Alterations in the anterior hypothalamic dopamine system in aggressive adolescent AAS-treated hamsters

Initial study on the possible mechanisms involved in the effects of high doses of perfluorooctane sulfonate (PFOS) on prolactin secretion

“…The augmented concentration of dopamine reported in the anterior hypothalamus in PFOS-treated rats could lead to several alterations in the thermoregulation (Hasegawa et al, 2000), in defense (Sweidan et al, 1991) and aggressive (Ricci et al, 2009) behavior as well as in the reproductive axis activity (Henderson et al, 2008). In fact, PFOS inhibits the reproductive axis function (L opez-Doval et al, 2014(L opez-Doval et al, , 2015 and this effect could be mediated by the increased concentration of dopamine, observed in the anterior hypothalamus after PFOS administration.…”

Neurophysiological Repercussions of Anabolic Steroid Abuse: A Road into Neurodegenerative Disorders

“…Specifically, down-regulation of these neurotransmitters throughout limbic regions can increase the susceptibility to depression and anxiety. Interestingly, chronic exposure to AS elicited significant decrease of serotonin levels in the hippocampus, hypothalamus, cortex, and amygdala of rats [65], whereas norepinephrine and dopamine levels are up-regulated in these regions [66,67]. In the amygdala and hypothalamus, ASs modulate the main excitatory and inhibitory neurotransmitters, namely glutamate and GABA, respectively.…”

γ-Aminobutyric acid neural signaling in the lateroanterior hypothalamus modulates aggressive behavior in adolescent anabolic/androgenic steroid-treated hamsters

“…In hamsters, the AH exists at the center of a neural network of reciprocal connections between the bed nucleus of the stria terminalis, lateral septum, medial amygdala, and ventrolateral hypothalamus that regulate offensive aggression (Delville et al, 2000). Recently we showed that adolescent hamsters stimulated to respond aggressively following AAS administration display significant alterations in the development and function of several neurotransmitter systems implicated in the control of aggressive behavior, i.e., the vasopressin (AVP) (Carrillo et al, 2011; Grimes et al, 2006, 2007; Harrison et al, 2000b; Melloni and Ricci, 2010), serotonin (5HT) (Grimes and Melloni, 2002, 2005; Ricci et al, 2006) and dopamine (DA) neural systems (Melloni and Ricci, 2010; Ricci et al, 2009; Schwartzer et al, 2009; Schwartzer and Melloni, 2010a, 2010b). Notably, these alterations were each observed in a ventrolateral subregion of the AH designated the latero-anterior hypothalamus (LAH) (DeLeon et al, 2002; Grimes and Melloni, 2005; Harrison et al, 2000b; Ricci et al, 2006).…”

“…This increase was not localized specifically to the LAH as we observed previously with AVP, 5HT, and DA afferents, suggesting that AH GABA neurons provide a diffuse inhibitory influence over neurons throughout the AH, and that this inhibitory influence is increased by adolescent AAS exposure. Conversely, an increase in GABA-containing neuronal somata were found exclusively within the LAH brain region after AAS exposure (Ricci et al, 2009), suggesting that the source of increased GABA afferents within the AH originate from GABA neurons in this brain region, and that adolescent AAS-induced increases in LAH GABA activity contribute to the mature and highly escalated adolescent AAS-induced aggressive phenotype. In contrast, while adolescent AAS exposure increases GABA production within the LAH and afferent development across the AH, subsequent studies from our laboratory have shown that aggressive, adolescent AAS-treated hamsters have fewer GABA Aα1 subunit-containing receptors in the LAH (Schwartzer et al, 2009), bringing into question whether the development of the mature, highly aggressive phenotype in AAS-treated animals is due to an increase in the overall activity of GABA within the LAH.…”