Neurosecretions formed in the brain in response to environmental stimuli regulate the synthesis and release of hormones known as gonadotropins, which, in turn, stimulate the gonads.
Neuroendocrine tumors (NETs) consist of a heterogeneous group of neoplasms originating from cells characterized by the synthesis and release of amines/peptides [1].
However, these bacteria are capable of synthesizing and releasing many neurotransmitters and neuromodulators themselves, or evoke the synthesis and release of neuropeptides from enteroendocrine cells.
Activation of the vagal/NTS pathway, by adrenaline and noradrenaline, stimulates the synthesis and release of noradrenaline and dopamine in the brain.
Collectively, we demonstrate that B-cells can be easily programmed toward the synthesis and release of multiple sncRNAs, including sncRNA-laden EVs, efficiently and specifically.
Triggered by the septic inflammatory response, endogenous glucocorticoids are being released, presumably in an attempt to modulate and counterbalance the synthesis and release of inflammatory mediators on a cellular level [13].
Later, these peptides were shown to increase the synthesis and release of anti-inflammatory molecules like IL-10 and the IL-1 receptor antagonist (IL-1Ra), leading to a decrease in the inflammatory response [34].
For example, female sex steroids enhance neuronal excitability by elevating Ca2+ and decreasing Mg2+ concentrations; and these play a role in the synthesis and release of nitric oxide and of neuropeptides; and in the function of receptors inducing vasoconstriction.
Therefore, blocking the synthesis and release of the inflammatory markers could potentially prevent asthma pathogenesis.
Here I investigate the synthesis and release of neuropeptide Y from pancreatic beta cells.
Presynaptic H3Rs located on histaminergic nerve endings, act as autoreceptors to control the synthesis and release of histamine [5], [17].
