Activity-Dependent Inhibitory Synaptic Plasticity Mediated by Chloride Regulation

Balena, Trevor; Acton, Brooke A.; Woodin, Melanie A.

doi:10.1007/978-1-4419-6978-1_10

Cited by 2 publications

(1 citation statement)

References 74 publications

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“…In adult hippocampal slices, when GABA is hyperpolarizing and exerts an inhibitory action, homosynaptic plasticity of GABAergic synapses is successfully induced when presynaptic action potentials are elicited at inhibitory axons coincidentally with the generation of postsynaptic action potentials in CA1 pyramidal neurons (STD-long-term depression of inhibition, STD-LTDi: Figure 2(a) , right panel) [ 33 , 39 – 41 ]. STD-LTDi induction depends on postsynaptic Ca 2+ influx through voltage-gated Ca 2+ channels and on the depolarization of the equilibrium potential for chloride by the neuron-specific chloride extruding transporter KCC2 [ 33 ] ( Figure 2(a) , right panel).…”

Section: Homosynaptic Inhibitory Plasticitymentioning

confidence: 99%

The Many Forms and Functions of Long Term Plasticity at GABAergic Synapses

Maffei

2011

Neural Plasticity

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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.

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Section: Homosynaptic Inhibitory Plasticitymentioning

confidence: 99%

The Many Forms and Functions of Long Term Plasticity at GABAergic Synapses

Maffei

2011

Neural Plasticity

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Chloride transporters controlling neuronal excitability

Pressey

Saint-Rome

Raveendran

et al. 2023

Physiological Reviews

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Synaptic inhibition plays a crucial role in regulating neuronal excitability, which is the foundation of nervous system function. This inhibition is largely mediated by the neurotransmitters GABA and glycine that activate Cl--permeable ion channels, which means that the strength of inhibition depends on the Cl- gradient across the membrane. In neurons, the Cl- gradient is primarily determined by two secondarily-active cation-chloride cotransporters (CCCs), NKCC1 and KCC2. CCC-mediated regulation of the neuronal Cl- gradient is critical for healthy brain function, as dysregulation of CCCs has emerged as a key mechanism underlying neurological disorders including epilepsy, neuropathic pain, and autism spectrum disorder. This Review begins with an overview of neuronal chloride transporters before explaining the dependent relationship between these CCCs, Cl- regulation, and inhibitory synaptic transmission. We then discuss the evidence for how CCCs can be regulated, including by activity and their protein interactions, which underlie inhibitory synaptic plasticity. For readers who may be interested in conducting experiments on CCCs and neuronal excitability, we have included a section on techniques for estimating and recording intracellular Cl-, including their advantages and limitations. While the focus of this Review is on neurons, we also examine how Cl- is regulated in glial cells, which in turn regulate neuronal excitability through the tight relationship between this non-neuronal cell type and synapses. Lastly, we discuss the relatively extensive and growing literature on how CCC-mediated neuronal excitability contributes to neurological disorders.

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Activity-Dependent Inhibitory Synaptic Plasticity Mediated by Chloride Regulation

Cited by 2 publications

References 74 publications

The Many Forms and Functions of Long Term Plasticity at GABAergic Synapses

The Many Forms and Functions of Long Term Plasticity at GABAergic Synapses

Chloride transporters controlling neuronal excitability

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