Abstract
On February 12th 1973, Bliss and Lomo submitted their findings on activity-dependent plasticity of glutamatergic synapses. After this groundbreaking discovery, long-term potentiation (LTP) and depression (LTD) gained center stage in the study of learning, memory, and experience-dependent refinement of neural circuits. While LTP and LTD are extensively studied and their relevance to brain function is widely accepted, new experimental and theoretical work recently demonstrates that brain development and function relies on additional forms of plasticity, some of which occur at nonglutamatergic synapses. The strength of GABAergic synapses is modulated by activity, and new functions for inhibitory synaptic plasticity are emerging. Together with excitatory neurons, inhibitory neurons shape the excitability and dynamic range of neural circuits. Thus, the understanding of inhibitory synaptic plasticity is crucial to fully comprehend the physiology of brain circuits. Here, I will review recent findings about plasticity at GABAergic synapses and discuss how it may contribute to circuit function.
Highlights
Bidirectional inhibitory plasticity was observed in many areas of the brain—neonatal hippocampus [2], deep cerebellar nuclei [3, 4], lateral superior olive [5], brain stem [6], and onto dopaminergic neurons in the ventral tegmental area (VTA) [7, 8]
There are significant differences in the induction and expression mechanisms of high-frequency long-term inhibitory plasticity (HF-long-term potentiation (LTPi) and HF-LTDi, Figure 1), some common features have been identified across several brain circuits
Postsynaptic activation of glutamatergic receptors is often required for the induction of HF-LTPi, while GABAA receptor activity is involved in maintaining the plasticity [1, 8]
Summary
Plasticity of GABAergic synapses onto excitatory neurons, in the form of long-term potentiation (LTPi) and/or depression (LTDi) of inhibitory postsynaptic potentials (IPSPs), was initially reported in layer 5 of the rodent primary visual cortex [1]. A second widely investigated form of heterosynaptic LTDi is induced by low-frequency (LF) activation of glutamatergic axons, which can heterosynaptically depress GABAergic inputs converging onto the activated postsynaptic neuron (LF-LTDi or I-LTD, Figure 1(b)) [23] This form of plasticity has been reported in several areas of the brain including VTA [24], basolateral amygdala (BLA) [25], dorsal striatum [26], prefrontal cortex [27], and corticotectal cocultures [28]. ECBI-LTD may contribute to the integration of local associative inputs elicited by long-lasting presynaptic activity in the lowfrequency range
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
