Journal: The Journal of Physiology
Article Title: 5‐HT 2A receptor activation enhances NMDA receptor‐mediated glutamate responses through Src kinase in the dendrites of rat jaw‐closing motoneurons
doi: 10.1113/JP275440
Figure Lengend Snippet: A, C and E, representative glutamate responses in masseter motoneurons before (Ctrl, black) and during application of 10 μm TCB‐2 (A: blue), 10 μm BW723C86 (C: green) or 10 μm MK212 (E: purple) in the presence of 1 μm TTX. The baselines of traces before and during drug application were adjusted to be the same. B, D and F, expanded traces of ‘a’, ‘b’, and ‘c’ in A, C and E. G, representative glutamate responses in masseter motoneurons in the presence of 2 μm ketanserin alone (grey) and during the addition of 10 μm 5‐HT (red) in the presence of 1 μm TTX. H, expanded traces of ‘a’, ‘b’ and ‘c’ in G. The baselines of traces before and during drug application were adjusted to be the same. I and J, pooled data for the effects of TCB‐2, BW723C86, MK212, 1 μm 8‐OH‐DPAT, 8‐OH‐DPAT with 1 μm WAY‐100635, ACSF, 5‐HT and 5‐HT with ketanserin on the glutamate response amplitude (I) and resting membrane potential (J). * P < 0.05 vs. before agonist application (paired Student's t test); †† P < 0.01 (unpaired Student's t test). Data are expressed as mean ± SEM.
Article Snippet: Drug application The following components were added to the bath medium when required: MNI‐glutamate; 5‐HT (Sigma‐Aldrich; Merck KGaA); 4‐bromo‐3,6‐dimethoxybenzocyclobuten‐1‐yl methylamine hydrobromide (TCB‐2; Tocris Bioscience); α‐methyl‐5‐(2‐thienylmethoxy)‐1H‐indole‐3‐ethanamine hydrochloride (BW723C86; Tocris Bioscience); 6‐chloro‐2‐(1‐piperazinyl)pyrazine hydrochloride (MK 212; Tocris Bioscience); (±)‐8‐hydroxy‐2‐dipropylaminotetralin hydrobromide (8‐OH‐DPAT; Sigma‐Aldrich; Merck KGaA); N ‐[2‐[4‐(2‐methoxyphenyl)‐1‐piperazinyl]ethyl]‐ N ‐2‐pyridinylcyclohexanecarboxamide maleate (WAY 100635; Sigma‐Aldrich; Merck KGaA); 3‐[2‐[4‐(4‐fluorobenzoyl)‐1‐piperidinyl]ethyl]‐2,4(1H,3H)‐quinazolinedione (ketanserin; Sigma‐Aldrich; Merck KGaA); CNQX (Sigma‐Aldrich; Merck KGaA); 2,3‐dioxo‐6‐nitro‐1,2,3,4‐tetrahydrobenzo[f]quinoxaline‐7‐sulfonamide disodium salt (NBQX; Sigma‐Aldrich; Merck KGaA); dl ‐2‐amino‐5‐phosphonopentanoic acid (APV; Sigma‐Aldrich; Merck KGaA); dl ‐3‐(2‐carboxypiperazin‐4‐yl)‐propyl‐1‐phosphonic acid (CPP; Sigma‐Aldrich; Merck KGaA); 3‐(4‐chlorophenyl) 1‐(1,1‐dimethylethyl)‐1H‐pyrazolo[3,4‐d]pyrimidin‐4‐amine (PP2; Tocris Bioscience); 1‐phenyl‐1H‐pyrazolo[3,4‐d]pyrimidin‐4‐amine (PP3; Tocris Bioscience); 1‐[6‐[[(17β)‐3‐methoxyestra‐1,3,5(10)‐trien‐17‐yl]amino]hexyl]‐1H‐pyrrole‐2,5‐dione (U73122; Tocris Bioscience); ( S ,2 R ,2′ R )‐3,3′‐disulfanediylbis(2‐amino‐1‐(( S )‐8‐(cyclohexylmethyl)‐2‐phenyl‐5,6‐dihydroimidazo[1,2‐a]pyrazin‐7(8H)‐yl)propan‐1‐one) tetrahydrochloride (BIM‐46187; Millipore, Billerica, MA, USA); ( RS )‐α‐methyl‐4‐carboxyphenylglycine (MCPG; Tocris Bioscience); N ‐[(3 R )‐3‐([1,1′‐biphenyl]‐4‐yloxy)‐3‐(4‐fluorophenyl)propyl]‐ N ‐methylglycine hydrochloride (ALX 5407; Tocris Bioscience); dl ‐threo‐β‐benzyloxyaspartic acid ( dl ‐TBOA; Tocris Bioscience); α‐(4‐hydroxyphenyl)‐β‐methyl‐4‐benzyl‐1‐piperidineethanol (+)‐tartrate salt (ifenprodil; Sigma‐Aldrich; Merck KGaA); 3‐chloro‐4‐fluoro‐ N ‐[4‐[[2‐(phenylcarbonyl)hydrazino]carbonyl]benzyl]benzenesulfonamide(TCN 201; Tocris Bioscience); and 1‐[3‐(dimethylamino)propyl]‐1‐(4‐fluorophenyl)‐1,3‐dihydroisobenzofuran‐5‐carbonitrile hydrobromide (citalopram; Tokyo Chemical Industry Co., Ltd., Tokyo, Japan).
Techniques: Membrane