Publications by authors named "Juliana A Hutter"

Objective: To characterize SARS-CoV-2 transmission following a COVID-19 outbreak in an emergency childcare centre (ECCC) in April 2020 in Quebec, Canada.

Methods: The study population consisted of all the children and employees who attended the ECCC as well as household contacts of the confirmed COVID-19 cases. Of the 120 individuals in the study, five cases were confirmed by epidemiological link and 25 were identified as COVID-19 by RT-PCR among which 19 were analyzed by viral whole genome sequencing.

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Background: The lateral entorhinal cortex receives inputs from ventral tegmental area dopamine neurons that are activated by exposure to food-related cues, and exogenously applied dopamine is known to modulate excitatory synaptic responses within the entorhinal cortex.

Methods: The present study used in vivo synaptic field potential recording techniques to determine how exposure to cues associated with food reward modulates synaptic responses in the entorhinal cortex of the awake rat. Chronically implanted electrodes were used to monitor synaptic potentials in the entorhinal cortex evoked by stimulation of the piriform (olfactory) cortex, and to determine how synaptic responses are modulated by food-related cues.

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The entorhinal cortex receives inputs from sensory and associational cortices, as well as a substantial input from midbrain dopaminergic neurons. Dopamine is likely to modulate the responsiveness of entorhinal cortex neurons to sensory inputs, and excitatory synaptic responses in layers I/II of the entorhinal cortex in vitro can be either facilitated or suppressed by dopamine depending upon the concentration applied. Rewarding stimulation of the lateral hypothalamus leads to activation of dopamine neurons, and the present study evaluated the effect of rewarding stimulation on synaptic responses in the lateral entorhinal cortex evoked by stimulation of the primary olfactory (piriform) cortex in behaving rats.

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Stress exerts a profound impact on learning and memory, in part, through the actions of adrenal corticosterone (CORT) on synaptic plasticity, a cellular model of learning and memory. Increasing findings suggest that CORT exerts its impact on synaptic plasticity by altering the functional properties of glutamate receptors, which include changes in the motility and function of α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid subtype of glutamate receptor (AMPAR) that are responsible for the expression of synaptic plasticity. Here we provide evidence that CORT could also regulate synaptic plasticity by modulating the function of synaptic N-methyl-D-aspartate receptors (NMDARs), which mediate the induction of synaptic plasticity.

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