rabbit polyclonal antibodies for trpc5  (Millipore)

Journal: International Journal of Molecular Sciences

Article Title: Effects of Transient Receptor Potential Cation 5 (TRPC5) Inhibitor, NU6027, on Hippocampal Neuronal Death after Traumatic Brain Injury

doi: 10.3390/ijms21218256

Figure Lengend Snippet: ( A ) Fluorescent images show that the TRPC5 channel expression level was detected by TRPC5 (TRPC5, red color) and counter-staining with neuronal nuclei (NeuN, green color) from the hippocampal CA3 region 24 h after TBI. NU6027 (1 mg/kg) administration after TBI at 24 h decreased a channel expression in the hippocampal CA3 region via inhibition of the TRPC5 channel. ( B ) The intensity of TRPC5 channel expression in the hippocampal CA3 region. The fluorescence intensity displayed a significant difference between groups (sham-vehicle, n = 5; sham-NU6027, n = 5; TBI-vehicle, n = 6; TBI-NU6027, n = 6). Data are mean ± S.E.M. * Significantly different from the vehicle-treated group, p < 0.05. Scale bar = 100 μm.

Article Snippet: After this, tissues were soaked in a PBS containing 0.3% TritonX-100 with polyclonal rabbit anti- TRPC5 serum (diluted 1:200, Alomone Laboratories, Jerusalem, Israel) overnight in an incubator at 4 °C.

Techniques: Expressing, Staining, Inhibition, Fluorescence

Journal: International Journal of Molecular Sciences

Article Title: Effects of Transient Receptor Potential Cation 5 (TRPC5) Inhibitor, NU6027, on Hippocampal Neuronal Death after Traumatic Brain Injury

doi: 10.3390/ijms21218256

Figure Lengend Snippet: When TBI occurs, edema is caused by a primary inflammatory reaction and the secondary injury oxidative stress occurs, which results in the activation of astrocyte and microglia, loss of many microtubules, and the accumulation of zinc in the neuron. ( A ) (1) Vesicular zinc is released from the presynaptic neuron by TBI , and the released vesicular zinc enters the neuron through the TRPC5 channel ; (2) NADPH oxidase is activated by vesicular zinc entering the neuron [ , ]; (3) oxidative stress is increased by NADPH oxidase activated by vesicular zinc [ , , , ] and excessive free zinc is released into the neuron due to oxidative stress [ , , ]; (4) TRPC5 channels are activated by the accumulated free zinc and the excess free zinc released causes injury to neurons ; (5) zinc and calcium influx due to the activated TRPC5 channel [ , ]; (6) neuronal death occurs. ( B ) (1) Vesicular zinc is released from the presynaptic neuron by TBI ; (2) NU6027 is injected immediately after TBI; (3) NU6027 prevents the entrance of vesicular zinc from the TRPC5 channel, thus reducing NADPH oxidase activation and NU6027 also reduces the H 2 O 2 , reducing oxidative stress ; (4) oxidative stress is reduced by NU6027, thereby reducing the accumulation of free zinc ; (5) the TRPC5 channel is inhibited by the inhibitor NU6027 and there is a reduction of zinc accumulation in neurons ; (6) inhibition of the TRPC5 channel reduces the influx of calcium and zinc; (7) neuron death is limited.

Article Snippet: After this, tissues were soaked in a PBS containing 0.3% TritonX-100 with polyclonal rabbit anti- TRPC5 serum (diluted 1:200, Alomone Laboratories, Jerusalem, Israel) overnight in an incubator at 4 °C.

Techniques: Activation Assay, Injection, Inhibition