The Effect of Chronic Overcrowding on Social Behavior and Expression of Neuroinflammation-Associated Genes in Rats

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Irina V. Pavlova^1,a*, Nadezhda D. Broshevitskaya¹, Anastasiya A. Potekhina¹, Anastasiya M. Shvadchenko¹

¹Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, 117485 Moscow, Russia

^* To whom correspondence should be addressed.

Received: April 24, 2024; Revised: July 15, 2024; Accepted: August 6, 2024

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The effect of chronic overcrowding on the social behavior of adult male Wistar rats was studied. From postnatal day 30 (P30) to P180, the rats lived under standard (STND) or overcrowded (CRWD) conditions. Starting from P100, rat behavior was studied in the social preference and tube dominance tests, and aggressive behavior was investigated in the resident-intruder test. After decapitation of rats on P180, amygdala, dorsal hippocampus, ventromedial hypothalamus, and medial prefrontal cortex were collected and analyzed for expression of the IL-1β, TNF, TGF-β1, and IL-6 mRNAs by quantitative polymerase chain reaction. Compared to the STND group, rats from the CRWD group demonstrated shorter interaction time with a social object in the social preference test. They also had more wins in the tube test and initiated more attacks in the resident-intruder test. Expression of the IL1β gene in the hippocampus and medial prefrontal cortex and of the TGFβ1 gene in the hippocampus, amygdala, and prefrontal cortex was increased in the CRWD group. The stress induced by overcrowding increased social dominance and aggressiveness and decreased social motivation in rats. The changes in the social behavior of CRWD rats were accompanied by upregulation of expression of genes for the proinflammatory cytokine IL-1β and the anti-inflammatory cytokine TGF-β1 in a number of brain structures, which can be considered as manifestations of neuroinflammation and compensatory processes, respectively.

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KEY WORDS: overcrowding, social dominance tube test, resident-intruder test, social preference test, pro-inflammatory cytokines IL-1β, TNF, IL-6, anti-inflammatory cytokine TGF-β1

DOI: 10.1134/S0006297924090050

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