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Cotella, E.

Publications and source records attributed to Cotella, E..

2 recordsLinked to original sources

Adolescent Stress Confers Resilience to Traumatic Stress Later in Life: Role of the Prefrontal Cortex

Stress during adolescence is usually associated with psychopathology later in life. However, under certain circumstances, developmental stress can promote an adaptive phenotype, allowing individuals to cope better with adverse situations in adulthood, thereby contributing to resilience. The aim of the study was to understand how adolescent stress alters behavioral and physiological responses to traumatic stress in adulthood. Sprague Dawley rats were subjected to adolescent chronic variable stress (adol CVS) followed by single prolonged stress (SPS) in adulthood. One week after SPS, animals were tested for acquisition, extinction, extinction recall and reinstatement of auditory-cued fear conditioning, with neuronal recruitment during reinstatement assessed by Fos expression. Patch clamp electrophysiology was performed to examine physiological changes associated with resilience. We observed that adol CVS blocked SPS-induced impairment of extinction learning (males) and enhancement fear reinstatement (both sexes). SPS effects were associated with a reduction of infralimbic (IL) cortex neuronal recruitment after reinstatement in males and increased engagement of the central amygdala in females, both of which were also prevented by adol CVS. We explored the mechanism behind reduced IL recruitment in male rats by studying the intrinsic excitability of IL pyramidal neurons. SPS reduced excitability of IL neurons and prior adol CVS prevented this effect, indicating that adolescent stress can impart resilience to the effects of traumatic stress by modification of IL output in males. Overall, our study suggests that prior stress exposure can limit the impact of a subsequent severe stress exposure in adulthood, effects that are mediated by sex-specific modification of infralimbic and amygdala signaling.

neuroscience↗

Chemogenetic Inhibition of Infralimbic Prefrontal Cortex GABA-ergic Parvalbuminpositive Interneurons Attenuates Chronic Stress Adaptions in Male Mice

Hypofunction of the prefrontal cortex (PFC) contributes to stress-related neuropsychiatric illnesses. Mechanisms leading to prefrontal hypoactivity remain to be determined. Prior evidence suggests that enhanced activity of parvalbumin (PV) expressing GABAergic interneurons (INs) play a role in chronic stress related pathologies. In this study, the role of PFC PV INs in stress related phenotypes were explored using Cre inducible inhibitory DREADDs (Designer Receptors Exclusively Activated by Designer Drugs). Mice were first tested in the tail suspension test (TST) to determine the effects of PV IN inhibition during acute stress. Following this, the long term impact of PV IN inhibition during chronic variable stress (CVS) was tested in the forced swim test (FST). Acute PV IN inhibition reduced active (struggling) and increased passive coping behaviors (immobility) in the TST. In contrast, inhibition of PV INs during CVS increased active and reduced passive coping behaviors in the FST. Moreover, chronic inhibition of PV INs attenuated CVS-induced changes in Fos expression in the prelimbic cortex, basolateral amygdala and ventrolateral periaqueductal gray and also prevented adrenal hypertrophy and body weight loss associated with chronic stress. Our results suggest differential roles of PV INs to acute vs chronic stress, indicative of distinct biological mechanisms underlying acute vs. chronic stress responses. Our results also indicate a role for PV INs in driving chronic stress adaptation and support literature evidence suggesting cortical GABAergic interneurons as a therapeutic target in stress related diseases.\n\nSIGNIFICANCEStress related diseases are associated with prefrontal hypoactivity, the mechanism of which is currently not known. In this study we showed that by inhibiting prefrontal GABA-ergic Parvalbumin interneurons (PV INs) using DREADDs, we can attenuate some of chronic stress related phenotypes. Additionally, we showed that modulation of PV IN activity during acute vs chronic stress had opposing effects on stress coping strategies, suggesting different underlying mechanisms behind acute vs chronic stress paradigms. Our findings indicate that GABA-ergic PV INs may be involved in driving stress related phenotypes and thereby an important target for treatment of stress-related illnesses. Our data suggest that reducing PV IN activity to promote prefrontal output may be an effective treatment strategy for stress related disorders.

neuroscience↗