Electrical Stimulation of the Medial Prefrontal Cortex Increases Dopamine Release in the Striatum

Taber, Matthew T.; Fibiger, Hans C.

doi:10.1038/npp.1993.63

Cited by 94 publications

(42 citation statements)

References 17 publications

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“…This highly specific effect was current-dependent, not-lateralized, and was found in both anesthetized and awake rats. The absence of motor or behavioral reactions during low-current stimulation of mPFC in behaving animals is in agreement with previous studies (Fuster 1997;Taber and Fibiger 1993). The effect of prefrontal stimulation on the 5-HT output was more pronounced in these rats than in the urethane-anesthetized rats.…”

Section: Discussionsupporting

confidence: 92%

Electrical Stimulation of Rat Medial Prefrontal Cortex Enhances Forebrain Serotonin Output Implications for Electroconvulsive Therapy and Transcranial Magnetic Stimulation in Depression

Juckel

1999

Neuropsychopharmacology

103

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Decreased activity of the prefrontal cortex (PFC), as well as reduced serotonergic neurotransmission, is considered as a characteristic feature of major depression. The mechanism by which electroconvulsive therapy (ECT) and transcranial magnetic stimulation (TMS) achieve their antidepressant effects may involve changes in PFC activity. It is, however, still unclear whether these changes are accompanied by increased synaptic availability of serotonin (5-HT). In the present study, 5-HT efflux in the rat ventral hippocampus and amygdala was analyzed using in vivo microdialysis during low-current electrical stimulation of PFC and other cortical regions. Electrical stimulation of the medial PFC produced current-dependent increases in limbic 5-HT output in both urethane-anesthetized and behaving rats. No effects on 5-HT levels were seen after comparable stimulation of either the lateral parts of the PFCAn extensive body of clinical evidence suggests that prefrontal cortex (PFC) abnormalities are involved in the pathophysiology of major depression. Significantly decreased cerebral blood flow as well as reduced rates of glucose metabolism have been consistently found in the PFC of depressed patients (Soares and Mann 1997;Kennedy et al. 1997;George et al. 1993). This reduction seems to be localized predominantly in the left hemisphere (Baxter et al. 1989;Martinot et al. 1990). This is supported by structural neuroimaging studies demonstrating that poststroke depression is more likely to occur following a lesion in the left PFC rather than either in the right PFC or elsewhere in the left hemisphere (Morris et al. 1996;Robinson et al. 1984). Both neuropsychological and oculomotor functioning of prefrontal cortex is impaired in depression (Goodwin 1997;Sweeney et al. 1998). Furthermore, symptom improvement and remission of depressed patients have been associated with increases in cerebral blood flow and glucose metabolism in this region (Goodwin et al. 1993;Bench et al. 1995;Bonne and Krausz 1997;Buchsbaum et al. 1997 NO . 3 This close association between prefrontal cortical dysfunction and depression suggests that enhancement of PFC activity might be beneficial in the treatment of this disorder. Consistent with this idea, electroconvulsive therapy (ECT), as well as transcranial magnetic stimulation (TMS), seems to achieve its antidepressant effects by altering PFC activity. ECT leads to pronounced prefrontal EEG changes, which are directly related to the therapeutic outcome. Hence, the efficacy of ECT seems to be critically linked to prefrontal cortex involvement in ECT-induced seizure activity (Sackeim et al. 1996). This is further supported by studies that have reported changes in cerebral blood flow in prefrontal cortex of ECT responders (Nobler et al. 1994;Bonne et al. 1996;Petracca et al. 1995). In recent years, repetitive TMS of the left dorsolateral prefrontal cortex has emerged as a successful antidepressant treatment (Pascual-Leone et al. 1996;George et al. 1997). Although the exact mechanism underlying the ef...

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Section: Discussionsupporting

confidence: 92%

Electrical Stimulation of Rat Medial Prefrontal Cortex Enhances Forebrain Serotonin Output Implications for Electroconvulsive Therapy and Transcranial Magnetic Stimulation in Depression

Juckel

1999

Neuropsychopharmacology

103

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“…Our results complement and extend recent studies showing that chemical or electrical activation of the PFC induces dopamine release in the striatum (Nieoullon et al, 1978;Murase et al, 1993;Taber and Fibiger, 1993;Moghaddam, 1994, 1996; and that an excitatory amino acid projection to the VTA is the most likely source of this modulation of the mesostriatal dopamine systems Tong et al, 1996a,b). Further functional relevance for the glutamatergic regulation of dopamine systems in the cell body region is provided by the recent finding that stress, which induces dopamine release from dopamine nerve terminals (Abercrombie et al, 1989) and Fos expression in dopamine cell bodies (Deutch et al, 1991), is associated with increased levels of glutamate and dopamine in the VTA (Rossetti and Wise, 1996).…”

Section: Discussionsupporting

confidence: 90%

Increase of Extracellular Glutamate and Expression of Fos‐Like Immunoreactivity in the Ventral Tegmental Area in Response to Electrical Stimulation of the Prefrontal Cortex

Rossetti¹,

Marcangione

Wise

1998

Journal of Neurochemistry

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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 and was blocked by the infusion of the sodium channel blocker tetrodotoxin (10 1iM) through the dialysis probe. The stimulation also induced bilateral Fos-like immunoreactivity in ventral tegmental neurons, with a significantly greater number of Fos-positive cells on the stimulated side. These findings add to a growing body of evidence suggesting that the medial prefrontal cortex regulates dopamine release in the nucleus accumbens via its projection to dopamine cell bodies in the VTA. Key Words: Prefrontal cortexVentral tegmental area-Glutamate-Fos-like immunoreactivity-Microdialysis-Electrical stimulation. J. Neurochem. 70, 1503-1512 (1998).There has been considerable recent interest in the possibility that glutamatergic fibers from the medial prefrontal cortex (PFC) to the striatum might presynaptically regulate striatal dopamine release (Giorguieff et al., 1977;Chesselet, 1984;Cheramy et al., 1986;Romo et al., 1986b;Abercrombie and Zigmond, 1990;Grace, 1993;Greenamyre, 1993). Glutamate infusion into the striatum elevates extracellular dopamine, but this effect is insensitive to the perfusion of the sodium channel blocker tetrodotoxin (TTX) (Giorguieff et al., 1977;Roberts and Sharif, 1978;Roberts and Anderson, 1979; Marien et al., 1983;Clow and Jhamandas, 1989;Lonart and Zigmond, 1991; but see Youngren et al., 1993). Disinhibition of prefrontal cortex by local interference with GABAergic transmission (Karremann and Moghaddam, 1996) or by GABA infusion into the medial thalamus (Romo et al., 1986a,b) similarly increases striatal dopamine levels while, at least in the latter case, inhibiting the firing of the ventral tegmental dopaminergic neurons that project to the striatum. However, glutamate antagonists infused into the striaturn tend to have no effect (Carter et al., 1988;Imperato et al., 1990;Leviel et al., 1990; Moghaddarn and Gruen, 1991; Rao et al., 1991;Keefe et al., 1992; or tend to increase extracellular dopamine levels (Barbeito et al., 1990; Moghaddarn and Gruen, 1991). Moreover, prefrontal neurons do not appear to make synaptic contact with doparninergic terminals in the striatum; rather, glutamatergic and dopaminergic terminals each synapse primarily on medium spiny neurons, often on adjacent regions of the same dendritic spine (Bouyer et al., 1984;Sesack and Pickel, 1992;Smith et al., 1994). Thus, a number of groups have begun to look for alternate avenues by which glutamatergic projections from the frontal cortex might influence dopamine levels in the striatum.The PFC sends ...

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“…In the striatum, DEHP also caused a decrease in the expression. The striatum is a region rich in NMDA receptors (Gracy, 1999;Petralia, 1994;Tarazi, 1999), and corticostriatal glutamatergic neurons stimulate DA release from the striatum (Taber, 1993) via NMDA receptors (Ochi, 1995 (Madras, 2002;Roman, 2001). The expression of Datl can be increased in DA neurons that are resistant to 6-OHDA treatment and/or in non-DA elements (Hoffman, 1998 (Counts, 2002) and striatum (Ericson, 1999;Tsuda, 1998).…”

Section: Resultsmentioning

confidence: 99%

Effects of Neonatal Treatment With 6‐Hydroxydopamine and Endocrine Disruptors on Motor Activity and Gene Expression in Rats

et al. 2004

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Electrical Stimulation of the Medial Prefrontal Cortex Increases Dopamine Release in the Striatum

Cited by 94 publications

References 17 publications

Electrical Stimulation of Rat Medial Prefrontal Cortex Enhances Forebrain Serotonin Output Implications for Electroconvulsive Therapy and Transcranial Magnetic Stimulation in Depression

Electrical Stimulation of Rat Medial Prefrontal Cortex Enhances Forebrain Serotonin Output Implications for Electroconvulsive Therapy and Transcranial Magnetic Stimulation in Depression

Increase of Extracellular Glutamate and Expression of Fos‐Like Immunoreactivity in the Ventral Tegmental Area in Response to Electrical Stimulation of the Prefrontal Cortex

Effects of Neonatal Treatment With 6‐Hydroxydopamine and Endocrine Disruptors on Motor Activity and Gene Expression in Rats

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