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Related Concept Videos

Excitatory and Inhibitory Effects of Neurotransmitters01:29

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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...
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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...
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γ-aminobutyric acid or GABA, plays a pivotal role as an inhibitory neurotransmitter in the brain. GABA pathway potentiators, also known as GABAergic drugs, are a class of pharmaceutical agents designed to enhance the functioning of the GABAergic system. These medications primarily treat epilepsy, a neurological disorder characterized by recurrent seizures.
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Depolarizing Blockers: Mechanism of Action01:28

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Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
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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.
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Integration of Synaptic Events01:28

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Synaptic integration mainly includes the summation of graded potentials. Graded potentials, regardless of their type, cause subtle alterations in membrane voltage, resulting in either depolarization or hyperpolarization. These incremental changes, when combined or summed, can propel the neuron toward its threshold. Consider, for example, a membrane experiencing a +15 mV shift, causing it to depolarize from -70 mV to -55 mV. In this scenario, graded potentials govern the membrane's ability to...
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Related Experiment Video

Updated: Oct 10, 2025

Inhibitory Synapse Formation in a Co-culture Model Incorporating GABAergic Medium Spiny Neurons and HEK293 Cells Stably Expressing GABAA Receptors
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When Are Depolarizing GABAergic Responses Excitatory?

Werner Kilb1

  • 1Institute of Physiology, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.

Frontiers in Molecular Neuroscience
|December 13, 2021
PubMed
Summary
This summary is machine-generated.

Even when GABAergic responses depolarize neurons, GABA can still inhibit. This occurs because GABA receptors reduce neuronal input resistance, shunting excitatory signals, particularly during development.

Keywords:
KCC2NKCC1SLC12A2SLC12A5chloride homeostasisgaba receptorneuronal development

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Area of Science:

  • Neuroscience
  • Cellular Neuroscience
  • Developmental Neuroscience

Background:

  • Intracellular chloride concentration ([Cl-]i) dictates GABA(A) receptor responses.
  • During development and in pathophysiology, NKCC1 and KCC2 transporter expression leads to elevated [Cl-]i and depolarizing GABAergic responses.
  • Depolarizing GABAergic responses are not inherently excitatory due to shunting inhibition.

Purpose of the Study:

  • To review the effects of depolarizing GABA responses on neuronal excitability.
  • To explore the interplay between GABA conductances, reversal potential, and neuronal excitability.
  • To summarize evidence on GABA's role as an excitatory or inhibitory neurotransmitter during early development.

Main Methods:

  • Theoretical considerations of GABAergic signaling.
  • Analysis of experimental studies on GABAergic and glutamatergic interactions.
  • Review of in vitro and in vivo investigations into GABA's function.

Main Results:

  • GABA conductances and reversal potential influence neuronal excitability.
  • Complex spatiotemporal interactions exist between depolarizing GABAergic and glutamatergic inputs.
  • Mechanisms beyond transporter expression affect intracellular chloride levels.

Conclusions:

  • GABA can function as an inhibitory neurotransmitter despite causing depolarizing membrane responses.
  • Neuronal excitability is modulated by shunting inhibition from GABA(A) receptors.
  • GABA's inhibitory role is maintained even with elevated intracellular chloride concentrations.