Central control of penile erection: A re-visitation of the role of oxytocin and its interaction with dopamine and glutamic acid in male rats

Neurophysiological effects of acute oxytocin administration: systematic review and meta-analysis of placebo-controlled imaging studies

“…[95][96][97][98] Furthermore, OXT has been implicated in helping to mediate addiction and withdrawal in the mesolimbic dopaminergic pathways, 99 and differences in peripheral and central levels of OXT have been found in patients with disorders with potential DA abnormalities, such as autism, [100][101][102][103] schizophrenia [104][105][106][107][108] and social anxiety disorder. [109][110][111][112] In addition, preclinical studies have shown that dopaminergic fibres may regulate OXT release 113,114 and that the receptor binding sites and neuronal fibres of both of these neurochemicals reside in the same regions of the central nervous system and are often next to each other. 92,99,115 Further evidence suggests that, at least in the ventral and dorsal striatum, DA D2 receptors and OXT are heteromers with facilitatory receptor-to-receptor interactions.…”

Mechanisms of Penile Erection and Basis for Pharmacological Treatment of Erectile Dysfunction

“…Evidence from animal studies indicates that the central supraspinal systems controlling sexual arousal are localized predominantly in the limbic system (e.g., olfactory nuclei, medial preoptic area, nucleus accumbens, amygdala, and hippocampus) and hypothalamus (paraventricular and ventromedial nuclei). In particular, medial amygdala, medial preoptic area (MPOA), paraventricular nucleus (PVN), the periaqueductal gray, and ventral tegmentum are recognized as key structures in the central control of the male sexual response (Andersson and Wagner, 1995;Giuliano and Rampin, 2000a,b;Argiolas and Melis, 2005;Hull and Dominguez, 2007;Melis and Argiolas, 2011). In rats, electrical stimulation of the MPOA, the PVN, or the hippocampal formation can elicit an erectile response.…”

“…Not unexpectedly, the central neurotransmission of penile erection is complex and only partly known. However, progress continues to be made to identify effectors involved in this function, and the field has recently been reviewed (Melis and Argiolas, 2011). Much of the knowledge gained in this area of research relates to morphological and pharmacological studies in experimental animal models (e.g., rodents, rabbits, primates).…”

“…However, it is well established that the balance between contractant and relaxant factors controls the degree of tone of the penile vasculature and of the smooth muscle of the corpora cavernosa (CC) and determines the functional state of the penis: detumescence and flaccidity, tumescence and erection. Several pharmacological, physiological, and clinical aspects of erectile function and dysfunction have been reviewed previously (e.g., Andersson and Wagner, 1995;Argiolas and Melis, 1995, 2004, 2005Giuliano andRampin, 2000, 2004;, but the field expands continuously and has been subject to several recent reviews (Baskerville and Douglas, 2008;Burnett et al, 2010;Gratzke et al, 2010a;Melis and Argiolas, 2011). The present review is an attempt to update the rapidly expanding information on some of the transmit-1 Abbreviations: ␣-MSH, ␣-melanocyte-stimulating hormone; ABT-724, 2-[(4-pyridin-2-ylpiperazin-1-yl)methyl]-1H-benzimidazole); ACE, angiotensin-converting enzyme; ACh, acetylcholine; AM251, 1-(2,4-dichlorophenyl)-5-(4-iodophenyl)-4-methyl-N-(1-piperidyl)pyrazole-3-carboxamide; AM630, 6-iodo-2-methyl-1-[2-(4-morpholinyl)ethyl]-1H-indol-3-yl-(4-methoxyphenyl)methanone; AMPA, amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid; Ang II, angiotensin II; ANP, atrial natriuretic peptide; AR, adrenergic receptor; ARB, angiotensin receptor blocker; BNP, brain natriuretic peptide; cAK, protein kinase A; CB, cannabinoid; CC, corpora cavernosa; cGK, cGMP-dependent protein kinase; CGRP, calcitonin gene-related peptide; CNP, C-type natriuretic peptide; CNS, central nervous system; CV, cardiovascular; ED, erectile dysfunction; eNOS, endothelial nitric-oxide synthase; ET, endothelin; GC, guanylyl cyclase; HO, heme oxygenase; 5-HT, 5-hydroxytryptamine; ICP, intracavernosal pressure; IPA, internal pudendal artery; IP 3 , inositol 1,4,5-trisphosphate; L-NAME, N G -nitro-L-arginine methyl ester; MC, melanocortin; m-CCP, m-chlorophenylpiperazine; MK-801, dizocilpine maleate; MLC, regulatory light-chain subunits of myosin; MLCK, myosin light-chain kinase; MPOA, medial preoptic area; MT-II, melanotan-II; NA, noradrenaline; NANC, nonadrenergic, noncholinergic; NMDA, N-methyl-D-aspartic acid; nNOS, neuronal nitric-oxide synthase; NOS, nitric-oxide synthase; PACAP, pituitary adenylate cyclase-activating polypeptide; PDE, phosphodiesterase; PG, prostaglandin; pGC, particulate GC; PKC, protein kinase C; PKG, protein kinase G; PVN, paraventricular nucleus; R 141716A, N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboximide hydrochloride; RAS, renin-angiotensin system; ROS, reactive oxygen species; sGC, soluble guanylyl cyclase; SHU-9119, Ac-Nlecyclo(Asp-His-D-2-Nal-Arg-Trp-Lys)-NH; SIN-1, 3-morpholinosydnonimin hydrochloride (linsidomine); SM, smooth muscle; SNP, sodium nitroprusside; TNF, tumor necrosis factor; 304,VIP,vasoactive intestinal peptide;VPAC,VIP receptor;…”

Oxytocin Nasal Spray in the Treatment of Binge Eating Disorder and Obesity: A Pilot, Randomized, Double-Blind Trial

“…Hypothalamic oxytocinergic neurons also project to specific central areas involved in the modulation of motivation, sense of well-being, and sexual performance [6,7]. A large number of studies found that administration of oxytocin reduces food intake and body weight in animal models of obesity [5,8].…”