Neuroendocrine signaling

Other cell lines are available for in vitro studies, including the Y1 mouse adrenocortical cell line, with different advantages and disadvantages (for review, see [49]). PC-12 cells are from a rat pheochromocytoma, and they produce norepinephrine and dopamine [60], They have been used to study neuroendocrine signaling of the adrenal medulla and differentiate and stop proliferating following exposure to neural growth factor. Adrenal slices have also been used for short-term experiments, especially those that required the presence of both medulla and cortex, but this model has rarely if ever been used to study toxicity of endocrine disruptors. 

Neurotransmitter and biogenic amine derived from the amino acid histidine synthesized in hypothalamic tuber-omamillary neurons (TMN) to maintain wakefulness, feeding rhythms, energy balance, neuroendocrine autonomic control, and memory functions prominent immu-nomodulator and proinflammatory signal released from mast cells in response to allergic reactions or tissue damage. 

Blask, D. E., Dauchy, R. T. Sauer, L. A. (2005). Putting cancer to sleep at night the neuroendocrine/circadian melatonin signal. Endocrine 27, 179-88. 

The sympathetic nervous system (SNS) and the hypothalamic-pituitary axis work together as important modulators of the immune system after exposure to stressors. Norepinephrine (NE) and epinephrine (EPI) (catecholamines from the SNS) and neuroendocrine hormones modulate a range of immune cell activities, including cell proliferation, cytokine and antibody production, lytic activity, and migration. This chapter will focus on these two major pathways of brain-immune signaling, briefly summarizing the evidence for SNS and hypothalamic-pituitary-adrenal (HPA) modulation of immune function, their influence on immune-mediated diseases, immune modulation in aging, and early life influences on these pathways. 

In my admittedly biased view, the most coherent approach is that of a profoundly disturbed stress system that under specific conditions paves the way to development of mood disorders. These stress-system alterations can be genetic or acquired through trauma in early life or even in utero. Consistent with this neuroendocrine hypothesis are findings that centrally released neuropeptides that drive the HPA system also have behavioral effects that are similar to affective symptoms. This view is further supported by the documented ability of various antidepressants to enhance corticosteroid receptor synthesis and efficacy. Moreover, the stress system, particularly the corticosteroids and their receptors, interferes with all of the neurotransmitter receptor systems, including intracellular signaling, that have been considered in the context of mood disorders. New drugs targeted directly to various elements of the stress system will constitute a major step forward. 

We have already discussed the co-occurrence of small amine and peptide neurotransmitters their release is normally Ca + dependent, and they operate through signal transmission. They are also capable of regulating each other s release and even the synthesis, clustering, and affinity of receptors. Neuroendocrine cells are capable of producing more than one peptide, and thus an amine-peptide as well as a peptide-peptide combination is possible. It is known, for instance, that the vagus nerve contains substance P, vasointestinal peptide, enkephalin, cholecystokinin, and somatostatin— peptides with a hybrid combination of neural and hormonal communication properties. 

Collado B, Sanchez MG, Diaz-Laviada I, Prieto JC, Carmena MJ. 2005. Vasoactive intestinal peptide (VIP) induces c-fos expression in LNCaP prostate cancer cells through a mechanism that involves Ca2 + signalling. Implications in angiogenesis and neuroendocrine differentiation. Biochim Biophys Acta 1744 224-233. 

Stern JE. Nitric oxide and homeostatic control an intercellular signalling molecule contributing to autonomic and neuroendocrine integration Prog Biophys Mol Biol. 2004 84 197-215. 

As a-LTXN4C (see Section 2.3) does not form pores, it probably stimulates exocy-tosis by receptor mediated signaling. Therefore, the activity of a-LTXN4C has been investigated in Ca2+-dependent and Ca2+-independent exocytosis from neurons and Ca2+-dependent exocytosis from neuroendocrine cells. 

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