Alcohol drinking during early adolescence activates microglial cells and increases frontolimbic Interleukin-1 beta and Toll-like receptor 4 gene expression, with heightened sensitivity in male rats compared to females

Silva-Gotay, Andrea; Davis, Jillian; Tavares, Elizabeth R.; Richardson, H. G.

doi:10.1016/j.neuropharm.2021.108698

Cited by 20 publications

(24 citation statements)

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“…This result seems to match the demyelination-remyelination hypothesis proposed by Tavares et al (2019) . The increased vulnerability of PFC myelin in males may be due to sex differences in expression of inflammatory markers following adolescent drinking ( Silva-Gotay et al, 2021 ). Expression of some pro-inflammatory genes, including interleukin 1-beta, increases in the PFC of both males and females after adolescent alcohol, while expression of the gene encoding Toll-like receptor 4 (TLR4) is increased in the PFC only in males ( Silva-Gotay et al, 2021 ).…”

Section: Animal Studies Of Alcohol Exposurementioning

confidence: 99%

“…The increased vulnerability of PFC myelin in males may be due to sex differences in expression of inflammatory markers following adolescent drinking ( Silva-Gotay et al, 2021 ). Expression of some pro-inflammatory genes, including interleukin 1-beta, increases in the PFC of both males and females after adolescent alcohol, while expression of the gene encoding Toll-like receptor 4 (TLR4) is increased in the PFC only in males ( Silva-Gotay et al, 2021 ). Because TLR4 has been implicated in alcohol-induced myelin loss ( Montesinos et al, 2015 ), Silva-Gotay et al (2021) argue that this sex difference in inflammatory gene expression may contribute to the increased sensitivity to adolescent alcohol in males.…”

Section: Animal Studies Of Alcohol Exposurementioning

confidence: 99%

“…Expression of some pro-inflammatory genes, including interleukin 1-beta, increases in the PFC of both males and females after adolescent alcohol, while expression of the gene encoding Toll-like receptor 4 (TLR4) is increased in the PFC only in males ( Silva-Gotay et al, 2021 ). Because TLR4 has been implicated in alcohol-induced myelin loss ( Montesinos et al, 2015 ), Silva-Gotay et al (2021) argue that this sex difference in inflammatory gene expression may contribute to the increased sensitivity to adolescent alcohol in males. Overall, these results indicate that myelination during adolescence is susceptible to alcohol exposure in both males and females.…”

Section: Animal Studies Of Alcohol Exposurementioning

confidence: 99%

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Adolescent Alcohol and Stress Exposure Rewires Key Cortical Neurocircuitry

et al. 2022

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Human adolescence is a period of development characterized by wide ranging emotions and behavioral risk taking, including binge drinking (Konrad et al., 2013). These behavioral manifestations of adolescence are complemented by growth in the neuroarchitecture of the brain, including synaptic pruning (Spear, 2013) and increases in overall white matter volume (Perrin et al., 2008). During this period of profound physiological maturation, the adolescent brain has a unique vulnerability to negative perturbations. Alcohol consumption and stress exposure, both of which are heightened during adolescence, can individually and synergistically alter these neurodevelopmental trajectories in positive and negative ways (conferring both resiliency and susceptibility) and influence already changing neurotransmitter systems and circuits. Importantly, the literature is rapidly changing and evolving in our understanding of basal sex differences in the brain, as well as the interaction between biological sex and life experiences. The animal literature provides the distinctive opportunity to explore sex-specific stress- and alcohol- induced changes in neurocircuits on a relatively rapid time scale. In addition, animal models allow for the investigation of individual neurons and signaling molecules otherwise inaccessible in the human brain. Here, we review the human and rodent literature with a focus on cortical development, neurotransmitters, peptides, and steroids, to characterize the field’s current understanding of the interaction between adolescence, biological sex, and exposure to stress and alcohol.

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Section: Animal Studies Of Alcohol Exposurementioning

confidence: 99%

Section: Animal Studies Of Alcohol Exposurementioning

confidence: 99%

Section: Animal Studies Of Alcohol Exposurementioning

confidence: 99%

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Adolescent Alcohol and Stress Exposure Rewires Key Cortical Neurocircuitry

et al. 2022

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“…The hippocampus is an important brain area that processes cognition and emotion. Chronic exposure to alcohol causes neuroinflammation in the hippocampus resulting from increased proinflammatory cytokine production and microglial cell activation [ 11 , 12 , 13 , 14 ]. Accumulating evidence suggests that neuroinflammation in the hippocampus contributes to the impairment of synaptic transmission efficacy, which is important for cognitive performance [ 15 , 16 ].…”

Section: Introductionmentioning

confidence: 99%

“…In support of this idea, a recent study indicated that the binge drinking of alcohol in adolescence increases the pathological processes of early Alzheimer’s disease during adulthood through the enhancement of neuroimmune activation [ 17 ]. In animal studies, adolescent intermittent ethanol (AIE) exposure would increase the release of pro-inflammatory factors, decrease the release of anti-inflammatory factors and increase the activation of microglia [ 13 ]. Additionally, anti-inflammatory treatments can attenuate the AIE-induced neurological disorders in animal models [ 16 , 18 , 19 ].…”

Section: Introductionmentioning

confidence: 99%

Treadmill Exercise Prevents Cognitive Impairments in Adolescent Intermittent Ethanol Rats by Reducing the Excessive Activation of Microglia Cell in the Hippocampus

Guo

Yan

et al. 2022

IJMS

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The excessive activation of microglia cell induced by adolescent intermittent ethanol (AIE) leads to neuroinflammation in the hippocampus. The endocannabinoid system plays a key role in the modulation of microglia activation. Accumulating evidence suggests that regular exercise improves learning and memory deficits in AIE models. The purpose of this study was to explore the effects of treadmill exercise intervention on the cognitive performance, activation of microglia cells and the expression of monoacylglycerol lipase (MAGL), cannabinoid receptor type 1 (CB1R) and cannabinoid receptor type 2 (CB2R) in the hippocampus of AIE rats. Here, we show that AIE rats exhibited cognitive impairments, whereas the treadmill exercise improves the cognitive performance in AIE rats. In order to explore the possible mechanisms for the exercise-induced attenuation of cognitive disorder, we examined the neuroinflammation in the hippocampus. We found that treadmill exercise led to the decrease in the level of proinflammatory cytokines (IL-1β, IL-6 and TNF-α) and the increase in the level of anti-inflammatory cytokine (IL-10). In addition, we found that treadmill exercise reduced the excessive activation of the microglia cell in the hippocampus of AIE rats. Finally, we found that AIE led to a decrease in the expression of CB1R and CB2R in the hippocampus; however, the treadmill exercise further decreased the expression of CB2R in the hippocampus of AIE rats. Our results suggest that treadmill exercise attenuates AIE-induced neuroinflammation and the excessive activation of hippocampus microglial cells, which may contribute to the exercise-induced improvement of cognitive performance in AIE rats.

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