Peptides in brain

Prokai L, Kim HS, Zharikova A, Roboz J, Ma L, et al. 1998. Electrospray ionization mass spectrometric and liquid chromatographic-mass spectrometric studies on the metabolism of synthetic dynorphin A peptides in brain tissue in vitro and in vivo. J Chromatogr A 800 59. 

Boonen K, Baggerman G, Hertog WD, Husson SJ, Overbergh L, Mathieu C, Schoofs L. Neuropeptides of the islets of Langerhans A peptidomics study. Gen. Comp. Endocrinol. 2007 152 231-241. Haskins WE, Watson CJ, Cellar NA, Powell DH, Kennedy RT. Discovery and Neurochemical screening of peptides in brain extracellular fluid by chemical analysis of in vivo microdialysis samples. Anal. Chem. 2004 76 5523-5533. 

Pearse AGE. The diffuse neuroendocrine system and the APUD concept Related endocrine peptides in brain, intestine, pituitary, placenta, and aneurin cutaneous glands. Med Biol 55 5- 25, 1977. 

Prokai, L., Kim, H.-S., Zharikova, A., Roboz, J., Ma, L., Deng, L. and Simonsick Jr., W.J., Electrospray ionization mass spectrometric and LC/MS studies on the metabolism of synthetic dynorphin A peptides in brain tissue in vitro and in vivo. J. Chromatogr. A, 800, 59-68 (1998). Klintenberg, R. and Andren, P.E., Altered extracellular striatal in vivo biotransformation of the opioid neuropeptide dynorphin A(l-17) in the unilateral 6-OHDA rat model of Parkinson s disease. J. Mass Spectrom., 40, 261-270 (2005). 

Evidence soon emerged that the endogenous opioids were peptides rather than simple morphine-like molecules (9). The first direct evidence for endogenous opioids in brain extracts was provided in 1975 when two pentapeptides were purified that differed only in the carboxyl terminal amino acids (10) (Table 1). These peptides were called methionine- (Met-) and leucine- (Leu-) enkephalin, from the Greek term meaning "in the head."... 

This peptide itself has no selectivity for the two CCK receptors, CCK-A and B, which have so far been established to stimulate IP3/DAG while, like substance P, can close potassium channels to increase neuronal activity. The CCK-B receptor is thought to predominate in the CNS but species differences may make this interpretation difficult. It has a wide distribution in the CNS but is also found in the gut whereas the CCK-A receptor is more restricted but is found in the hypothalamus, hippocampus and in the brainstem. There are high levels of the natural peptide, CCK-8 in cortex, hippocampus, hypothalamus, ventral tegmentum, substantia nigra, brainstem and spinal cord. CCK is one of the most abundant peptides in the brain and CCK co-exists with dopamine, substance P, 5-HT and vasopressin. Interestingly, in the dopamine areas, CCK co-exists in the mesolimbic pathways but in the nigrostriatal projections, the peptide and... 

Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) are members of a family of so-called natriuretic peptides, synthesized predominantly in the cardiac atrium, ventricle, and vascular endothelial cells, respectively (G13, Y2). ANP is a 28-amino-acid polypeptide hormone released into the circulation in response to atrial stretch (L3). ANP acts (Fig. 8) on the kidney to increase sodium excretion and glomerular filtration rate (GFR), to antagonize renal vasoconstriction, and to inhibit renin secretion (Ml). In the cardiovascular system, ANP antagonizes vasoconstriction and shifts fluid from the intravascular to the interstitial compartment (G14). In the adrenal cortex, ANP is a powerful inhibitor of aldosterone synthesis (E6, N3). At the hypothalamic level, ANP inhibits vasopressin secretion (S3). It has been shown that some of the effects of ANP are mediated via a newly discovered hormone, called adreno-medullin, controlling fluid and electrolyte homeostasis (S8). The diuretic and blood pressure-lowering effect of ANP may be partially due to adrenomedullin (V5). 

Inhibition of monoamine oxidase has been proposed as a possible mechanism underlying the hydrogen sulfide-mediated disruption of neurotransmission in brain stem nuclei controlling respiration (Warenycia et al. 1989a). Administration of sodium hydrosulfide, an alkali salt of hydrogen sulfide, has been shown to increase brain catecholamine and serotonin levels in rats. It has also been suggested that persulfide formation resulting from sulfide interaction with tissue cystine and cystinyl peptides may underlie some... 

Peyron, C., Faraco, J., Rogers, W. et al. (2000). A mutation in a case of early onset narcolepsy and a generalized absence of hypocretin peptides in human narcoleptic brains. Nat. Med. 6, 991-7. 

Narcolepsy, a sleep disorder characterized by excessive daytime sleepiness and cataplexy, may be caused by the lack of hypocretin mRNA and peptides in humans (Peyron et al., 2000) or a disruption of the hypocretin receptor 2 or its ligand in dogs and mice (Lin et al., 1999 Chemelli et al., 1999). Hypocretin-containing neurons are located exclusively in the dorsomedial, lateral, and perifornical hypothalamic areas (Peyron et al., 1998). Two hypocretin sequences, Hcrt-1 (orexin-A) and Hcrt-2 (orexin-B), are generated from a single preprohypocretin (De Lecea et al., 1998 Peyron et al, 1998 Sakurai et al, 1998). Axons from these neurons are found in the hypothalamus, locus coeruleus (LC), raphe nuclei, tuberomamillary nucleus, midline thalamus, all levels of spinal cord, sympathetic and parasympathetic centers, and many other brain regions... 

---