Biology subjects

Courtemanche, R.

Publications and source records attributed to Courtemanche, R..

3 recordsLinked to original sources

bioRxiv2026

A Preventive Effect of Exercise in a Mouse Model of Essential Tremor

The effects of exercise have not been widely studied for potential benefits in essential tremor (ET), while this has been growing for other neurodegenerative disorders. This study examines the effects of two types of exercise [high-intensity interval training (HIIT) and resistance training (RT)] on mice that were subjected to harmaline injections to trigger tremor. We employed a repeated-measures design with three groups: a HIIT group, a RT group, and a sedentary (SED) control group. Each group received an injection before and after the intervention. Tremor kinetics (power within the 8-14 and 14-29 Hz bands) were assessed using accelerometry. Tremor kinematics were also assessed using high-speed video analysis, for validation. As potential signalling molecules from exercise, we also tested for blood lactate and BDNF in each group. Compared to pre-intervention measurements, we found a significant decrease in power within the 8-14 Hz band combined with an increase in the 14-29 Hz band, for the HIIT group, but not in the RT or SED groups. We also found a change in BDNF concentration for the HIIT group. These results suggest that the HIIT protocol may have helped the animal to shift tremor frequency to higher bands, thereby offering functional resistance to harmaline-induced tremor. This study supports high intensity aerobic physical exercise as a potential therapeutic/preventive intervention for ET, with translational implications for human studies.

neuroscience↗

bioRxiv2026

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

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.

neuroscience↗

bioRxiv2026

Region-specific Bmal1 deletion in the dorsal striatum alters alcohol consumption in a sex-specific manner

BackgroundCircadian disruption is strongly associated with alcohol use disorder (AUD), but insight into the underlying brain-region and sex-specific mechanisms is limited. The function of the circadian clock gene Bmal1 within the striatum has been linked to alcohol drinking, yet its role within functionally distinct striatal subregions has not been systematically examined. MethodsWe deleted Bmal1 in medium spiny neurons of the dorsomedial striatum (DMS) or dorsolateral striatum (DLS). Male and female mice were tested for anxiety-like behavior, depressive-like behavior, and motor coordination. Voluntary alcohol intake was measured with an intermittent two-bottle choice paradigm, followed by sucrose preference and quinine-adulterated alcohol tests. To assess hormonal contributions, a subset of female mice underwent ovariectomy before behavioral testing. ResultsDeletion of Bmal1 in the DLS did not alter alcohol intake, alcohol preference, or quinine-adulterated alcohol intake in either sex. In contrast, DMS Bmal1 deletion significantly reduced alcohol consumption and alcohol preference in female mice, with no effect in males. These effects were not accompanied by changes in depressive-like behavior or motor coordination and were not explained by generalized reward changes, as sucrose preference was unaffected. Ovariectomy eliminated the effect of DMS Bmal1 deletion on alcohol intake, indicating dependence on ovarian hormones. ConclusionsThe DMS is a critical site at which Bmal1 regulates alcohol consumption in a sex-specific manner. These findings support an interaction between local circadian mechanisms and ovarian hormones in controlling alcohol drinking and highlight a potential target for sex-specific therapeutics in AUD.

neuroscience↗