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This study was aimed to identify the neuronal pathways that mediate the handling stress induced increase in the release of dopamine in the medial prefrontal cortex (mPFC) of the rat brain. For that purpose a microdialysis probe was implanted in the ventral tegmental area (VTA) and a second probe was placed in the ipsilateral mPFC. Receptor specific compounds acting on GABA(A) (20 mu M muscimol), GABA(B) (50 mu M baclofen), acetylcholine (100 mu M atropine, 100 mu M mecamylamine), NMDA (30, 100 and 300 mu M CPP; 300 mu M AP-5, 1 mM (+)-HA-966) and non-NMDA receptors (500 mu M CNQX) were infused into the VTA by retrograde dialysis, whereas extracellular dopamine was recorded in the ipsilateral mPFC. Intrategmental infusion of muscimol, baclofen, CPP, AP-5, (+)-HA-966 and CNQX decreased extracellular dopamine in the ipsilateral mPFC; atropine and mecamylamine were without effect on the basal values. During infusion of the various compounds rats were gently handled for 15 min. The infusions of muscimol, atropine, mecamylamine and(+)-HA-966 did not modify the handling stress induced increase in extracellular dopamine in the mPFC. However, during intrategmental infusion of baclofen, CPP, AP-5 and CNQX the handling stress induced increase in extracellular dopamine (expressed as % of controls) in the mPFC was suppressed. These results indicate that a glutamatergic projection to the VTA, acting via both NMDA and non-NMDA-glutamate receptors, play a major role in the handling stress-induced increase in dopamine release in the mPFC. In addition the results suggest a certain role for GABAergic neurones, acting via GABA(B) receptors, in the handling response. (C) 1998 Elsevier Science B.V.

This study was aimed to identify the neuronal pathways that mediate the handling stress induced increase in the release of dopamine in the medial prefrontal cortex (mPFC) of the rat brain. For that purpose a microdialysis probe was implanted in the ventral tegmental area (VTA) and a second probe was placed in the ipsilateral mPFC. Receptor specific compounds acting on GABA(A) (20 mu M muscimol), GABA(B) (50 mu M baclofen), acetylcholine (100 mu M atropine, 100 mu M mecamylamine), NMDA (30, 100 and 300 mu M CPP; 300 mu M AP-5, 1 mM (+)-HA-966) and non-NMDA receptors (500 mu M CNQX) were infused into the VTA by retrograde dialysis, whereas extracellular dopamine was recorded in the ipsilateral mPFC. Intrategmental infusion of muscimol, baclofen, CPP, AP-5, (+)-HA-966 and CNQX decreased extracellular dopamine in the ipsilateral mPFC; atropine and mecamylamine were without effect on the basal values. During infusion of the various compounds rats were gently handled for 15 min. The infusions of muscimol, atropine, mecamylamine and(+)-HA-966 did not modify the handling stress induced increase in extracellular dopamine in the mPFC. However, during intrategmental infusion of baclofen, CPP, AP-5 and CNQX the handling stress induced increase in extracellular dopamine (expressed as % of controls) in the mPFC was suppressed. These results indicate that a glutamatergic projection to the VTA, acting via both NMDA and non-NMDA-glutamate receptors, play a major role in the handling stress-induced increase in dopamine release in the mPFC. In addition the results suggest a certain role for GABAergic neurones, acting via GABA(B) receptors, in the handling response. (C) 1998 Elsevier Science B.V.

This study was aimed to identify the neuronal pathways that mediate the handling stress induced increase in the release of dopamine in the medial prefrontal cortex (mPFC) of the rat brain. For that purpose a microdialysis probe was implanted in the ventral tegmental area (VTA) and a second probe was placed in the ipsilateral mPFC. Receptor specific compounds acting on GABA(A) (20 mu M muscimol), GABA(B) (50 mu M baclofen), acetylcholine (100 mu M atropine, 100 mu M mecamylamine), NMDA (30, 100 and 300 mu M CPP; 300 mu M AP-5, 1 mM (+)-HA-966) and non-NMDA receptors (500 mu M CNQX) were infused into the VTA by retrograde dialysis, whereas extracellular dopamine was recorded in the ipsilateral mPFC. Intrategmental infusion of muscimol, baclofen, CPP, AP-5, (+)-HA-966 and CNQX decreased extracellular dopamine in the ipsilateral mPFC; atropine and mecamylamine were without effect on the basal values. During infusion of the various compounds rats were gently handled for 15 min. The infusions of muscimol, atropine, mecamylamine and(+)-HA-966 did not modify the handling stress induced increase in extracellular dopamine in the mPFC. However, during intrategmental infusion of baclofen, CPP, AP-5 and CNQX the handling stress induced increase in extracellular dopamine (expressed as % of controls) in the mPFC was suppressed. These results indicate that a glutamatergic projection to the VTA, acting via both NMDA and non-NMDA-glutamate receptors, play a major role in the handling stress-induced increase in dopamine release in the mPFC. In addition the results suggest a certain role for GABAergic neurones, acting via GABA(B) receptors, in the handling response. (C) 1998 Elsevier Science B.V.

The present study examined whether the prefrontal cortex (PFC) exerts a tonic control over the basal release of dopamine in the limbic striatum and whether this control is mediated by glutamatergic afferents to the dopamine cell body or terminal regions. Using intracerebral microdialysis in freely moving rats, it was demonstrated that application of tetrodotoxin in the contralateral PFC significantly decreased the release of dopamine in the medial striatum. Conversely, blockade of the tonic inhibitory GABAergic input in the PFC with bicuculline increased the release of dopamine in the medial striatum. Application of excitatory amino acid receptor antagonists into the striatum, while bicuculline was perfused in the PFC, did not affect the bicuculline-evoked dopamine increase in the striatum, However, infusion of tetrodotoxin or excitatory amino acid receptor antagonists into the ventral tegmental area, a region containing dopamine cell bodies that project to the medial striatum, blocked the stimulation of striatal dopamine release induced by infusion of bicuculline into the PFC, These data demonstrate that the basal output of dopamine terminals in the medial striatum is under a tonic excitatory control of the PFC, Furthermore, this control occurs primarily through glutamatergic projections to the dopamine cell body area rather than the terminal regions.

The present study examined whether the prefrontal cortex (PFC) exerts a tonic control over the basal release of dopamine in the limbic striatum and whether this control is mediated by glutamatergic afferents to the dopamine cell body or terminal regions. Using intracerebral microdialysis in freely moving rats, it was demonstrated that application of tetrodotoxin in the contralateral PFC significantly decreased the release of dopamine in the medial striatum. Conversely, blockade of the tonic inhibitory GABAergic input in the PFC with bicuculline increased the release of dopamine in the medial striatum. Application of excitatory amino acid receptor antagonists into the striatum, while bicuculline was perfused in the PFC, did not affect the bicuculline-evoked dopamine increase in the striatum, However, infusion of tetrodotoxin or excitatory amino acid receptor antagonists into the ventral tegmental area, a region containing dopamine cell bodies that project to the medial striatum, blocked the stimulation of striatal dopamine release induced by infusion of bicuculline into the PFC, These data demonstrate that the basal output of dopamine terminals in the medial striatum is under a tonic excitatory control of the PFC, Furthermore, this control occurs primarily through glutamatergic projections to the dopamine cell body area rather than the terminal regions.

The present study examined whether the prefrontal cortex (PFC) exerts a tonic control over the basal release of dopamine in the limbic striatum and whether this control is mediated by glutamatergic afferents to the dopamine cell body or terminal regions. Using intracerebral microdialysis in freely moving rats, it was demonstrated that application of tetrodotoxin in the contralateral PFC significantly decreased the release of dopamine in the medial striatum. Conversely, blockade of the tonic inhibitory GABAergic input in the PFC with bicuculline increased the release of dopamine in the medial striatum. Application of excitatory amino acid receptor antagonists into the striatum, while bicuculline was perfused in the PFC, did not affect the bicuculline-evoked dopamine increase in the striatum. However, infusion of tetrodotoxin or excitatory amino acid receptor antagonists into the ventral tegmental area, a region containing dopamine cell bodies that project to the medial striatum, blocked the stimulation of striatal dopamine release induced by infusion of bicuculline into the PFC. These data demonstrate that the basal output of dopamine terminals in the medial striatum is under a tonic excitatory control of the PFC. Furthermore, this control occurs primarily through glutamatergic projections to the dopamine cell body area rather than the terminal regions.