Abstract
This study demonstrates how exposure to psychosocial crowding stress (CS) for 3, 7, and 14 days affects glutamate synapse functioning and signal transduction in the frontal cortex (FC) of rats. CS effects on synaptic activity were evaluated in FC slices of the primary motor cortex (M1) by measuring field potential (FP) amplitude, paired-pulse ratio (PPR), and long-term potentiation (LTP). Protein expression of GluA1, GluN2B mGluR1a/5, VGLUT1, and VGLUT2 was assessed in FC by western blot. The body’s response to CS was evaluated by measuring body weight and the plasma level of plasma corticosterone (CORT), adrenocorticotropic hormone (ACTH), and interleukin 1 beta (IL1B). CS 3 14d increased FP and attenuated LTP in M1, while PPR was augmented in CS 14d. The expression of GluA1, GluN2B, and mGluR1a/5 was up-regulated in CS 3d and downregulated in CS 14d. VGLUTs expression tended to increase in CS 7d. The failure to blunt the effects of chronic CS on FP and LTP in M1 suggests the impairment of habituation mechanisms by psychosocial stressors. PPR augmented by chronic CS with increased VGLUTs level in the CS 7d indicates that prolonged CS exposure changed presynaptic signaling within the FC. The CS bidirectional profile of changes in glutamate receptors’ expression seems to be a common mechanism evoked by stress in the FC.
Highlights
Data showing effects of social stress in animal models are scarce and limited to models that are based on strong social interactions and related with behaviors like isolation, aggression, or subordination [1]
The initial mean body weight ± standard error of the mean (SEM) of the animal groups analyzed in the experiment was as follows: control for CS3d—185 ± 2.99 g, n = 12; crowding stress (CS) 3d—192 ± 2.99 g, n = 12; control for CS 7d and CS 14d—210 ± 2.03 g, n = 7; CS 7d—216 ± 2.34 g, n = 24; CS
Our study provides new information about time-dependent changes in the synaptic properties and expression levels of selected subunits of glutamate receptors as well as vesicular glutamate transporters in the frontal cortex (FC) of rats undergoing psychosocial stress
Summary
Data showing effects of social stress in animal models are scarce and limited to models that are based on strong social interactions and related with behaviors like isolation, aggression, or subordination [1]. The psychosocial model of crowding stress (CS) is connected with the proximity to companions and competition for access to drinking water or food rather than the expression of antagonistic behaviors. For this reason, the CS model is similar to common social stressors in humans that may lead to stress-related pathology. Data obtained from the CS model suggest that animals exposed chronically to CS do not develop habituation or homeostatic adaptation to crowd exposure—which is a typical response to physical stressors, observed on the level of endocrine signaling, synaptic transmission, and intracellular signal transduction [2,3,4].
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