@article {2291, title = {The same stress has divergent effects on social versus asocial manifestations of anxiety-like behavior over time.}, journal = {Stress}, volume = {24}, year = {2021}, month = {2021 07}, pages = {474-480}, abstract = {

Stress may lead to augmented anxiety, which may, with time culminate in some form of anxiety disorder. Behavioral alterations related to increased anxiety can be broadly classified into two types-social, affecting interactions between individuals, and self-oriented, affecting the anxious individual only. While a growing body of literature now exists describing the effects of stress-induced anxiety on self-oriented behavior in animal models of anxiety disorders, the effects of such aberrant anxiety on social behavior has largely remained uncharacterized in these models. This study aims to fill this gap in our understanding by examining changes in social behavior following a single 2-hour episode of immobilization stress, which has been shown to cause delayed structural and functional changes in the amygdala. To this end, we examined social behavior, measured as active social interactions, anogenital sniffing, nose-to-nose contacts, allogrooming, actively following and crawling under, as well as self-oriented asocial behavior, manifested as self-grooming and rearing, in adult male rats. Stressed animals showed reduced social interaction 1 day after immobilization stress and this decrease was persistent for at least 10 days after stress. In contrast, individualistic behaviors were impaired only 10 days, but not 1 day later. Together, these results not only show that the same single episode of stress can elicit divergent effects on social and asocial measures of anxiety in the same animal, but also suggest that enhanced social anxiety soon after stress may also serve as an early indicator of its delayed behavioral effects.

}, keywords = {Amygdala, Animals, Anxiety, Anxiety Disorders, Behavior, Animal, Disease Models, Animal, Male, Rats, Social Behavior, Stress, Psychological}, issn = {1607-8888}, doi = {10.1080/10253890.2020.1855421}, author = {Saxena, Kapil and Chakraborty, Prabahan and Chattarji, Sumantra} } @article {2111, title = {Stress-induced modulation of endocannabinoid signaling leads to delayed strengthening of synaptic connectivity in the amygdala.}, journal = {Proc Natl Acad Sci U S A}, volume = {117}, year = {2020}, month = {2020 01 07}, pages = {650-655}, abstract = {

Even a brief exposure to severe stress strengthens synaptic connectivity days later in the amygdala, a brain area implicated in the affective symptoms of stress-related psychiatric disorders. However, little is known about the synaptic signaling mechanisms during stress that eventually culminate in its delayed impact on the amygdala. Hence, we investigated early stress-induced changes in amygdalar synaptic signaling in order to prevent its delayed effects. Whole-cell recordings in basolateral amygdala (BLA) slices from rats revealed higher frequency of miniature excitatory postsynaptic currents (mEPSCs) immediately after 2-h immobilization stress. This was replicated by inhibition of cannabinoid receptors (CBR), suggesting a role for endocannabinoid (eCB) signaling. Stress also reduced -arachidonoylethanolamine (AEA), an endogenous ligand of CBR. Since stress-induced activation of fatty acid amide hydrolase (FAAH) reduces AEA, we confirmed that oral administration of an FAAH inhibitor during stress prevents the increase in synaptic excitation in the BLA soon after stress. Although stress also caused an immediate reduction in synaptic inhibition, this was not prevented by FAAH inhibition. Strikingly, FAAH inhibition during the traumatic stressor was also effective 10 d later on the delayed manifestation of synaptic strengthening in BLA neurons, preventing both enhanced mEPSC frequency and increased dendritic spine-density. Thus, oral administration of an FAAH inhibitor during a brief stress prevents the early synaptic changes that eventually build up to hyperexcitability in the amygdala. This framework is of therapeutic relevance because of growing interest in targeting eCB signaling to prevent the gradual development of emotional symptoms and underlying amygdalar dysfunction triggered by traumatic stress.

}, keywords = {Administration, Oral, Amidohydrolases, Animals, Basolateral Nuclear Complex, Cannabinoid Receptor Antagonists, Disease Models, Animal, Emotions, Endocannabinoids, Enzyme Inhibitors, Excitatory Postsynaptic Potentials, Humans, Male, Rats, Receptor, Cannabinoid, CB1, Signal Transduction, Stress, Psychological}, issn = {1091-6490}, doi = {10.1073/pnas.1910322116}, author = {Yasmin, Farhana and Colangeli, Roberto and Morena, Maria and Filipski, Sarah and van der Stelt, Mario and Pittman, Quentin J and Hillard, Cecilia J and Teskey, G Campbell and McEwen, Bruce S and Hill, Matthew N and Chattarji, Sumantra} }