The modulatory role of serotonin-1A receptors of the basolateral amygdala and dorsal periaqueductal gray on the impact of hormonal variation on the conditioned fear response.

Despite significant advances in the study of fear and fear memory formation, little is known about fear learning and expression in females. This omission has been proven surprising, as normal and pathological behaviors are highly influenced by ovarian hormones, particularly estradiol and progesterone. In the current study, we investigated the joint influence of serotonin (5-HT) neurotransmission and estrous cycle phases (low or high levels of estradiol and progesterone) on the expression of conditioned fear in a group of female rats that were previously divided according to their response to stressful stimuli into low or high anxiety-like subjects.

Contributions of the GABAergic system of the prelimbic cortex and basolateral amygdala to morphine withdrawal-induced contextual fear.

Morphine withdrawal can trigger disruptions in neuronal pathways involved in the modulation and expression of anxiety and fear-related behaviors, particularly those involved in associative learning. When it comes to contextual fear, specific subdivisions of the medial prefrontal cortex (mPFC) regulate the expression of defensive behaviors through projections to specific amygdala (AM) nuclei, such as the prelimbic cortex (PrL). The basolateral nucleus (BLA) of the AM has been shown to be involved in the modulation and expression of associative memories of fear, including those associated with opiate withdrawal-related aversive events.

Differential effects of early exposure to alcohol on alcohol preference and blood alcohol levels in low- and high-anxious rats.

Emotional disturbances emerge following alcohol withdrawal. The anxiolytic effect of alcohol may be one important motivation for its consumption in conditions where alcohol intake is anxiety reducing. Besides, early alcohol experience will predict future alcohol-related problems at some point in their lives.