Commentary - Neurophysiology Research (2023) Volume 5, Issue 2

Balancing Excitation and Inhibition: Inhibitory Postsynaptic Potentials in the Brain

Department of Neuroscience, Physiology & Pharmacology University, UCL, Gower Street, London, UK

*Corresponding Author:

Jack Michael
Department of Neuroscience
Physiology & Pharmacology University
UCL, Gower Street, London, UK
E-mail: michaeljack@ucl.ac.uk

Received: 03-Apr-2023, Manuscript No. AANR-23-96224; Editor assigned: 07-Apr-2023, PreQC No. AANR-23-96224(PQ); Reviewed: 221-Apr-2023, QC No. AANR-23-96224; Revised: 25-Apr-2023, Manuscript No. AANR-23-96224(R); Published: 28-Apr-2023, DOI: 10.35841/aanr-5.2.145

Citation: Michael J. Balancing excitation and inhibition: inhibitory postsynaptic potentials in the brain. Neurophysiol Res. 2023;5(2):145

Abstract

 An inhibitory postsynaptic potential (IPSP) is a type of electrical potential change that occurs in the postsynaptic neuron in response to the release of neurotransmitters by the presynaptic neuron. IPSPs result in a hyperpolarization of the postsynaptic neuron, making it less likely to fire an action potential and reducing its excitability.

Keywords

Neurotransmitters, Gamma-amino butyric acid, Inhibitory postsynaptic potential, Hyperpolarization, Nervous system.

Introduction

The primary cause of an IPSP is the binding of inhibitory neurotransmitters, such as gamma-amino butyric acid (GABA) or glycine, to their respective receptors on the postsynaptic neuron. These inhibitory neurotransmitters are released by the presynaptic neuron and bind to receptors on the postsynaptic neuron's membrane, leading to an influx of negatively charged ions, such as chloride (Cl-) or potassium (K+), or an efflux of positively charged ions, such as potassium (K+). This influx or efflux of ions causes the postsynaptic neuron's membrane potential to become more negative, resulting in hyperpolarization and making it less likely for the neuron to generate an action potential [1].

IPSPs play a crucial role in shaping the overall electrical activity of neural circuits and contribute to the fine-tuning of neuronal signaling and information processing in the brain. They work in concert with excitatory postsynaptic potentials (EPSPs), which result in depolarization of the postsynaptic neuron and increase its excitability, to modulate the overall activity and output of neural networks. The balance between IPSPs and EPSPs in a neuron's synaptic inputs determines its overall firing rate and output, which is critical for proper functioning of the nervous system. Inhibitory postsynaptic potentials (IPSPs) are crucial for the proper functioning of the central nervous system (CNS) as they help regulate neural activity and maintain the balance between excitation and inhibition. IPSPs are localized changes in the electrical potential of a postsynaptic neuron that occur when inhibitory neurotransmitters bind to their receptors on the postsynaptic membrane. IPSPs play a significant role in shaping neuronal output, modulating synaptic transmission, and regulating overall circuit activity [2].

Hyperpolarization: The binding of inhibitory neurotransmitters, such as gamma-aminobutyric acid (GABA) or glycine, to their respective receptors on the postsynaptic neuron leads to an increase in chloride (Cl-) or potassium (K+) conductance, resulting in an efflux of positive ions or an influx of negative ions, respectively. This causes the postsynaptic membrane to become more negative, leading to hyperpolarization, or a decrease in the neuron's membrane potential, making it less likely to generate an action potential.

Shunting Inhibition: IPSPs can also be generated by shunting inhibition, which occurs when the opening of inhibitory ion channels creates a conductance pathway that shunts, or bypasses, the excitatory current generated by other synapses. This effectively reduces the effectiveness of excitatory inputs, limiting the depolarization of the postsynaptic neuron and reducing the probability of generating an action potential [3].

Presynaptic Inhibition: In addition to postsynaptic mechanisms, IPSPs can also be regulated presynaptically. Presynaptic inhibition occurs when an inhibitory neuron releases inhibitory neurotransmitters onto the presynaptic terminal of an excitatory synapse, reducing the release of excitatory neurotransmitters from the presynaptic neuron. This can effectively decrease the strength of the excitatory input onto the postsynaptic neuron, leading to a reduction in the amplitude of IPSPs [4].

Neuromodulator: IPSPs can also be modulated by neuromodulators, which are chemical messengers that regulate the strength of synaptic transmission. Neuromodulators can influence the activity of inhibitory neurotransmitters, receptors, or ion channels, altering the properties of IPSPs. For example, the release of neuromodulators such as serotonin, dopamine, or norepinephrine can modulate the strength of IPSPs, affecting the overall inhibitory tone in a neural circuit [5].

Conclusion

In summary, IPSPs are critical for regulating neural activity in the CNS, and their mechanisms and regulation involve hyperpolarization through changes in ion conductance, shunting inhibition, presynaptic inhibition, and modulation by neuromodulators. Understanding the mechanisms and regulation of IPSPs is fundamental to our understanding of how the CNS maintains the balance between excitation and inhibition, and how it processes information and generates complex behaviours.

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