ABSTRACT
Concerning the matter of depression, its full understanding pushes the envelope beyond clinical psychology and moves the subject further into the areas of Neuropsychopharmacology and Neuromolecular Imaging (NMI). Here, we studied, with the BRODERICK PROBE® acute and chronic stress-induced depression via the hypothalamic-pituitary-adrenal (HPA) axis. The “axis” is responsible for the emission of glucocorticoids during sympathetic nervous system activation. Negative feedback systems within areas of the hippocampus (HPC) and prefrontal cortex (PFC) prevent excessive amounts of glucocorticoids in the neurochemical environment and regulate the HPA axis production of these hormones. In depression, whether or not stress-induced, an increased concentration of glucocorticoids is present. In fact, when released by psychological or physical insult, glucocorticoids are accompanied by cytokines. The purpose of this work is to neuroimage a cytokine storm in the brain as it relates to COVID-19 SARS-CoV-2 patients. The advanced sensor nanobiotechnology, BRODERICK PROBE® transduced a small, protein cytokine, interleukin 1 alpha (IL-1α) to hippocampal Cornu Ammonis (CA-1) in two groups of animal subjects who are walking during neurotransmitter signaling. One genetically normal group was devoid of comorbidity to depression and indeed was also bred without viruses. The other genetic group was bred genetically depressed having platelet storage pool deficiency of the neurotransmitter, serotonin (5-HT);this group presented with Chediak-Higashi Syndrome and are Fawn-Hooded. Microdosing the pro-inflammatory IL-1α showed inherent neuroprotection of the hippocampal cytokine storm during real-time video tracking in Cornu Ammonis neurons in both nondepressed and depressed freely moving and walking subjects. The depressed subjects showed that the cytokine-induced storm began earlier than in nondepressed subjects while walking was increased in addition to enhanced stereotypy. Longer term studies in the same freely moving, walking subjects showed that the nondepressed were adapted to this cytokine brainstorm according to reliable sensor signaling signatures whereas the depressed subjects remained depressed. Thus, at the same time that we watched the brain immune derived cytokine storm directly coming to us online from HPC (CA-1) neurons, we monitored these motor skills with infrared photocell beams. Stereotypic grooming, nasopharyngeal systems were carefully assessed. These skills are important as they are related to respiratory SARS-CoV-2 insults and trauma. We watched online as the feared “hippocampal cytokine storm” was imaged in the depressed subject while immune T cell ratio CD4/CD8 was reversed. Tracking cytokine neuroinflammation transduced to HPC CA-1 neurons directly online while the subject is walking enables direct extrapolation to immune brain dysfunction in SARS-CoV-2 virus (Covid 19) patient data. © 2021 Elsevier Inc. All rights reserved.