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Related Concept Videos

G-Protein Gated Ion Channels01:21

G-Protein Gated Ion Channels

GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory organs,...
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
The Role of Ion Channels in Neuronal Computation01:19

The Role of Ion Channels in Neuronal Computation

A postsynaptic neuron usually receives numerous impulses from several other presynaptic neurons. The axon hillock of the postsynaptic neuron integrates all these signals and determines the likelihood of firing an action potential.
Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron. However, multiple presynaptic inputs must often create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential.
Excitatory and Inhibitory Effects of Neurotransmitters01:29

Excitatory and Inhibitory Effects of Neurotransmitters

When an action potential reaches the presynaptic axon terminal, it releases neurotransmitters from the neuron into the synaptic cleft at a chemical synapse. The released neurotransmitter can be excitatory or inhibitory. The critical criteria commonly used to determine whether a molecule is a neurotransmitter at a chemical synapse are the molecule's presence in the presynaptic neuron. Second, its release is in response to strong presynaptic depolarization. And lastly, the presence of specific...
Non-gated Ion Channels01:24

Non-gated Ion Channels

Ion channels are specialized proteins on the plasma membrane that allow charged ions to pass down their electrochemical gradient. Their main function is to maintain the membrane potential which is critical for cell viability. These channels are either gated or non-gated and can transport more than a thousand ions within milliseconds for the cellular event to occur.
Compared to the gated ion channels, the non-gated channels, also known as leakage or passive channels, have no gating mechanism.
Non-gated Ion Channels01:24

Non-gated Ion Channels

Ion channels are specialized proteins on the plasma membrane that allow charged ions to pass down their electrochemical gradient. Their main function is to maintain the membrane potential which is critical for cell viability. These channels are either gated or non-gated and can transport more than a thousand ions within milliseconds for the cellular event to occur.
Compared to the gated ion channels, the non-gated channels, also known as leakage or passive channels, have no gating mechanism.

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Related Experiment Video

Updated: May 27, 2026

Study of the Functions and Activities of Neuronal K-Cl Co-Transporter KCC2 Using Western Blotting
10:08

Study of the Functions and Activities of Neuronal K-Cl Co-Transporter KCC2 Using Western Blotting

Published on: December 9, 2022

Hyperpolarizing GABAergic transmission depends on KCC2 function and membrane potential.

Tarek Z Deeb1, Henry H C Lee, Joshua A Walker

  • 1Tufts University, Boston, MA, USA.

Channels (Austin, Tex.)
|November 16, 2011
PubMed
Summary
This summary is machine-generated.

Glutamate impairs KCC2, altering GABA responses from inhibitory to excitatory. This shift, driven by chloride loading via GABA(A) receptors, increases neuronal excitability, impacting neurological conditions.

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Inhibitory Synapse Formation in a Co-culture Model Incorporating GABAergic Medium Spiny Neurons and HEK293 Cells Stably Expressing GABAA Receptors
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Inhibitory Synapse Formation in a Co-culture Model Incorporating GABAergic Medium Spiny Neurons and HEK293 Cells Stably Expressing GABAA Receptors

Published on: November 14, 2014

Whole-cell Currents Induced by Puff Application of GABA in Brain Slices
07:32

Whole-cell Currents Induced by Puff Application of GABA in Brain Slices

Published on: October 12, 2017

Related Experiment Videos

Last Updated: May 27, 2026

Study of the Functions and Activities of Neuronal K-Cl Co-Transporter KCC2 Using Western Blotting
10:08

Study of the Functions and Activities of Neuronal K-Cl Co-Transporter KCC2 Using Western Blotting

Published on: December 9, 2022

Inhibitory Synapse Formation in a Co-culture Model Incorporating GABAergic Medium Spiny Neurons and HEK293 Cells Stably Expressing GABAA Receptors
07:51

Inhibitory Synapse Formation in a Co-culture Model Incorporating GABAergic Medium Spiny Neurons and HEK293 Cells Stably Expressing GABAA Receptors

Published on: November 14, 2014

Whole-cell Currents Induced by Puff Application of GABA in Brain Slices
07:32

Whole-cell Currents Induced by Puff Application of GABA in Brain Slices

Published on: October 12, 2017

Area of Science:

  • Neuroscience
  • Cellular Biology
  • Physiology

Background:

  • Potassium-chloride cotransporter 2 (KCC2) is crucial for neuronal inhibition via hyperpolarizing GABAergic transmission.
  • Glutamate exposure has been shown to impair KCC2 function through phosphorylation, leading to excitatory GABA responses.

Purpose of the Study:

  • To investigate methods for estimating changes in the GABA reversal potential (E(GABA)).
  • To characterize the mechanisms underlying depolarizing GABA responses and their impact on neuronal excitability.
  • To explore the role of tonic inhibition in facilitating depolarizing GABA responses.

Main Methods:

  • Utilized current-clamp recordings of membrane potential responses to GABA to determine E(GABA) limits.
  • Analyzed the contribution of persistently active GABA(A) receptors to chloride loading during glutamate exposure.
  • Investigated the interplay between hyperpolarizing GABA responses and afterhyperpolarizations.

Main Results:

  • Established current-clamp recordings as a viable method for quantifying E(GABA) shifts.
  • Demonstrated that depolarizing GABA responses can both excite and inhibit neurons.
  • Identified tonic inhibition via GABA(A) receptors as a facilitator of depolarizing GABA responses and increased excitability.
  • Observed transient shifts from hyperpolarizing to depolarizing GABA responses coinciding with afterhyperpolarizations.

Conclusions:

  • KCC2 dysfunction and subsequent depolarizing GABA responses contribute to increased neuronal excitability, particularly after pathophysiological insults.
  • Tonic inhibition plays a significant role in chloride loading and the development of excitatory GABAergic signaling.
  • Understanding these mechanisms is critical for developing therapeutic strategies targeting neurological disorders involving altered GABAergic signaling.