Electrical Stimulation of the Medial Prefrontal Cortex Increases Dopamine Release in the Striatum
Abstract
Exogenous and endogenous glutamate has been shown to evoke dopamine (DA) release in the striatum using both in vitro and in vivo techniques. We hypothesized that stimulation of the prefrontal cortex (PFC) would phasically enhance striatal DA release via the glutamatergic corticostriatal pathway. To test this hypothesis, in vivo brain microdialysis was employed to measure extracellular concentrations of DA in the striatum during electrical stimulation of the PFC. Five rats were implanted with bilateral electrodes located in the medial PFC and dialysis probes in the dorsal striatum. Two days later the PFC of these awake, freely moving rats was stimulated first at 50 microA and then at 100 microA for 20 minutes at 2-hour intervals. Both currents significantly increased DA release. Extracellular DA rose rapidly during stimulation, peaked immediately afterward, and then slowly returned to baseline values. Dopamine reached 118% of baseline values with 50 microA stimulation and 138% with 100 microA stimulation. Histologic analysis using the fluorescent retrograde dye Fluoro Gold confirmed that cells projecting to the vicinity of the striatal dialysis probe originated in the vicinity of the PFC electrodes. These results provide direct evidence for phasic, excitatory modulation of striatal DA release by the PFC.
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In rats, inactivation of the ventral ACC converts burst-firing patterns to pacemaker-like firing activity.
“In rats, stimulation of these ventral ACC areas elicits burst-firing patterns in the VTA-DA neurons whereas inactivation of the ventral ACC converts burstfiring patterns to pacemaker-like firing activity (Drevets et al, 1998;Murase et al, 1993;Taber and Fibiger, 1993;Gariano and Groves, 1988).”
From Neurocircuitry of Mood Disorders (2010) · cites this paper as Taber and Fibiger, 1993
The Results and Discussion (page numbers unavailable) describe increased striatal dopamine release during medial prefrontal cortex stimulation in rats. A search for ventral ACC inactivation and burst-to-pacemaker firing found no passage addressing the claimed change in VTA dopamine-neuron activity. (LLM, conf=0.75)
Experimental — accuracy not yet measuredIn rats, stimulation of ventral ACC areas elicits burst-firing patterns in VTA-DA neurons.
“In rats, stimulation of these ventral ACC areas elicits burst-firing patterns in the VTA-DA neurons whereas inactivation of the ventral ACC converts burstfiring patterns to pacemaker-like firing activity (Drevets et al, 1998;Murase et al, 1993;Taber and Fibiger, 1993;Gariano and Groves, 1988).”
From Neurocircuitry of Mood Disorders (2010) · cites this paper as Taber and Fibiger, 1993
The Results report increased striatal dopamine after medial prefrontal cortex stimulation in rats. The Discussion mentions a possible projection to the ventral tegmental area, but neither passage reports whether stimulation of ventral ACC areas elicits burst firing in VTA dopamine neurons. Searches for burst firing and pacemaker activity found no passage addressing that outcome. (LLM, conf=0.75)
Experimental — accuracy not yet measuredIn rats, stimulation of ventral ACC areas elicits burst firing patterns in the VTA-DA neurons, while inactivation of the ventral ACC converts burst firing patterns to pacemaker-like firing activity.
“In rats, stimulation of these ventral ACC areas elicits burst firing patterns in the VTA-DA neurons, while inactivation of the ventral ACC converts burst firing patterns to pacemaker-like firing activity (Drevets et al. 1998; Murase et al. 1993; Taber and Fibiger 1993; Gariano and Groves 1988).”
From Brain structural and functional abnormalities in mood disorders: implications for neurocircuitry models of depression (2008) · cites this paper as Taber and Fibiger 1993
The Results and Discussion (page not available in our copy) report that medial prefrontal cortex stimulation increased dopamine release in the rat striatum. They do not report VTA dopamine-neuron burst firing after ventral ACC stimulation or a change to pacemaker-like firing after ventral ACC inactivation; searches for those firing patterns found no supporting passage. (LLM, conf=0.76)
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- Authors
- Taber, M. T., & Fibiger, H. C.
- Affiliations
- University of British Columbia (CA)
- Venue
- Neuropsychopharmacology
- Published
- 1993-12
- Volume
- 9
- Issue
- 4
- Pages
- 271-275
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- OpenAlex
- W2047628735
- Cited by
- 99
- References
- 18
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2022: 1 · 2021: 1 · 2020: 2 · 2018: 3 · 2016: 1 · 2015: 2 · 2014: 2 · 2013: 2 · 2012: 5
- FWCI
- 1.32
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Neuropsychopharmacology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Bristol-Myers Squibb
- Medical Research Council Canada
- Medical Research Council
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Neurology › Neurological disorders and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- medial prefrontal cortex, striatum, dopamine release, electrical stimulation, phasic dopamine release, extracellular dopamine, cerebral microdialysis
- MeSH terms
- Animals, Dopamine, Electric Stimulation, Extracellular Space, Fluorescent Dyes, Male, Stilbamidines, Neostriatum, Rats, Wistar, Prefrontal Cortex, Microdialysis, Rats
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