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Published on: February 15, 2017
Accommodation enhances depolarizing inhibition in central neurons
1Graduate Program in Neurobiology and Behavior and Virginia Merrill Bloedel Hearing Research Center, University of Washington, Seattle, Washington 98195, USA.
Summary
In avian cochlear nucleus neurons, inhibitory GABAergic inputs depolarize cells. This surprising finding reveals that depolarizing inhibitory postsynaptic potentials (dIPSPs) enhance inhibition by shifting spike threshold.
Area of Science:
- Neuroscience
- Auditory Neuroscience
- Synaptic Plasticity
Background:
- Neurons in the avian cochlear nucleus receive GABAergic synaptic input.
- Typically, inhibitory inputs hyperpolarize neurons, moving them away from spike threshold.
Purpose of the Study:
- To investigate the nature and function of GABAergic synaptic input in avian cochlear nucleus neurons.
- To determine the reversal potential (V(rev)) of GABAergic currents and its relation to spike threshold.
Main Methods:
- Gramicidin-perforated-patch recordings to measure GABAergic synaptic currents.
- Experimental manipulation to assess the impact of inhibitory postsynaptic potentials (IPSPs) on neuronal excitability.
Main Results:
- GABAergic synaptic input resulted in a depolarized reversal potential (V(rev)) relative to spike threshold.
- Depolarizing IPSPs (dIPSPs) were observed, kept below spike threshold by a dendrotoxin-I-sensitive, voltage-gated K+ conductance.
- dIPSPs were found to be more inhibitory than hyperpolarizing IPSPs due to induced accommodation and a positive shift in spike threshold.
Conclusions:
- Depolarizing GABAergic inputs can function as a potent inhibitory mechanism in neurons.
- This inhibitory mechanism, involving dIPSPs and voltage-gated K+ conductances, may amplify inhibition when excitatory conductances are large.
- Similar mechanisms may exist in other neuronal systems, suggesting a general principle for enhancing inhibition.
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