Effects of Chlordiazepoxide on Predator Odor-Induced Reductions of Playfulness in Juvenile Rats

The extent to which a non-sedative dose of chlordiazepoxide (CDP) is able to modify the behavioral responses toward a predator odor was assessed in juvenile rats. Play behavior was suppressed and defensive behaviors were enhanced in the presence of a collar previously worn by a cat, when tested 24 hours later in the same context as that where the exposure occurred, and when tested in a context different than that in which the exposure occurred for up to 3 hours after exposure. CDP had no effect on the ability of cat odor to suppress play when rats were tested in the presence of the odor or when tested 24 hours later in the same context where that exposure occurred. When rats were exposed to a worn cat collar in their home cage and tested in a different context CDP attenuated the ability of cat odor to reduce one measure of play (nape contacts) but not another measure (pins). Rats had an opportunity to hide during testing and CDP either decreased hiding or increased risk assessment from within the hide box in all of the testing scenarios. These data suggest that CDP can alter the defensive strategy used by juvenile rats that are confronted with a predatory threat and can also lead to an earlier return to pre-threat levels of playfulness when that threat becomes less immediate

Acute Ethanol Inhibition of γ Oscillations Is Mediated by Akt and GSK3β

Hippocampal network oscillations at gamma band frequency (γ, 30–80 Hz) are closely associated with higher brain functions such as learning and memory. Acute ethanol exposure at intoxicating concentrations (≥50 mM) impairs cognitive function. This study aimed to determine the effects and the mechanisms of acute ethanol exposure on γ oscillations in an in vitro model. Ethanol (25–100 mM) suppressed kainate-induced γ oscillations in CA3 area of the rat hippocampal slices, in a concentration-dependent, reversible manner. The ethanol-induced suppression was reduced by the D1R antagonist SCH23390 or the PKA inhibitor H89, was prevented by the Akt inhibitor triciribine or the GSk3β inhibitor SB415286, was enhanced by the NMDA receptor antagonist D-AP5, but was not affected by the MAPK inhibitor U0126 or PI3K inhibitor wortmanin. Our results indicate that the intracellular kinases Akt and GSk3β play a critical role in the ethanol-induced suppression of γ oscillations and reveal new cellular pathways involved in the ethanol-induced cognitive impairment

Chronic alcohol remodels prefrontal neurons and disrupts NMDAR-mediated fear extinction encoding

Alcoholism is frequently co-morbid with post-traumatic stress disorder, but it is unclear how alcohol affects the neural circuits mediating recovery from trauma. We found that chronic intermittent ethanol (CIE) impaired fear extinction and remodeled the dendritic arbor of medial prefrontal cortical (mPFC) neurons in mice. CIE impaired extinction encoding by infralimbic mPFC neurons in vivo and functionally downregulated burst-mediating NMDA GluN1 receptors. These findings suggest that alcohol may increase risk for trauma-related anxiety disorders by disrupting mPFC-mediated extinction of fear