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REVIEW: Mechanisms of Long-Term Plasticity of Hippocampal GABAergic Synapses

A. V. Rozov1,2, F. F. Valiullina1, and A. P. Bolshakov3,4*

1Kazan Federal University, OpenLab of Neurobiology, 420008 Kazan, Russia

2Division of Neuro- and Sensory Physiology, Institute of Physiology and Pathophysiology, Heidelberg University, 69120 Heidelberg, Germany

3Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, 117485 Moscow, Russia; E-mail: al230679@yandex.ru, ocrachek@yahoo.com

4Russian National Research Medical University, 117997 Moscow, Russia

* To whom correspondence should be addressed.

Received October 19, 2016; Revision received December 5, 2016
Long-term potentiation and depression of synaptic transmission have been considered as cellular mechanisms of memory in studies conducted in recent decades. These studies were predominantly focused on mechanisms underlying plasticity at excitatory synapses. Nevertheless, normal central nervous system functioning requires maintenance of a balance between inhibition and excitation, suggesting existence of similar modulation of glutamatergic and GABAergic synapses. Here we review the involvement of G-protein-coupled receptors in the generation of long-term changes in synaptic transmission of inhibitory synapses. We considered the role of endocannabinoid and glutamate systems, GABAB and opioid receptors in the induction of long-term potentiation and long-term depression in inhibitory synapses. The pre- and postsynaptic effects of activation of these receptors are also discussed.
KEY WORDS: long-term synaptic plasticity, GABAergic synapses, endocannabinoids, GABAB receptor, G-protein-coupled receptors, hippocampus, opioid receptors

DOI: 10.1134/S0006297917030038