First-pass extracted concept

GABAergic signaling

Candidate: concept label2 source documents4 linked claims

Jump to explainers Jump to evidence Jump to sources Jump to claims

Live refresh every 5sNext refresh in 5s

Extracted Explainers

What the tool is doing

GABAergic signaling is presented as a relevant component of local prefrontal circuitry involved in affective pain processing.

Source 1DOI PubMed

The review presents GABAergic signaling as a key regulator of neuronal circuit building and refinement during development. It is discussed as a mechanism whose disruption can alter network excitatory/inhibitory balance in ASD.

Source 2DOI PubMed

What problem it solves

It identifies inhibitory signaling as a mechanistic theme for chronic pain-associated mPFC dysfunction.

Source 1DOI PubMed

This concept helps explain how early developmental signaling abnormalities could propagate into circuit-level dysfunction associated with autism.

Source 2DOI PubMed

What it does not solve

The abstract does not specify which GABAergic cells, receptors, or interventions should be used.

Source 1DOI PubMed

The abstract does not present GABAergic signaling as a discrete intervention, assay, or engineered tool.

Source 2DOI PubMed

Alternatives

The abstract contrasts this mechanism with neuroligin-neurexin-mediated transsynaptic regulation as another route to E/I imbalance.

Source 2DOI PubMed

Evidence Snippets

A multitude of neurotransmitter systems contributes to the fine-tuning of the local circuitry, of which cholinergic and GABAergic signaling are particularly emerging as relevant components of affective pain processing within the prefrontal cortex.

Evidence 1Source 1DOI PubMedprovenance

Here, we summarize recent data concerning the functional role of GABA in building up and refining neuronal circuits early in development and the molecular mechanisms regulating the E/I balance.

Evidence 2Source 2DOI PubMedprovenance

Supporting Sources

Source 1review2020International Journal of Molecular SciencesDOI PubMed

1 evidence snippet 1 linked claim Claim 1

Source 2review2011Neural PlasticityDOI PubMed

1 evidence snippet 3 linked claims Claim 1 Claim 2 Claim 3

Linked Claims

Claim 1mechanism summarysupports2020Source 1DOI PubMed

Cholinergic and GABAergic signaling are emerging as relevant components of affective pain processing within the prefrontal cortex.

Quoted textsource-backed

cholinergic and GABAergic signaling are particularly emerging as relevant components of affective pain processing within the prefrontal cortex

Claim 2developmental mechanismsupports2011Source 2DOI PubMed

During late embryonic and early postnatal stages, GABA can depolarize and excite target cells through outwardly directed chloride flux.

Quoted textsource-backed

GABA, the main inhibitory neurotransmitter in adult life, at late embryonic/early postnatal stages has been shown to depolarize and excite targeted cell through an outwardly directed flux of chloride.

Claim 3developmental role summarysupports2011Source 2DOI PubMed

Depolarizing GABA action and associated calcium influx regulate developmental processes including cell migration, differentiation, and synapse formation.

Quoted textsource-backed

The depolarizing action of GABA and associated calcium influx regulate a variety of developmental processes from cell migration and differentiation to synapse formation.

Claim 4disease model summarysupports2011Source 2DOI PubMed

Early developmental dysfunction of GABAergic signaling can lead to severe excitatory/inhibitory imbalance in neuronal circuits that may account for some behavioral deficits observed in ASD patients.

Quoted textsource-backed

A dysfunction of the GABAergic signaling early in development leads to a severe E/I unbalance in neuronal circuits, a condition that may account for some of the behavioral deficits observed in ASD patients.