The role of afferents to the ventral tegmental area in the handling stress-induced increase in the release of dopamine in the medial prefrontal cortex: a dual-probe microdialysis study in the rat brain

Acute Handling Stress Modulates Methylphenidate-induced Catecholamine Overflow in the Medial Prefrontal Cortex

“…Enrico et al (1998) demonstrated that infusion of a GABA B agonist (baclofen), though not a GABA A agonist (muscimol) suppressed stress-induced increases of extracellular mPFC DA. These findings are of particular interest in light of the clinical anxiolytic utility of GABA A agonists.…”

“…This augmented response might be due to cross innervation of the mPFC from several brain stem projections, such as the A10 pathway from the ventral tegmental area (VTA) and/or noradrenergic connections from the locus coeruleus (LC). More specifically, systemic stressors such as handling, restraint, or immobilization increase mPFC levels of DA by 150-300% (Enrico et al 1998;Feenstra et al 1995), and NE levels by 160-250% Kawahara et al 2000;Shimizu et al 1994). These responses can be modulated by infusion of pharmacologic agents directly into the LC and the VTA, indicating the influence of these regions on mPFC function.…”

Local Activation of Metabotropic Glutamate Receptors Inhibits the Handling‐Induced Increased Release of Dopamine in the Nucleus Accumbens but Not that of Dopamine or Noradrenaline in the Prefrontal Cortex: Comparison with Inhibition of Ionotropic Receptors

“…These combined results suggest that handling-induced mPFC catecholamine release is not or is only marginally regulated by excitatory amino acids at the terminal level. The regulation at the cell-body level recently received support from several groups (Kalivas, 1993;Morrow et al, 1993;Enrico et al, 1997).…”

Differential involvement of dopamine D1 receptor and MEK signaling pathway in the ventromedial prefrontal cortex in consolidation and reconsolidation of recognition memory

“…These disorders involve memory deficits caused by PFC dysfunction (Mattes 1980;Weinberger et al 1986;Deutch 1993;Fibiger 1995). Experimental evidence has shown that acute mild stressful stimuli such as exposure to novelty increases dopamine (DA) and dopamine metabolism in the PFC, producing working memory impairment that can be blocked by agents that prevent the increase in DA turnover (Murphy et al 1996;Enrico et al 1998;Takahata and Moghaddam 1998;Ihalainen et al 1999;Feenstra et al 2000;Del Arco and Mora 2001).We have recently shown that novelty or familiarity with the experimental arena, which differentially affects the arousal level of the rat, also has a differential effect on consolidation and reconsolidation of object recognition memory. Specifically, learning was tested under two arousal conditions: no previous habituation to the experimental context (high novelty stress/arousal level) or extensive prior habituation to the experimental context (reduced novelty stress/arousal level).…”

“…These disorders involve memory deficits caused by PFC dysfunction (Mattes 1980;Weinberger et al 1986;Deutch 1993;Fibiger 1995). Experimental evidence has shown that acute mild stressful stimuli such as exposure to novelty increases dopamine (DA) and dopamine metabolism in the PFC, producing working memory impairment that can be blocked by agents that prevent the increase in DA turnover (Murphy et al 1996;Enrico et al 1998;Takahata and Moghaddam 1998;Ihalainen et al 1999;Feenstra et al 2000;Del Arco and Mora 2001).…”