Abstract
Glutamate release and reuptake play a key role in the pathophysiology of depression. glutamatergic nerves in the hippocampus region are modulated by histaminergic afferents. Excessive accumulation of glutamate in the synaptic area causes degeneration of neuron cells. The H4 receptor is defined as the main immune system histamine receptor with a pro-inflammatory role. To understand the role of this receptor, the drug JNJ7777120 was used to reveal the chronic depression-glutamate relationship. We have important findings showing that the H4 antagonist increases the glutamate transporters’ instantaneous activity. In our experiment, it has been shown that blocking the H4 receptor leads to increased neuron cell viability and improvement in behavioral ability due to glutamate. Therefore, JNJ can be used to prevent neurotoxicity, inhibit membrane phospholipase activation and free radical formation, and minimize membrane disruption. In line with our findings, results have been obtained that indicate that JNJ will contribute to the effective prevention and treatment of depression.
Highlights
Chronic depression is a mental disorder that affects around 5% of the adult population globally and was one of the top 25 leading causes of burden worldwide in 2019 [1] and increased in prevalence during 2020 due to the COVID-19 pandemic [2]
They reported that hopeless animals expressed significantly lower levels of GLT1 in the hippocampus and cortex compared to offspring that did not display helpless behavior [8,10]. glut release and reuptake play a key role in the pathophysiology of depression [33,34,35,36]
It is known that glutamatergic nerves in the hippocampus region are modulated by histaminergic afferents [14,37] We found a modulation role of the H4 antagonist with glut receptor-transporters in chronic depression
Summary
Chronic depression is a mental disorder that affects around 5% of the adult population globally and was one of the top 25 leading causes of burden worldwide in 2019 [1] and increased in prevalence during 2020 due to the COVID-19 pandemic [2]. The current situation regarding the increasing prevalence of chronic depression requires health systems to find a solution for promoting mental wellbeing and treating those affected in order to prevent the socioeconomic impact of this disorder. Tathophysiology of depression continues to be incompletely known and associated with the heterogeneous pattern determined by multiple mechanisms of development and several aetiologies [3]. These ideas are supported by the high number of patients that don’t respond to antidepressant therapy [4]. There are several mechanisms considered responsible for the pathophysiology of depression, such as the involvement of dysregulation in biogenic amine, dysregulation of HPA (hypothalamic-pituitary-adrenal) axis, dysregulation in neurogenesis and second messenger systems, genetic, immunological factors, environmental factors, and the upregulation of CRF (corticotrophin-releasing factor), but none of these can explain all the signs and symptoms observed in these patients [3]
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