科研之友
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摘要
With oxygen deprivation, the mammalian brain undergoes hyperactivity and neuronal death while this does not occur in the anoxia-tolerant goldfish (Carassius auratus). Anoxic survival of the goldfish may rely on neuromodulatory mechanisms to suppress neuronal hyper-excitability. As gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the brain, we decided to investigate its potential role in suppressing the electrical activity of goldfish telencephalic neurons. Utilizing whole-cell patch-clamp recording, we recorded the electrical activities of both excitatory (pyramidal) and inhibitory (stellate) neurons. With anoxia, membrane potential (V-m) depolarized in both cell types from -72.2 mV to -57.7 mV and from -64.5 mV to -46.8 mV in pyramidal and stellate neurons, respectively. While pyramidal cells remained mostly quiescent, action potential frequency (AP(f)) of the stellate neurons increased 68-fold. Furthermore, the GABA(A) receptor reversal potential (E-GABA) was determined using the gramicidin perforated-patch-clamp method and found to be depolarizing in pyramidal (-53.8 mV) and stellate neurons (-42.1 mV). Although GABA was depolarizing, pyramidal neurons remained quiescent as E-GABA was below the action potential threshold (-36 mV pyramidal and -38 mV stellate neurons). Inhibition of GABA(A) receptors with gabazine reversed the anoxia-mediated response. While GABA(B) receptor inhibition alone did not affect the anoxic response, co-antagonism of GABA(A) and GABA(B) receptors (gabazine and CGP-55848) led to the generation of seizure-like activities in both neuron types. We conclude that with anoxia, V-m depolarizes towards E-GABA which increases AP(f) in stellate neurons and decreases AP(f) in pyramidal neurons, and that GABA plays an important role in the anoxia tolerance of goldfish brain.
- 出版日期2017-2-15
