Neurochemical interaction between dopaminergic and noradrenergic neurons in the medial prefrontal cortex

Pan, Wynn H.T.; Yang, Sze-Yuan; Lin, Shi-Kwang

doi:10.1002/syn.20034

Cited by 61 publications

(41 citation statements)

References 32 publications

(45 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Blockade of α 1 adrenoceptor reduces releases of dopamine, serotonin, and norepinephrine in the mPFC, while inhibition of the α 2 adrenoceptor increases the same releases Devoto and Flore. 2006;Pan et al 2004;Pudovkina et al 2001;Weikop et al 2004). Therefore, the paradoxical effects of QTP on norepinephrine, dopamine, and serotonin release in the mPFC are not attributable to the blockade of adrenoceptors.…”

Section: Discussionmentioning

confidence: 88%

Effects of quetiapine on monoamine, GABA, and glutamate release in rat prefrontal cortex

et al. 2009

View full text Add to dashboard Cite

The dopaminergic terminal projecting from the VTA received inhibitory GABA-mediated NMDA/glutamatergic regulation, but not stimulatory AMPA/glutamatergic regulation. However, both dopaminergic and noradrenergic terminals from the LC received stimulatory AMPA/glutamatergic regulation from the MTN, but not inhibitory GABA-mediated NMDA/glutamatergic regulation. These findings correlating neuronal activities in nuclei with neurotransmitter release suggested that the effects of QTP on neurotransmission in the mPFC depend on activated neuronal projections located outside the mPFC. Furthermore, positive interaction between LC and MTN afferents are potentially important in the pharmacological mechanisms of neurotransmitter regulation by QTP and hint at mechanisms underlying the atypical profile of this drug for treatment of schizophrenia and as a mood stabilizer and proconvulsive agent.

show abstract

Section: Discussionmentioning

confidence: 88%

Effects of quetiapine on monoamine, GABA, and glutamate release in rat prefrontal cortex

et al. 2009

View full text Add to dashboard Cite

show abstract

“…Possibly the slight change by M100907, and absence by MDL 11,939, is due to their differential a1 adrenergic receptor-binding properties (K i ¼ 128 vs 1800, respectively; see Table 1). Local antagonism of adrenergic a1 receptors diminish DA levels in the mPFC (Pan et al, 2004). Nonetheless, selective antagonism of cortical 5-HT2A receptors clearly does not increase basal DA efflux in the mPFC.…”

Section: Discussionmentioning

confidence: 88%

Evidence for the Preferential Involvement of 5-HT2A Serotonin Receptors in Stress- and Drug-Induced Dopamine Release in the Rat Medial Prefrontal Cortex

Pehek

Nocjar

Roth

et al. 2005

Neuropsychopharmacol

172

104

View full text Add to dashboard Cite

The mechanism(s) by which serotonin modulates dopamine release in the medial prefrontal cortex is not known, although studies suggest an involvement of 5-HT2 family receptors. We employed in vivo microdialysis and putatively selective 5-HT2A antagonists (M100907, MDL 11,939, SR46349B) to determine if 5-HT2A receptors are responsible for both drug-and stress-induced DA release in the medial prefrontal cortex. MDL 11,939 and SR46349B receptor-binding studies indicated, for the first time, that only MDL 11,939 had greater selectivity for the 5-HT2A vs the 5-HT2C receptor subtypes similar to M100907, and that both showed low or no affinity for non-5-HT2 receptors. Reverse dialysis with 5-HT2A antagonists had little or no effect on basal dopamine efflux. However, intracortical administration of MDL 11,939 or M100907 attenuated dopamine release induced by systemic administration of the 5-HT2 agonist DOI. Dual-probe microdialysis demonstrated that systemic DOI also increased glutamate concentrations in the ventral tegmental area (VTA). This was blocked by intracortical M100907. Cortical perfusion with M100907, or the atypical antipsychotic drug risperidone, but not the 5-HT2B/C ligand SB 206553, also decreased dopamine release induced physiologically by stress. These results indicate that stimulation of cortical 5-HT2A receptors increases the release of dopamine from the mesocortical system. They suggest that this effect may be mediated by increases in glutamate release from corticotegmental projections to the VTA. Additionally, they indicate that cortical 5-HT2A receptors modulate evoked dopamine release, such as that observed physiologically following mild stress. These findings may have implications for the pharmacological treatment of disorders resulting from or exacerbated by stress.

show abstract

“…While ␣ 1 -adrenoreceptors are mostly postsynaptic, some might also be located presynaptically (Nakadate et al, 2006), and although ␣ 1 -adrenoreceptor activation was initially reported to increase EPSCs in PFC pyramidal neurons (Marek and Aghajanian,1999), recent evidence suggests instead that it suppresses GLU-, AMPA-, and NMDA-induced EPSCs (Kobayashi et al, 2009). Furthermore, locally applied NE increases PFC DA levels, an effect that is inhibited by local ␣ 1 -adrenoreceptor blockade (Pan et al, 2004). Thus it is presently unclear whether the effects of benoxathian were mediated directly by ␣ 1 -adrenoreceptors on callosal neurons or indirectly via a DA-dependent mechanism.…”

Section: Involvement Of Ne and Gabamentioning

confidence: 99%

Interhemispheric Regulation of the Medial Prefrontal Cortical Glutamate Stress Response in Rats

Lupinsky¹,

Moquin²,

Gratton³

2010

J. Neurosci.

View full text Add to dashboard Cite

While stressors are known to increase medial prefrontal cortex (PFC) glutamate (GLU) levels, the mechanism(s) subserving this response remain to be elucidated. We used microdialysis and local drug applications to investigate, in male Long-Evans rats, whether the PFC GLU stress response might reflect increased interhemispheric communication by callosal projection neurons. We report here that tail-pinch stress (20 min) elicited comparable increases in GLU in the left and right PFC that were sodium and calcium dependent and insensitive to local glial cystine-GLU exchanger blockade. Unilateral ibotenate-induced PFC lesions abolished the GLU stress response in the opposite hemisphere, as did contralateral mGlu 2/3 receptor activation. Local dopamine (DA) D 1 receptor blockade in the left PFC potently enhanced the right PFC GLU stress response, whereas the same treatment applied to the right PFC had a much weaker effect on the left PFC GLU response. Finally, the PFC GLU stress response was attenuated and potentiated, respectively, following ␣ 1 -adrenoreceptor blockade and GABA B receptor activation in the opposite hemisphere. These findings indicate that the PFC GLU stress response reflects, at least in part, activation of callosal neurons located in the opposite hemisphere and that stress-induced activation of these neurons is regulated by GLU-, DA-, norepinephrine-, and GABA-sensitive mechanisms. In the case of DA, this control is asymmetrical, with a marked regulatory bias of the left PFC DA input over the right PFC GLU stress response. Together, these findings suggest that callosal neurons and their afferentation play an important role in the hemispheric specialization of PFC-mediated responses to stressors.

show abstract

Neurochemical interaction between dopaminergic and noradrenergic neurons in the medial prefrontal cortex

Cited by 61 publications

References 32 publications

Effects of quetiapine on monoamine, GABA, and glutamate release in rat prefrontal cortex

Effects of quetiapine on monoamine, GABA, and glutamate release in rat prefrontal cortex

Evidence for the Preferential Involvement of 5-HT2A Serotonin Receptors in Stress- and Drug-Induced Dopamine Release in the Rat Medial Prefrontal Cortex

Interhemispheric Regulation of the Medial Prefrontal Cortical Glutamate Stress Response in Rats

Contact Info

Product

Resources

About