Transient gain adjustment in the inferior colliculus is serotonin- and calcium-dependent.

摘要: In the inferior colliculus (IC), a brief period of acoustic conditioning can transiently enhance evoked discharge rate. The cellular basis this phenomenon was assessed with whole cell current-clamp recordings in gerbil IC brain slice preparation. current needed to elicit single action potential first established for each neuron. A 5s synaptic stimulus train delivered lateral lemniscus (LL), and followed immediately by initial pulse assess change postsynaptic gain. majority neurons (66%) displayed an increase current-evoked potentials (Positive Gain). Despite blockade ionotropic glutamate receptors, effect correlated membrane depolarization that occurred during train. mechanism positive gain examined selective specific neurotransmitter receptors. Gain enhanced antagonists metabotropic glutamate, acetylcholine, GABAA glycine contrast, blocked or reduced antagonist serotonin receptors (5-HT3R). Blocking voltage-activated calcium channels verapamil also effect. These results suggest 5-HT3R activation, coupled increased intracellular calcium, alter excitability neurons.