First-pass extracted concept

optogenetic activation

Candidate: concept label4 source documents5 linked claims
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Evidence Snippets

The functional role of the CeA in feeding regulation was examined using chemogenetic and optogenetic activation.
Evidence 1Source 1DOIPubMedprovenance
Further, we demonstrate that optogenetic activation of CIII md neurons evokes calcium increases in these neurons.
Evidence 2Source 2DOIPubMedprovenance
The abstract reports optogenetic activation of GABAergic LPBN neurons and optogenetic activation of glutamatergic LPBN neurons.
Evidence 3Source 3DOIPubMedprovenance
We show that optogenetic activation of these neurons is sufficient to induce CTA in the absence of anorexigenic substances
Evidence 4Source 4DOIPubMedprovenance

Supporting Sources

Source 1primary paper2026MEDDOIPubMed

Linked Claims

Claim 1activity readoutsupports2025Source 2DOIPubMed

Optogenetic activation of CIII md neurons evokes calcium increases in these neurons.

Claim 2coactivation effectsupports2025Source 2DOIPubMed

Co-activation of CIII md neurons with additional cell types facilitates larval contraction responses.

Claim 3causal perturbation effectsupports2020Source 3DOIPubMed

Optogenetic activation of GABAergic LPBN neurons alleviates neuropathic pain-like behavior without affecting basal nociception.

Claim 4causal perturbation effectsupports2020Source 3DOIPubMed

Optogenetic activation of glutamatergic LPBN neurons or inhibition of GABAergic LPBN neurons induces neuropathic pain-like behavior in naive mice.

Claim 5sufficiencysupports2015Source 4DOIPubMed

Optogenetic activation of PBel CGRP neurons is sufficient to induce conditioned taste aversion in mice in the absence of anorexigenic substances.

Quoted textsource-backed
We show that optogenetic activation of these neurons is sufficient to induce CTA in the absence of anorexigenic substances