( a ). Top, schematic for selected glutamatergic input regions to VTA. Bottom, experimental timeline. ( b ). Summary data showing the percentage of failures after local infusion of ketamine or ACSF in mPFC, and ketamine in PAG, PPTg, and VTA. Two-way ANOVA, Sidak’s multiple comparison test, LH vs LH+ KET, mPFC, p< 0.0001, PAG, p = 0.4965, PPTg, p = 0.9998, VTA, p = 0.9986. LH vs LH+ ACSF (mPFC), p = 0.9993. ( c ). Schematic for viral transduction and VTA photometry recording of Ca 2+ transients with local ketamine delivery in mPFC. ( d ). Left, average Ca 2+ transients (mean ± SEM) in response to foot shocks at the start of induction, at the end of induction, and following local ketamine infusion. Traces are aligned to shock start time (20 trials/animal, 6 animals). Right, quantification of peak Ca 2+ transient amplitude during and after foot shock stimuli across conditions. Both positive and negative values are quantified. n = 6 animals, repeated measures one-way ANOVA, Holm-Sidak’s multiple comparison test, Peak: During shock, F (1.948, 9.739) = 5.547, p = 0.0252, Induction start vs Induction end p = 0.0433, Induction end vs LH + KET, p = 0.0823. After shock, F (1.468, 7.341) = 10.05, p = 0.0105, Induction start vs Induction end, p = 0.0462, Induction end vs LH + KET, p = 0.0147. *p < 0.05, *** p < 0.001, **** p < 0.0001. Error bars reflect SEM. Figure 5—source data 1. Numerical data for the graphs in .

Journal: eLife

Article Title: Attenuated dopamine signaling after aversive learning is restored by ketamine to rescue escape actions

doi: 10.7554/eLife.64041

Figure Lengend Snippet: ( a ). Top, schematic for selected glutamatergic input regions to VTA. Bottom, experimental timeline. ( b ). Summary data showing the percentage of failures after local infusion of ketamine or ACSF in mPFC, and ketamine in PAG, PPTg, and VTA. Two-way ANOVA, Sidak’s multiple comparison test, LH vs LH+ KET, mPFC, p< 0.0001, PAG, p = 0.4965, PPTg, p = 0.9998, VTA, p = 0.9986. LH vs LH+ ACSF (mPFC), p = 0.9993. ( c ). Schematic for viral transduction and VTA photometry recording of Ca 2+ transients with local ketamine delivery in mPFC. ( d ). Left, average Ca 2+ transients (mean ± SEM) in response to foot shocks at the start of induction, at the end of induction, and following local ketamine infusion. Traces are aligned to shock start time (20 trials/animal, 6 animals). Right, quantification of peak Ca 2+ transient amplitude during and after foot shock stimuli across conditions. Both positive and negative values are quantified. n = 6 animals, repeated measures one-way ANOVA, Holm-Sidak’s multiple comparison test, Peak: During shock, F (1.948, 9.739) = 5.547, p = 0.0252, Induction start vs Induction end p = 0.0433, Induction end vs LH + KET, p = 0.0823. After shock, F (1.468, 7.341) = 10.05, p = 0.0105, Induction start vs Induction end, p = 0.0462, Induction end vs LH + KET, p = 0.0147. *p < 0.05, *** p < 0.001, **** p < 0.0001. Error bars reflect SEM. Figure 5—source data 1. Numerical data for the graphs in .

Article Snippet: In vivo injections included intraperitoneal and subcutaneous injections of ketamine (10 mg/kg, Vedco, St. Joseph, MO) and Clozapine N-oxide (3 mg/kg in vivo, 1 μM in vitro, Sigma-Aldrich); intracranial injections of ketamine (12.5 μg in 500 nl ACSF) and Chicago Sky Blue 6B (50 μg in 500 nl ACSF, Tocris, Bristol, United Kingdom).

Techniques: Comparison, Transduction

Journal: eLife

Article Title: Attenuated dopamine signaling after aversive learning is restored by ketamine to rescue escape actions

doi: 10.7554/eLife.64041

Figure Lengend Snippet:

Article Snippet: In vivo injections included intraperitoneal and subcutaneous injections of ketamine (10 mg/kg, Vedco, St. Joseph, MO) and Clozapine N-oxide (3 mg/kg in vivo, 1 μM in vitro, Sigma-Aldrich); intracranial injections of ketamine (12.5 μg in 500 nl ACSF) and Chicago Sky Blue 6B (50 μg in 500 nl ACSF, Tocris, Bristol, United Kingdom).

Techniques: Recombinant, Plasmid Preparation, RNAscope, Fluorescence, Multiplex Assay, Software

Enrichment recoveries obtained with the different extraction solvents evaluated for the extraction of drugs by dispersive liquid–liquid microextraction (DLLME).

Journal: Forensic Sciences Research

Article Title: Determination of multiple drugs of abuse in human urine using dispersive liquid–liquid microextraction and capillary electrophoresis with PDA detection

doi: 10.1080/20961790.2021.1986771

Figure Lengend Snippet: Enrichment recoveries obtained with the different extraction solvents evaluated for the extraction of drugs by dispersive liquid–liquid microextraction (DLLME).

Article Snippet: 6-Monoacetylmorphine (6-MAM) hydrochloride, morphine hydrochloride, codeine phosphate, methamphetamine hydrochloride, amphetamine hydrochloride, 3,4-methylenedioxymethamphetamine (MDMA) hydrochloride, 3,4-methylenedioxyamphetamine (MDA) hydrochloride and ketamine hydrochloride were purchased from Cerilliant (Merck KGaA, Darmstadt, Germany).

Techniques:

Enrichment recoveries obtained with the different dispersive solvents evaluated for the extraction of drugs by dispersive liquid–liquid microextraction (DLLME).

Journal: Forensic Sciences Research

Article Title: Determination of multiple drugs of abuse in human urine using dispersive liquid–liquid microextraction and capillary electrophoresis with PDA detection

doi: 10.1080/20961790.2021.1986771

Figure Lengend Snippet: Enrichment recoveries obtained with the different dispersive solvents evaluated for the extraction of drugs by dispersive liquid–liquid microextraction (DLLME).

Article Snippet: 6-Monoacetylmorphine (6-MAM) hydrochloride, morphine hydrochloride, codeine phosphate, methamphetamine hydrochloride, amphetamine hydrochloride, 3,4-methylenedioxymethamphetamine (MDMA) hydrochloride, 3,4-methylenedioxyamphetamine (MDA) hydrochloride and ketamine hydrochloride were purchased from Cerilliant (Merck KGaA, Darmstadt, Germany).

Techniques:

The performance of the proposed methods in spiked urine samples.

Journal: Forensic Sciences Research

Article Title: Determination of multiple drugs of abuse in human urine using dispersive liquid–liquid microextraction and capillary electrophoresis with PDA detection

doi: 10.1080/20961790.2021.1986771

Figure Lengend Snippet: The performance of the proposed methods in spiked urine samples.

Article Snippet: 6-Monoacetylmorphine (6-MAM) hydrochloride, morphine hydrochloride, codeine phosphate, methamphetamine hydrochloride, amphetamine hydrochloride, 3,4-methylenedioxymethamphetamine (MDMA) hydrochloride, 3,4-methylenedioxyamphetamine (MDA) hydrochloride and ketamine hydrochloride were purchased from Cerilliant (Merck KGaA, Darmstadt, Germany).

Techniques:

Electropherograms obtained for the spiked biological samples before (a) and after (b) dispersive liquid–liquid microextraction (DLLME) extraction under the optimum conditions. Extraction conditions: dispersive solvent, 0.5 mL isopropyl alcohol; extraction solvent, 41.0 µL CHCl 3 ; room temperature; pH of sample, 9.0; analytes concentration spiked, urine: 50 ng/mL; internal standard: 3 µg/mL lidocaine. Peak identification: (IS) lidocaine, (1) AM: amphetamine, (2) MA: methamphetamine, (3) MDA: methy­lenedioxyamphetamine, (4) MDMA: methylenedioxymethamphetamine, (5) ketamine, (6) codeine, (7) morphine, (8) 6-MAM: 6-monoacetylmorphine.

Journal: Forensic Sciences Research

Article Title: Determination of multiple drugs of abuse in human urine using dispersive liquid–liquid microextraction and capillary electrophoresis with PDA detection

doi: 10.1080/20961790.2021.1986771

Figure Lengend Snippet: Electropherograms obtained for the spiked biological samples before (a) and after (b) dispersive liquid–liquid microextraction (DLLME) extraction under the optimum conditions. Extraction conditions: dispersive solvent, 0.5 mL isopropyl alcohol; extraction solvent, 41.0 µL CHCl 3 ; room temperature; pH of sample, 9.0; analytes concentration spiked, urine: 50 ng/mL; internal standard: 3 µg/mL lidocaine. Peak identification: (IS) lidocaine, (1) AM: amphetamine, (2) MA: methamphetamine, (3) MDA: methy­lenedioxyamphetamine, (4) MDMA: methylenedioxymethamphetamine, (5) ketamine, (6) codeine, (7) morphine, (8) 6-MAM: 6-monoacetylmorphine.

Article Snippet: 6-Monoacetylmorphine (6-MAM) hydrochloride, morphine hydrochloride, codeine phosphate, methamphetamine hydrochloride, amphetamine hydrochloride, 3,4-methylenedioxymethamphetamine (MDMA) hydrochloride, 3,4-methylenedioxyamphetamine (MDA) hydrochloride and ketamine hydrochloride were purchased from Cerilliant (Merck KGaA, Darmstadt, Germany).

Techniques: Concentration Assay

Electropherograms obtained for the real biological samples from the drug abuser before (a) and after (b) dispersive liquid–liquid microextraction (DLLME) extraction under the optimum conditions. Extraction conditions: dispersive solvent, 0.5 mL isopropyl alcohol; extraction solvent, 41.0 μL CHCl 3 ; room temperature; pH of sample, 9.0; analytes concentration spiked, urine: 50 ng/mL; internal standard: 3 μg/mL lidocaine. Peak identification: (IS) lidocaine, (1) AM: amphetamine, 42.1 ng/mL, (2) MA: methamphetamine, 102.6 ng/mL, (5) ketamine, 84.7 ng/mL.

Journal: Forensic Sciences Research

Article Title: Determination of multiple drugs of abuse in human urine using dispersive liquid–liquid microextraction and capillary electrophoresis with PDA detection

doi: 10.1080/20961790.2021.1986771

Figure Lengend Snippet: Electropherograms obtained for the real biological samples from the drug abuser before (a) and after (b) dispersive liquid–liquid microextraction (DLLME) extraction under the optimum conditions. Extraction conditions: dispersive solvent, 0.5 mL isopropyl alcohol; extraction solvent, 41.0 μL CHCl 3 ; room temperature; pH of sample, 9.0; analytes concentration spiked, urine: 50 ng/mL; internal standard: 3 μg/mL lidocaine. Peak identification: (IS) lidocaine, (1) AM: amphetamine, 42.1 ng/mL, (2) MA: methamphetamine, 102.6 ng/mL, (5) ketamine, 84.7 ng/mL.

Article Snippet: 6-Monoacetylmorphine (6-MAM) hydrochloride, morphine hydrochloride, codeine phosphate, methamphetamine hydrochloride, amphetamine hydrochloride, 3,4-methylenedioxymethamphetamine (MDMA) hydrochloride, 3,4-methylenedioxyamphetamine (MDA) hydrochloride and ketamine hydrochloride were purchased from Cerilliant (Merck KGaA, Darmstadt, Germany).

Techniques: Concentration Assay

Schemes for Experiments and post hoc analyses. (A) Scheme of the ketamine injection paradigm for Experiment 1 during development of LID (daily L-DOPA injections). FAS = Forelimb adjusting steps test. (B) Scheme of the injection paradigm in PD rats for Experiment 2 . AR = amphetamine-rotation test; RR = RotaRod test. (C) Scheme of the injection paradigm for Experiment 3 during development of LID (daily L-DOPA injections). (D) Verification of unilateral 6-OHDA lesion and evaluation of striatal dopamine (DA) levels after ketamine in the rats from the study shown in (A). Electrochemical detection of striatal DA content (mean ± SEM) is reduced by>95% in the lesioned side. Striatal DA content was unchanged by a 10-h-treatment of either ketamine (K; n =9), R -ketamine ( R -K; n =9) vs. vehicle (V; n = 9) 1-h before rats were euthanized, showing no effect on overall striatal DA levels by ketamine or R -ketamine-treatment compared to vehicle in either the lesioned (Lx) or the intact hemisphere. (E) Verification of unilateral 6-OHDA lesion from the study shown in (B) using semi-quantitative TH western analysis in striatal tissue plotting % loss (mean ± SEM) in Lx vs. intact (In) hemisphere ( n =9). Two-tailed t -test, *** p < .001. (F) Verification of unilateral 6-OHDA lesions in the rats from the study depicted in (C). The graph shows the quantification of the TH-ir plotting the % loss (mean ± SEM) in the Lx vs. intact SN hemispheres ( n =10/group; V =vehicle, K =ketamine, K +A = ketamine+ ANA-12). (G) Example photomicrograph of a SN in Experiment 3 shows the unilateral reduction in TH-ir post-lesion. Two-way ANOVAs, Bonferroni post hoc tests, *** p < .001. (H) Verification of unilateral 6-OHDA lesion from the ANA-12-only control study, the negative control for Experiment 3 , using semi-quantitative TH western analysis in striatal tissue, plotting % loss (mean ± SEM) in Lx vs. intact hemisphere ( n = 10). Two-tailed t -test, *** p < .001.

Journal: Experimental neurology

Article Title: Preclinical evidence in support of repurposing sub-anesthetic ketamine as a treatment for L-DOPA-induced dyskinesia

doi: 10.1016/j.expneurol.2020.113413

Figure Lengend Snippet: Schemes for Experiments and post hoc analyses. (A) Scheme of the ketamine injection paradigm for Experiment 1 during development of LID (daily L-DOPA injections). FAS = Forelimb adjusting steps test. (B) Scheme of the injection paradigm in PD rats for Experiment 2 . AR = amphetamine-rotation test; RR = RotaRod test. (C) Scheme of the injection paradigm for Experiment 3 during development of LID (daily L-DOPA injections). (D) Verification of unilateral 6-OHDA lesion and evaluation of striatal dopamine (DA) levels after ketamine in the rats from the study shown in (A). Electrochemical detection of striatal DA content (mean ± SEM) is reduced by>95% in the lesioned side. Striatal DA content was unchanged by a 10-h-treatment of either ketamine (K; n =9), R -ketamine ( R -K; n =9) vs. vehicle (V; n = 9) 1-h before rats were euthanized, showing no effect on overall striatal DA levels by ketamine or R -ketamine-treatment compared to vehicle in either the lesioned (Lx) or the intact hemisphere. (E) Verification of unilateral 6-OHDA lesion from the study shown in (B) using semi-quantitative TH western analysis in striatal tissue plotting % loss (mean ± SEM) in Lx vs. intact (In) hemisphere ( n =9). Two-tailed t -test, *** p < .001. (F) Verification of unilateral 6-OHDA lesions in the rats from the study depicted in (C). The graph shows the quantification of the TH-ir plotting the % loss (mean ± SEM) in the Lx vs. intact SN hemispheres ( n =10/group; V =vehicle, K =ketamine, K +A = ketamine+ ANA-12). (G) Example photomicrograph of a SN in Experiment 3 shows the unilateral reduction in TH-ir post-lesion. Two-way ANOVAs, Bonferroni post hoc tests, *** p < .001. (H) Verification of unilateral 6-OHDA lesion from the ANA-12-only control study, the negative control for Experiment 3 , using semi-quantitative TH western analysis in striatal tissue, plotting % loss (mean ± SEM) in Lx vs. intact hemisphere ( n = 10). Two-tailed t -test, *** p < .001.

Article Snippet: In Experiment 1 , ketamine (20 mg/kg; VetOne), R -ketamine (10 mg/kg; Cayman Chemicals, Ann Arbor, MI), and L-DOPA (6 and 12 mg/kg; Sigma-Aldrich) combined with benserazide hydrochloride (14 mg/kg; Sigma-Aldrich) were formulated in the vehicle solution, 0.9% USP grade sterile saline (VetOne).

Techniques: Injection, Western Blot, Two Tailed Test, Negative Control

Low-dose racemic ketamine treatment once a week attenuates the development of LID in the preclinical model. In Experiment 1 6-OHDA-lesioned PD rats were injected daily with L-DOPA (days 0–13: 6 mg/kg; days 14–28: 12 mg/kg; i.p. ) to induce dyskinesia and tested for LAO-AIMs twice a week for 3 h by blinded investigators. (A) The mean LAO AIMs scores±SEM are plotted showing a 50% reduction after racemic low-dose ketamine treatments (K) when compared to the vehicle group (V) and a group treated with R -ketamine ( R -K), to test for contribution of the stereospecific ketamine isomer. The blue arrows point to the days of the 10-h racemic ketamine (20 mg/kg; i.p. ), R -ketamine (10 mg/kg; i.p. ) or vehicle treatment paradigm; n = 9 per group, * p < .05, ** p < .01, Kruskal-Wallis test with Dunn’s multiple comparisons post hoc tests. (B) Example time course of the LAO-AIMs data showed in (A) for day 11. (C) Example time course of the LAO-AIMs data showed in (A) for day 25. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Journal: Experimental neurology

Article Title: Preclinical evidence in support of repurposing sub-anesthetic ketamine as a treatment for L-DOPA-induced dyskinesia

doi: 10.1016/j.expneurol.2020.113413

Figure Lengend Snippet: Low-dose racemic ketamine treatment once a week attenuates the development of LID in the preclinical model. In Experiment 1 6-OHDA-lesioned PD rats were injected daily with L-DOPA (days 0–13: 6 mg/kg; days 14–28: 12 mg/kg; i.p. ) to induce dyskinesia and tested for LAO-AIMs twice a week for 3 h by blinded investigators. (A) The mean LAO AIMs scores±SEM are plotted showing a 50% reduction after racemic low-dose ketamine treatments (K) when compared to the vehicle group (V) and a group treated with R -ketamine ( R -K), to test for contribution of the stereospecific ketamine isomer. The blue arrows point to the days of the 10-h racemic ketamine (20 mg/kg; i.p. ), R -ketamine (10 mg/kg; i.p. ) or vehicle treatment paradigm; n = 9 per group, * p < .05, ** p < .01, Kruskal-Wallis test with Dunn’s multiple comparisons post hoc tests. (B) Example time course of the LAO-AIMs data showed in (A) for day 11. (C) Example time course of the LAO-AIMs data showed in (A) for day 25. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: In Experiment 1 , ketamine (20 mg/kg; VetOne), R -ketamine (10 mg/kg; Cayman Chemicals, Ann Arbor, MI), and L-DOPA (6 and 12 mg/kg; Sigma-Aldrich) combined with benserazide hydrochloride (14 mg/kg; Sigma-Aldrich) were formulated in the vehicle solution, 0.9% USP grade sterile saline (VetOne).

Techniques: Injection

LAO-AIMs scores from Experiment 1 separated by sub-type of dyskinesia. Low-dose racemic ketamine treatment once a week attenuates the development of (A) limb (B) axial (C) orolingual AIMs in the preclinical model. 6-OHDA-lesioned PD rats were injected daily with L-DOPA (days 0–13: 6 mg/kg; days 14–28: 12 mg/kg; i.p. ) to induce dyskinesia and tested for LAO AIMs twice a week for 3 h by blinded investigators. The mean LAO AIMs scores ± SEM are plotted showing a 50% reduction after racemic low-dose ketamine treatments (K) when compared to the vehicle group (V) and a group treated with R -ketamine ( R -K), to test for contribution of the stereospecific ketamine isomer. The blue arrows point to the days of the 10-h racemic ketamine (20 mg/kg; i.p. ), R -ketamine (10 mg/kg; i.p. ) or vehicle treatment paradigm; n = 9 per group, * p < .05, ** p < .01, Kruskal-Wallis tests with Dunn’s post hoc tests. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Journal: Experimental neurology

Article Title: Preclinical evidence in support of repurposing sub-anesthetic ketamine as a treatment for L-DOPA-induced dyskinesia

doi: 10.1016/j.expneurol.2020.113413

Figure Lengend Snippet: LAO-AIMs scores from Experiment 1 separated by sub-type of dyskinesia. Low-dose racemic ketamine treatment once a week attenuates the development of (A) limb (B) axial (C) orolingual AIMs in the preclinical model. 6-OHDA-lesioned PD rats were injected daily with L-DOPA (days 0–13: 6 mg/kg; days 14–28: 12 mg/kg; i.p. ) to induce dyskinesia and tested for LAO AIMs twice a week for 3 h by blinded investigators. The mean LAO AIMs scores ± SEM are plotted showing a 50% reduction after racemic low-dose ketamine treatments (K) when compared to the vehicle group (V) and a group treated with R -ketamine ( R -K), to test for contribution of the stereospecific ketamine isomer. The blue arrows point to the days of the 10-h racemic ketamine (20 mg/kg; i.p. ), R -ketamine (10 mg/kg; i.p. ) or vehicle treatment paradigm; n = 9 per group, * p < .05, ** p < .01, Kruskal-Wallis tests with Dunn’s post hoc tests. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: In Experiment 1 , ketamine (20 mg/kg; VetOne), R -ketamine (10 mg/kg; Cayman Chemicals, Ann Arbor, MI), and L-DOPA (6 and 12 mg/kg; Sigma-Aldrich) combined with benserazide hydrochloride (14 mg/kg; Sigma-Aldrich) were formulated in the vehicle solution, 0.9% USP grade sterile saline (VetOne).

Techniques: Injection

Ketamine does not interfere with the anti-PD effect of L-DOPA and reduces PD-motor behavior post-6-OHDA-lesion (Post-Lx) by itself. (A) Mean % contralateral/ipsilateral ratios of steps ± SEM using the FAS test paradigm in the LID cohort of Experiment 1 , are plotted after normalization to pre-lesion (Pre-Lx) indicate a significant anti-PD effect of ketamine * p < .05; repeated measures ANOVA. Ketamine does also not interfere with the anti-PD effect of L-DOPA, and a significant increase of stepping contralateral to the lesioned side after either L-DOPA alone or L-DOPA + Ketamine vs. all Post-Lx time points is seen: *** p < .001; one-way ANOVA on data prior to normalization, Tukey-Kramer corrected post hoc tests; n = 9 per group. (B) In Experiment 2 we tested ketamine treatment in a separate cohort of hemi-parkinsonian 6-OHDA-lesioned rats and used the RotaRod test to evaluate the deficit. The graph shows the mean latency to fall ± SEM, normalized to pre-lesion baseline (Pre-Lx). Post-lesion (Post-Lx) the latency to fall was reduced by 50% in these PD animals. This motor deficit was reversed by ketamine treatment (blue bars), already at the 1st injection, and the animals performed as good as at baseline. One-way ANOVA, with Tukey-Kramer corrected post hoc tests, on raw data before normalization. n = 9, * p < .05, ** p < .01. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Journal: Experimental neurology

Article Title: Preclinical evidence in support of repurposing sub-anesthetic ketamine as a treatment for L-DOPA-induced dyskinesia

doi: 10.1016/j.expneurol.2020.113413

Figure Lengend Snippet: Ketamine does not interfere with the anti-PD effect of L-DOPA and reduces PD-motor behavior post-6-OHDA-lesion (Post-Lx) by itself. (A) Mean % contralateral/ipsilateral ratios of steps ± SEM using the FAS test paradigm in the LID cohort of Experiment 1 , are plotted after normalization to pre-lesion (Pre-Lx) indicate a significant anti-PD effect of ketamine * p < .05; repeated measures ANOVA. Ketamine does also not interfere with the anti-PD effect of L-DOPA, and a significant increase of stepping contralateral to the lesioned side after either L-DOPA alone or L-DOPA + Ketamine vs. all Post-Lx time points is seen: *** p < .001; one-way ANOVA on data prior to normalization, Tukey-Kramer corrected post hoc tests; n = 9 per group. (B) In Experiment 2 we tested ketamine treatment in a separate cohort of hemi-parkinsonian 6-OHDA-lesioned rats and used the RotaRod test to evaluate the deficit. The graph shows the mean latency to fall ± SEM, normalized to pre-lesion baseline (Pre-Lx). Post-lesion (Post-Lx) the latency to fall was reduced by 50% in these PD animals. This motor deficit was reversed by ketamine treatment (blue bars), already at the 1st injection, and the animals performed as good as at baseline. One-way ANOVA, with Tukey-Kramer corrected post hoc tests, on raw data before normalization. n = 9, * p < .05, ** p < .01. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: In Experiment 1 , ketamine (20 mg/kg; VetOne), R -ketamine (10 mg/kg; Cayman Chemicals, Ann Arbor, MI), and L-DOPA (6 and 12 mg/kg; Sigma-Aldrich) combined with benserazide hydrochloride (14 mg/kg; Sigma-Aldrich) were formulated in the vehicle solution, 0.9% USP grade sterile saline (VetOne).

Techniques: Injection

Ketamine’s long-term anti-dyskinetic activity was driven by BDNF signaling. (A) The mean LAO-AIMs scores ± SEM of Experiment 3 are plotted. The sustained anti-dyskinetic effect of low-dose ketamine is reduced by blocking the BDNF receptor TrkB, with co-injection of the TrkB antagonist ANA-12 (0.5 mg/kg; i.p. ) with ketamine (K + A). The blue arrows point to the days of the 10-h racemic (K) ketamine (20 mg/kg; i.p. ), or vehicle treatment paradigm (V). ANA-12 co-injection (green bars) did reduce the sustained anti-dyskinetic effect seen in ketamine-only injected LID (blue bars) leading to LAO AIMs comparable to those of the vehicle group (grey bars), indicating an involvement of BDNF in the sustained anti-dyskinetic effects of ketamine. n = 10 per group, * p < .05, ** p < .01, ANOVAs, Tukey-Kramer corrected post hoc tests. (B) Example time course of the LAO-AIMs for day 14 showed in (A). (C) A control study using 10-h ANA-12-only treatments on days 0 and 7 of daily L-DOPA-treatment (6 mg/kg; i.p .) verified that, while systemic TrkB antagonism does block the ketamine effect, it does not change development of LID in this model, and serves as an important negative control for the data shown in (A). The graph depicts the mean LAO-AIMs scores ± SEM from the vehicle control groups in Experiment 1 (V- E1 ; n = 9) and Experiment 3 (V- E3 ; n = 10), as well as the ANA-12-only control study (ANA-12; n = 10). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Journal: Experimental neurology

Article Title: Preclinical evidence in support of repurposing sub-anesthetic ketamine as a treatment for L-DOPA-induced dyskinesia

doi: 10.1016/j.expneurol.2020.113413

Figure Lengend Snippet: Ketamine’s long-term anti-dyskinetic activity was driven by BDNF signaling. (A) The mean LAO-AIMs scores ± SEM of Experiment 3 are plotted. The sustained anti-dyskinetic effect of low-dose ketamine is reduced by blocking the BDNF receptor TrkB, with co-injection of the TrkB antagonist ANA-12 (0.5 mg/kg; i.p. ) with ketamine (K + A). The blue arrows point to the days of the 10-h racemic (K) ketamine (20 mg/kg; i.p. ), or vehicle treatment paradigm (V). ANA-12 co-injection (green bars) did reduce the sustained anti-dyskinetic effect seen in ketamine-only injected LID (blue bars) leading to LAO AIMs comparable to those of the vehicle group (grey bars), indicating an involvement of BDNF in the sustained anti-dyskinetic effects of ketamine. n = 10 per group, * p < .05, ** p < .01, ANOVAs, Tukey-Kramer corrected post hoc tests. (B) Example time course of the LAO-AIMs for day 14 showed in (A). (C) A control study using 10-h ANA-12-only treatments on days 0 and 7 of daily L-DOPA-treatment (6 mg/kg; i.p .) verified that, while systemic TrkB antagonism does block the ketamine effect, it does not change development of LID in this model, and serves as an important negative control for the data shown in (A). The graph depicts the mean LAO-AIMs scores ± SEM from the vehicle control groups in Experiment 1 (V- E1 ; n = 9) and Experiment 3 (V- E3 ; n = 10), as well as the ANA-12-only control study (ANA-12; n = 10). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: In Experiment 1 , ketamine (20 mg/kg; VetOne), R -ketamine (10 mg/kg; Cayman Chemicals, Ann Arbor, MI), and L-DOPA (6 and 12 mg/kg; Sigma-Aldrich) combined with benserazide hydrochloride (14 mg/kg; Sigma-Aldrich) were formulated in the vehicle solution, 0.9% USP grade sterile saline (VetOne).

Techniques: Activity Assay, Blocking Assay, Injection, Negative Control

LAO-AIMs scores from Experiment 3 separated by sub-type of dyskinesia. Low-dose ketamine treatment (blue arrows) once a week attenuates the development of individual AIMs scores. 6-OHDA-lesioned PD rats were injected daily with L-DOPA (days 0–14: 6 mg/kg; i.p. ) to induce dyskinesia and tested for LAO-AIMs twice a week for 3 h by blinded investigators. The anti-dyskinetic effect of low-dose ketamine (K, blue bars) reduced the individual (A) limb (B) axial (C) and orolingual AIMs (mean ± SEM) scores, compared to the vehicle (V, grey bars) group and a group treated with the TrkB antagonist, ANA-12 (K + A, green bars). The blue arrows point to the days of the 10-h racemic ketamine (20 mg/kg; i.p. ), R -ketamine (10 mg/kg; i.p. ) n = 10 per group, *p < .05, **p < .01, Kruskal-Wallis tests with Dunn’s post hoc tests. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Journal: Experimental neurology

Article Title: Preclinical evidence in support of repurposing sub-anesthetic ketamine as a treatment for L-DOPA-induced dyskinesia

doi: 10.1016/j.expneurol.2020.113413

Figure Lengend Snippet: LAO-AIMs scores from Experiment 3 separated by sub-type of dyskinesia. Low-dose ketamine treatment (blue arrows) once a week attenuates the development of individual AIMs scores. 6-OHDA-lesioned PD rats were injected daily with L-DOPA (days 0–14: 6 mg/kg; i.p. ) to induce dyskinesia and tested for LAO-AIMs twice a week for 3 h by blinded investigators. The anti-dyskinetic effect of low-dose ketamine (K, blue bars) reduced the individual (A) limb (B) axial (C) and orolingual AIMs (mean ± SEM) scores, compared to the vehicle (V, grey bars) group and a group treated with the TrkB antagonist, ANA-12 (K + A, green bars). The blue arrows point to the days of the 10-h racemic ketamine (20 mg/kg; i.p. ), R -ketamine (10 mg/kg; i.p. ) n = 10 per group, *p < .05, **p < .01, Kruskal-Wallis tests with Dunn’s post hoc tests. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: In Experiment 1 , ketamine (20 mg/kg; VetOne), R -ketamine (10 mg/kg; Cayman Chemicals, Ann Arbor, MI), and L-DOPA (6 and 12 mg/kg; Sigma-Aldrich) combined with benserazide hydrochloride (14 mg/kg; Sigma-Aldrich) were formulated in the vehicle solution, 0.9% USP grade sterile saline (VetOne).

Techniques: Injection