SARS-CoV-2 Psychiatric Sequelae: A Review of Neuroendocrine Mechanisms and Therapeutic Strategies.

From the earliest days of the coronavirus disease 2019 (COVID-19) pandemic, there have been reports of significant neurological and psychological symptoms following Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection. This narrative review is designed to examine the potential psychoneuroendocrine pathogenic mechanisms by which SARS-CoV-2 elicits psychiatric sequelae as well as to posit potential pharmacologic strategies to address and reverse these pathologies. Following a brief overview of neurological and psychological sequelae from previous viral pandemics, we address mechanisms by which SARS-CoV-2 could enter or otherwise elicit changes in the CNS. We then examine the hypothesis that COVID-19-induced psychiatric disorders result from challenges to the neuroendocrine system, in particular the hypothalamic-pituitary-adrenal stress axis and monoamine synthesis, physiological mechanisms that are only further enhanced by the pandemic-induced social environment of fear, isolation, and socioeconomic pressure. Finally, we evaluate several FDA-approved therapeutics in the context of COVID-19-induced psychoneuroendocrine disorders.

Responsiveness of extracellular dopamine in the nucleus accumbens to systemic quinpirole and eticlopride is modulated by low-level lead exposure.

Environmental lead exposure has been linked to learning and memory impairments as well as psychosocial deficits in children. Although the precise mechanisms by which lead exerts these effects are not completely understood, experimental animal studies suggest the involvement of mesolimbic dopamine system. Here, we investigated the effects of post weaning, 90-day exposure to 50ppm lead on the responsiveness of extracellular dopamine in the nucleus accumbens core to quinpirole and eticlopride using in vivo microdialysis in anesthetized Long-Evans rats. Attenuation of dopamine release by 1mg/kg quinpirole was more pronounced in lead-exposed rats compared to control rats. In contrast, eticlopride did not significantly modulate extracellular dopamine in lead-exposed rats as it did in the control group. Taken together, these results provides further evidence that exposure to environmentally relevant levels of lead disrupts mesolimbic dopamine system function, at least in part, through perturbations of D(2) receptor systems.