“…in the range of normal, ambient KYNA levels in the mammalian brain (Schwarcz and Pellicciari, 2002). In experimental animals, comparatively minor increases in brain KYNA are neuroprotective against ischemic insults (Cozzi et al, 1999), exert anticonvulsant effects (Chiarugi et al, 1995;Nemeth et al, 2004;Pellicciari et al, 1994), affect the firing pattern of dopaminergic and noradrenergic neurons in the midbrain (Erhardt et al, 2001b;Nilsson et al, 2005), and reduce the extracellular levels of glutamate, dopamine and acetylcholine in the striatum (Carpenedo et al, 2001;Potter et al, 2005;Rassoulpour et al, 2005). Conversely, reductions in brain KYNA augment neuronal vulnerability to NMDA receptor-mediated excitotoxic insults (Sapko et al, 2006), enhance a7nACh receptor function (Alkondon et al, 2004), and cause an elevation of extracellular dopamine levels (Wu et al, in press).…”