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Gravel-Chouinard, A.

Publications and source records attributed to Gravel-Chouinard, A..

2 recordsLinked to original sources

Assessing accelerometry as an alternative to electromyography for mouse sleep scoring

For sleep scoring in rodents, the use of electromyography (EMG) is considered the gold standard to assess muscle tone; however, EMG electrodes require invasive surgical implantation, are sensitive to muscular placement, can have extensive noise due to non-muscular signal contamination, and are at risk of failure due to mechanical stress. The use of an accelerometer (Acc) integrated on the recording headstage offers an alternative for movement detection. However, the degree of agreement between these two approaches has never been systematically evaluated. To understand if these tools allow similar scoring outcomes, seven trained scorers manually classified mouse sleep recordings using hippocampal local field potential (LFP) together with EMG or Acc. When comparing scoring between EMG and Acc, overall epoch-by-epoch accuracy exceeded 90% with a kappa score above 0.8, indicating excellent agreement. However, Acc was found to under classify Wake by 4.92% while overclassifying NREM sleep by 3.29%, possibly reflecting a decreased sensitivity of Acc to subtle changes in muscle tone used in distinguishing Wake from NREM sleep. Comparing EMG and Acc signal for agreed epochs vs disagreed epochs revealed a weaker correlation between the two signals for disagreed epochs, especially for Wake and NREM, suggesting that disagreements reflected genuine signal differences rather than scorer subjectivity. These findings support LFP/Acc as a valid approach to sleep scoring, however, it is noted that Acc based scoring slightly underestimated Wake epochs, favoring NREM sleep, relative to traditional EMG approach.

neuroscience↗

Where and how does d-amphetamine act to reveal antipsychotic-induced dopamine supersensitivity in rats?

Antipsychotic treatment can produce a dopamine-supersensitive state, potentiating the response to dopamine receptor stimulation. In both schizophrenia patients and rats, this is linked to tolerance to ongoing antipsychotic treatment. In rodents, dopamine supersensitivity is often confirmed by an exaggerated psychomotor response to d-amphetamine after discontinuation of antipsychotic exposure. Here we examined in rats the dopaminergic mechanisms mediating this enhanced behavioural response, as this could uncover pathophysiological processes underlying the expression of antipsychotic-evoked dopamine supersensitivity. Rats received 0.5 mg/kg/day haloperidol via osmotic minipump for 2 weeks, before treatment was discontinued. After cessation of antipsychotic treatment, rats showed a supersensitive psychomotor response to the D2 agonist quinpirole, but not to the D1 partial agonist SKF38393 or the dopamine reuptake blocker GBR12783. Furthermore, acute D1 receptor blockade (using SCH39166) decreased the exaggerated psychomotor response to d-amphetamine in haloperidol-pretreated rats, whereas acute D2 receptor blockade (using sulpiride) enhanced it. Thus, after discontinuation of antipsychotic treatment, D1- and D2-mediated transmission differentially modulate the expression of a supersensitive response to d-amphetamine. This supersensitive behavioural response was accompanied by enhanced GSK3{beta} activity and suppressed ERK1/2 activity in the nucleus accumbens (but not caudate-putamen), suggesting increased mesolimbic D2 transmission. Finally, after discontinuing haloperidol treatment, neither increasing ventral midbrain dopamine impulse flow nor infusing d-amphetamine into the cerebral ventricles triggered the expression of already established antipsychotic-evoked dopamine supersensitivity, suggesting that peripheral effects are required. Thus, while dopamine receptor-mediated signalling regulates the expression of antipsychotic-evoked dopamine supersensitivity, a simple increase in central dopamine neurotransmission is insufficient to trigger this supersensitivity. HIGHLIGHTSO_LIAntipsychotic exposure can lead to a state of dopamine (DA) supersensitivity C_LIO_LIIn rats, this DA supersensitivity potentiates d-amphetamine-induced locomotion C_LIO_LIWe report that D2 transmission promotes DA supersensitivity and D1 transmission tempers it C_LIO_LID-amphetamines central effects are also insufficient to reveal DA supersensitivity C_LI

pharmacology and toxicology↗