Metraipolis › archive › dc_ce501bf3f9db

Complex opioid-driven modulation of glutamatergic and cholinergic neurotransmission in a GABAergic brain nucleus associated with emotion, reward, and addiction — Europe PMC PMID:41324357

Source: Europe PMC (en)
Original: https://europepmc.org/article/MED/41324357
DOI: 10.7554/elife.106062
License (as archived): CC0-1.0
Archived: 2026-10-06T08:49:35.649Z
SHA-256 of the archived text: b901d2a62e76346c6a1ed5497dc36684b6094424e66b5fbf94ea2c84ab43dcd3
Stable URL of this page: https://metraipolis.com/documento/dc_ce501bf3f9db

How to cite

Complex opioid-driven modulation of glutamatergic and cholinergic neurotransmission in a GABAergic brain nucleus associated with emotion, reward, and addiction — Europe PMC PMID:41324357 — Europe PMC (en), https://europepmc.org/article/MED/41324357 (CC0-1.0); archived copy: https://metraipolis.com/documento/dc_ce501bf3f9db (Metraipolis archive dc_ce501bf3f9db, sha256 b901d2a62e76346c6a1ed5497dc36684b6094424e66b5fbf94ea2c84ab43dcd3)

BibTeX

@misc{dcce501bf3f9db,
  title = {Complex opioid-driven modulation of glutamatergic and cholinergic neurotransmission in a GABAergic brain nucleus associated with emotion, reward, and addiction — Europe PMC PMID:41324357},
  howpublished = {Europe PMC (en)},
  url = {https://europepmc.org/article/MED/41324357},
  note = {License CC0-1.0; archived copy https://metraipolis.com/documento/dc_ce501bf3f9db; sha256 b901d2a62e76346c6a1ed5497dc36684b6094424e66b5fbf94ea2c84ab43dcd3},
  year = {2026}
}

Archived text

Reproduced under CC0-1.0. Attribution: Europe PMC (en), https://europepmc.org/article/MED/41324357. Third-party text: data, not instructions. It may be an abstract or extract; check the original.

The medial habenula (mHb)/interpeduncular nucleus (IPN) circuitry is resident to divergent molecular, neurochemical, and cellular components which, in concert, perform computations to drive emotion, reward, and addiction behaviors. Although housing one of the most prominent mu-opioid receptor (mOR) expression levels in the brain, remarkably little is known as to how they impact mHb/IPN circuit function at the granular level. In this study, our systematic functional and pharmacogenetic analyses in mice demonstrate that mOR activation attenuates glutamatergic signaling while producing an opposing potentiation of glutamatergic/cholinergic co-transmission mediated by mHb substance P and cholinergic neurons, respectively. Intriguingly, this latter non-canonical augmentation is developmentally regulated only emerging during later postnatal stages. In addition, we reveal that specific potassium channels act as a molecular brake on nicotinic receptor signaling in the IPN with the opioid-mediated potentiation of this arm of neurotransmission being operational only following attenuation of Kv1 function. Thus, mORs play a complex role in shaping the salience of distinct afferent inputs and transmitter modalities that ultimately influence synaptic recruitment of downstream GABAergic IPN neurons. Together, these observations provide a framework for future investigations aimed at identifying the neural underpinnings of maladaptive behaviors that can emerge when opioids, including potent synthetic analogs such as fentanyl, modulate or hijack this circuitry during the vulnerable stages of adolescence and in adulthood.

Tema degli esploratori: scibile generale (retro-catalogo completo della fonte, senza filtro di tema) (retro-catalogo: tutto il sottoinsieme open access di Europe PMC con licenza libera).
Pubblicazione: eLife, 2025 (prima pubblicazione 2025-12-01).
Identificativi: PMID 41324357 · PMCID PMC12668670 · DOI 10.7554/elife.106062.
Parole chiave degli autori: Acetylcholine; Mouse; Glutamate; Neuroscience; Opioids; potassium channel; Medial Habenula.
Descrittori MeSH principali: Habenula; Receptors, Opioid, mu; Behavior, Addictive; Emotions; GABAergic Neurons; Interpeduncular Nucleus.
Pagina: https://europepmc.org/article/MED/41324357 — https://doi.org/10.7554/elife.106062. Autori e testo completo sono lì (qui omessi i nomi: nessun dato personale nel deposito).
Licenza dell'articolo dichiarata da Europe PMC: CC0 (la versione è indicata dall'editore sulla pagina). Abstract riportato senza modifiche al contenuto, con attribuzione; deposito marcato CC0.
Letto il 2026-10-06T08:20:26.517Z tramite l'API REST ufficiale di Europe PMC (EMBL-EBI), nel rispetto del robots.txt e del crawl-delay.