2004
DOI: 10.1016/j.neuroscience.2004.01.022
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Nitric oxide mediates glutamate-evoked dopamine release in the medial preoptic area

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Cited by 62 publications
(51 citation statements)
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“…We observed that exogenous glutamate increased levels of extracellular DA by nearly three times that of basal levels [112], suggesting glutamate as a possible candidate for regulating MPOA DA release. Interestingly, however, while exogenous glutamate evoked increased DA release, it also inhibited levels of DA metabolites [homovanillic acid (HVA) and dihydroxyphenylacetic acid (DOPAC)] [112]. This may seem perplexing; however, these results are likely a function of NO activity rather than direct glutamatergic regulation (see below).…”
Section: Interactions Between Glutamate and Da In The Mpoamentioning
confidence: 67%
See 1 more Smart Citation
“…We observed that exogenous glutamate increased levels of extracellular DA by nearly three times that of basal levels [112], suggesting glutamate as a possible candidate for regulating MPOA DA release. Interestingly, however, while exogenous glutamate evoked increased DA release, it also inhibited levels of DA metabolites [homovanillic acid (HVA) and dihydroxyphenylacetic acid (DOPAC)] [112]. This may seem perplexing; however, these results are likely a function of NO activity rather than direct glutamatergic regulation (see below).…”
Section: Interactions Between Glutamate and Da In The Mpoamentioning
confidence: 67%
“…To determine whether NO was responsible for the aforementioned results, we performed a similar experiment, in which we co-administered l-NAME along with glutamate through the microdialysis probe. l-NAME did decrease basal DA levels and completely blocked the glutamate-evoked increase in extracellular DA, as well as the glutamate-evoked attenuation of DOPAC and HVA levels observed in animals receiving glutamate alone [112] (see Fig. 3).…”
Section: Interactions Between Glutamate and Da In The Mpoamentioning
confidence: 70%
“…There are no DA-containing neurons in the amygdala of male rats; however, some efferents from the MeA to the MPOA, and even more from the BNST, appeared to be glutamatergic (Dominguez et al, 2003). Reverse dialysis of glutamate into the MPOA increased DA release, an effect blocked by a NOS inhibitor (Dominguez et al, 2004). In addition, extracellular glutamate increased during copulation and rose to 300% of basal levels in the two-minute sample collected during ejaculation; reverse dialysis of glutamate reuptake inhibitors facilitated several measures of copulation (Dominguez et al, 2006).…”
Section: Ne Antagonists − (Clark and Smith 1990)mentioning
confidence: 92%
“…cGMP relaxes the blood vessels following exercise, increasing blood flow to muscles post exercise to facilitate glucose uptake [37]. In addition, glutamate-induced dopamine release is also mediated by NO [3]. Glutamate regulates the release of dopamine in several brain regions and has been implicated in the regulation of various behaviors and behavioral disorders [3].…”
Section: Discussionmentioning
confidence: 99%
“…In addition to being a potent vasodilator, NO is involved in the control of skeletal muscle function [2], skeletal muscle glucose uptake during exercise [2], and mitochondrial ATP production [2], all of which can modulate muscle strength. NO is also produced in the cerebral circulation affecting neuronal activity including the 2 ISRN Vascular Medicine release of dopamine [3]. Therefore, NO mediated actions can also influence behavior and cognition as well as voluntary movement and motivation [4].…”
Section: Introductionmentioning
confidence: 99%