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PreprintCC BY-NC-NDbioRxiv

Dorsomedial striatal Bmal1 deletion in medium spiny neurons alters EPSCs and dendritic morphology after chronic exposure to alcohol in female mice.

  • M. Darvishmolla
  • R. Courtemanche
  • S. Amir
  • A. Chapman1
  1. 1Concordia University
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Abstract

Circadian clock genes in the striatum modulate alcohol drinking behavior in female mice, but the underlying synaptic mechanisms remain unknown. Medium spiny neurons (MSNs) of the striatum express D1- or D2-type dopamine receptors, which are differentially modulated by alcohol. Here we used whole-cell patch-clamp recordings to examine how deletion of the clock gene Bmal1 affects spontaneous excitatory postsynaptic currents (sEPSCs) in electrophysiologically identified D1 and D2 neurons of the female mouse dorsomedial striatum (DMS). Prior intermittent access to alcohol increased sEPSC amplitude in putative D1 neurons of wildtype mice without affecting sEPSC frequency, and this increase was accompanied by greater dendritic branching and complexity in biocytin-filled D1 MSNs. Bmal1 knockout had the opposite effect in D1 neurons, reducing sEPSC amplitude in both alcohol-exposed and alcohol-naive animals. In D2 neurons, alcohol produced only a non-significant trend toward increased sEPSC amplitude in wildtype mice, but a significant increase in Bmal1 knockout mice. Thus, local disruption of Bmal1 appears to block the alcohol-induced enhancement of sEPSCs in D1 neurons while unmasking a similar enhancement in D2 neurons. These findings may help explain how Bmal1 deletion in the DMS reduces alcohol consumption in female mice.

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Cite

BibTeXRIS
BibTeX
@misc{darvishmolla2026dorsomedial,
  title = {{Dorsomedial striatal Bmal1 deletion in medium spiny neurons alters EPSCs and dendritic morphology after chronic exposure to alcohol in female mice.}},
  author = {M. Darvishmolla and R. Courtemanche and S. Amir and A. Chapman},
  howpublished = {bioRxiv},
  year = {2026},
  month = oct,
  doi = {10.64898/2026.10.03.753483},
  url = {https://www.biorxiv.org/content/10.64898/2026.10.03.753483v1},
  note = {CC BY-NC-ND},
}
RIS
TY  - UNPB
TI  - Dorsomedial striatal Bmal1 deletion in medium spiny neurons alters EPSCs and dendritic morphology after chronic exposure to alcohol in female mice.
AU  - M. Darvishmolla
AU  - R. Courtemanche
AU  - S. Amir
AU  - A. Chapman
PY  - 2026
DA  - 2026/10/03
PB  - bioRxiv
DO  - 10.64898/2026.10.03.753483
UR  - https://www.biorxiv.org/content/10.64898/2026.10.03.753483v1
AB  - Circadian clock genes in the striatum modulate alcohol drinking behavior in female mice, but the underlying synaptic mechanisms remain unknown. Medium spiny neurons (MSNs) of the striatum express D1- or D2-type dopamine receptors, which are differentially modulated by alcohol. Here we used whole-cell patch-clamp recordings to examine how deletion of the clock gene Bmal1 affects spontaneous excitatory postsynaptic currents (sEPSCs) in electrophysiologically identified D1 and D2 neurons of the female mouse dorsomedial striatum (DMS). Prior intermittent access to alcohol increased sEPSC amplitude in putative D1 neurons of wildtype mice without affecting sEPSC frequency, and this increase was accompanied by greater dendritic branching and complexity in biocytin-filled D1 MSNs. Bmal1 knockout had the opposite effect in D1 neurons, reducing sEPSC amplitude in both alcohol-exposed and alcohol-naive animals. In D2 neurons, alcohol produced only a non-significant trend toward increased sEPSC amplitude in wildtype mice, but a significant increase in Bmal1 knockout mice. Thus, local disruption of Bmal1 appears to block the alcohol-induced enhancement of sEPSCs in D1 neurons while unmasking a similar enhancement in D2 neurons. These findings may help explain how Bmal1 deletion in the DMS reduces alcohol consumption in female mice.
ER  -