1998
DOI: 10.1046/j.1471-4159.1998.70041503.x
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Increase of Extracellular Glutamate and Expression of Fos‐Like Immunoreactivity in the Ventral Tegmental Area in Response to Electrical Stimulation of the Prefrontal Cortex

Abstract: Electrical stimulation of the medial prefrontal cortex caused glutamate release in the ventral tegmental area (VTA) of freely moving animals. Cathodal stimulation was given through monopolar electrodes in 0.1-ms pulses at an intensity of 300 biA and frequencies of 4-120 Hz. Glutamate was measured in 10-min perfusate samples by HPLC coupled with fluorescence detection following precolumn derivatization with o-phthaldialdehyde/ß-mercaptoethanol. The stimulation-induced glutamate release was frequency dependent a… Show more

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Cited by 56 publications
(32 citation statements)
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“…Since blockade of an excitatory influence results in an increase in dopamine release, it is likely that the glutamate receptors being impacted are on GABAergic interneurons [13]. Consistent with this idea is the suggestion that efferent (presumably glutamatergic [39]) projections from the PFC to the VTA may synapse on GABAergic interneurons that ultimately modulate dopamine release in the NAcc [7]. Our results are in accord with this interpretation since GABA receptor blockade also induced partner preferences.…”
Section: Partner Preference Inductionsupporting
confidence: 86%
“…Since blockade of an excitatory influence results in an increase in dopamine release, it is likely that the glutamate receptors being impacted are on GABAergic interneurons [13]. Consistent with this idea is the suggestion that efferent (presumably glutamatergic [39]) projections from the PFC to the VTA may synapse on GABAergic interneurons that ultimately modulate dopamine release in the NAcc [7]. Our results are in accord with this interpretation since GABA receptor blockade also induced partner preferences.…”
Section: Partner Preference Inductionsupporting
confidence: 86%
“…Thus, release of GABA via activation of the 5-HT 2C R on parvalbumin-positive mPFC GABA interneurons would be expected to reduce excitatory output from the mPFC to the mesoaccumbens pathway, enabling mPFC 5-HT 2C R to indirectly regulate glutamate and DA levels in the NAc ( Figure 9). In support of this concept, iontophoretic application of the 5-HT 2C R agonist mCPP suppressed spontaneous and/or glutamate-activated firing of PFC neurons (Bergqvist et al, 1999), while electrical stimulation of the rat mPFC enhanced glutamate levels in the VTA (Rossetti et al, 1998) and NAc (You et al, 1998) as well as DA release in the NAc (You et al, 1998); but see (Jackson et al, 2001). Taken in conjunction with the observation that activation of mPFC GABA receptors inhibited both glutamate release in the VTA and NAc and DA release in the NAc (Karreman and Moghaddam, 1996;Harte and O'Connor, 2005), these data suggest that stimulation of mPFC 5-HT 2C R on parvalbumin-positive GABA interneurons would function to reduce excitatory glutamate output as well as subsequent DA neurotransmission within the mesoaccumbens pathway (Figure 9).…”
Section: Discussionmentioning
confidence: 89%
“…NIH-PA Author Manuscript NIH-PA Author Manuscript 1999), while electrical stimulation of the rat mPFC enhanced glutamate levels in the VTA (Rossetti et al, 1998) and NAc (You et al, 1998) as well as DA release in the NAc (You et al, 1998); but see (Jackson et al, 2001). Taken in conjunction with the observation that activation of mPFC GABA receptors inhibited both glutamate release in the VTA and NAc and DA release in the NAc (Karreman and Moghaddam, 1996;Harte and O'Connor, 2005), these data suggest that stimulation of mPFC 5-HT 2C R on parvalbumin-positive GABA interneurons would function to reduce excitatory glutamate output as well as subsequent DA neurotransmission within the mesoaccumbens pathway (Figure 9).…”
Section: Nih-pa Author Manuscriptmentioning
confidence: 99%
“…Electrical stimulation of the PFC increases glutamate efflux in the VTA (Rossetti et al 1998), whereas excitotoxic lesions of the PFC prevent amphetamine-induced increases in glutamate efflux in the VTA (Wolf and Xue 1999). There is evidence suggesting that glutamatergic transmission in the PFC-VTA pathway is crucial in the development of sensitization.…”
Section: Introductionmentioning
confidence: 99%