Interactions between the dopaminergic and GABAergic neural systems in the lateral anterior hypothalamus of aggressive AAS-treated hamsters

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

“…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. To examine this question, animals were treated with AAS throughout adolescent development and tested for aggressive behavior following direct pharmacological manipulations of LAH GABA signaling to determine whether alterations in GABA signaling through GABA A receptors in the LAH modulate adolescent AAS-induced offensive aggression.…”

“…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).…”

“…Similar to AVP, 5HT, and DA, GABA has been implicated in aggressive behavior in various species and behavioral models, yet its role appears complex, both suppressing (Clement et al, 1987; Earley and Leonard, 1977; Guillot and Chapouthier, 1996, 1998; Haug et al, 1984; Krsiak et al, 1981; Poshivalov, 1981; Potegal et al, 1982; Puglisi-Allegra et al, 1981) and facilitating (Christmas and Maxwell, 1970; Cole and Wolf, 1970; Depaulis and Vergnes, 1985; DiMascio, 1973; Rodgers and Waters, 1985; Stork et al, 2000; Weerts et al, 1993) aggression. Across the neuraxis, GABA has been localized to both neurons and axon terminals (Bowers et al, 1998; Chen et al, 1998; Feldblum et al, 1993; Fenelon et al, 1995; Sur et al, 1999; Tappaz and Brownstein, 1977; Tappaz et al, 1977), including those that comprise the reciprocal hypothalamic neural circuit regulating aggressive behavior in hamsters; in particular the AH and LAH (Grimes et al, 2003; Schwartzer et al, 2009). In the CNS, GABA has been shown to exert its inhibitory action mainly through post-synaptic GABA A receptors, and aggressive behavior has been shown to be mediated by alterations in GABA A receptor activity (de Almeida et al, 2005; Jorge et al, 2002; Miczek et al, 2003).…”

“…In the CNS, GABA has been shown to exert its inhibitory action mainly through post-synaptic GABA A receptors, and aggressive behavior has been shown to be mediated by alterations in GABA A receptor activity (de Almeida et al, 2005; Jorge et al, 2002; Miczek et al, 2003). Recently, we localized a dense concentration of GABA A receptors aligned across the LAH (Schwartzer et al, 2009), so it is possible that GABA activity alters the activity of LAH-GABA A receptor-containing neurons that normally function to modulate aggression.…”

Sex, Drugs, and Violence: Neuromodulation of Attachment and Conflict in Voles

“…For example, syrian hamsters treated during adolescence with cocaine (Harrison et al 2000a;Melloni et al 2001;DeLeon et al 2002a;Jackson et al 2005;Knyshevski et al 2005a, b) or anabolic-androgenic steroids (AAS) (Melloni and Ferris 1996;Melloni et al 1997;Harrison et al 2000b;DeLeon et al 2002b) display enhanced offensive aggression in adulthood. Interestingly, these drug experiences reorganize AVP (Harrison et al 2000b;Jackson et al 2005;Grimes et al 2007), DA Schwartzer et al 2009); and GABA ) signaling in the AH. When compared with nonaggressive vehicle-treated control males, aggressive AAS-treated males exhibit significant neuroplastic changes in the AH including increased AVP-ir fiber density and AVP content (Harrison et al 2000b), an increase in TH-ir cell and fiber density ), enhanced DA-D2R expression ), a higher number of GAD 67 -ir cells , and decreased GABA A receptor expression ).…”