PMID- 8739626
OWN - NLM
STAT- MEDLINE
DCOM- 19970114
LR  - 20141120
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 715
IP  - 1-2
DP  - 1996 Apr 9
TI  - Medial prefrontal cortical D1 receptor modulation of the meso-accumbens dopamine 
      response to stress: an electrochemical study in freely-behaving rats.
PG  - 86-97
AB  - Voltammetry was used to study the role of prefrontal cortex (PFC) dopamine (DA) 
      in modulating the nucleus accumbens (NAcc) DA response to stress. Signal 
      increases elicited in NAcc by 15 min of restraint were monitored in 
      freely-behaving rats following intra-PFC microinjections of D1 and D2 
      receptor-selective drugs. The exact site of injection was first determined by 
      assessing the electrochemical response to stress at two dorsal-ventral levels of 
      PFC. Consistent with previous reports, a pronounced stress response was observed 
      ventrally at sites within the infralimbic PFC but not dorsally within the 
      superficial layers of PFC. When microinjected into the infralimbic PFC, the D1 
      receptor antagonist SCH 23390 significantly enhanced the NAcc stress response. 
      While the D1 receptor agonist SKF 38393 tended to decrease the NAcc stress 
      response, it failed to do so reliably. Neither sulpiride (D2 receptor antagonist) 
      nor quinpirole (D2 receptor agonist) had a significant effect. Finally, systemic 
      administration of the selective DA uptake inhibitor GBR 12909 dose-dependently 
      potentiated stress-induced signal increases in NAcc and in PFC, indicating that 
      the electrochemical responses to stress in both regions were due primarily to 
      increases in extracellular DA levels. Together, these data add to other evidence 
      indicating that the PFC exerts an inhibitory influence on subcortical DA 
      transmission. Specifically, the present results suggest that the NAcc DA response 
      to stress is dampened by the concurrent activation of meso-PFC DA neurons and 
      that this action is mediated, at least in part, by D1 receptors in PFC.
FAU - Doherty, M D
AU  - Doherty MD
AD  - Douglas Hospital Research Center, McGill University, Department of Psychiatry, 
      Montreal, Que., Canada.
FAU - Gratton, A
AU  - Gratton A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Dopamine Agonists)
RN  - 0 (Dopamine Antagonists)
RN  - 0 (Dopamine D2 Receptor Antagonists)
RN  - 0 (Dopamine Uptake Inhibitors)
RN  - 0 (Receptors, Dopamine D1)
RN  - 0 (Receptors, Dopamine D2)
SB  - IM
MH  - Animals
MH  - Behavior, Animal/drug effects/*physiology
MH  - Calibration
MH  - Dopamine Agonists/administration & dosage/pharmacology
MH  - Dopamine Antagonists/administration & dosage/pharmacology
MH  - Dopamine D2 Receptor Antagonists
MH  - Dopamine Uptake Inhibitors/administration & dosage/pharmacology
MH  - Electrochemistry
MH  - Electrophysiology
MH  - Injections
MH  - Male
MH  - Nucleus Accumbens/anatomy & histology/metabolism/*physiology
MH  - Oxidation-Reduction
MH  - Prefrontal Cortex/anatomy & histology/metabolism/*physiology
MH  - Rats
MH  - Receptors, Dopamine D1/agonists/antagonists & inhibitors/*physiology
MH  - Receptors, Dopamine D2/agonists
MH  - Restraint, Physical
MH  - Stress, Psychological/*metabolism/psychology
EDAT- 1996/04/09 00:00
MHDA- 1996/04/09 00:01
CRDT- 1996/04/09 00:00
PHST- 1996/04/09 00:00 [pubmed]
PHST- 1996/04/09 00:01 [medline]
PHST- 1996/04/09 00:00 [entrez]
AID - 0006-8993(95)01557-4 [pii]
AID - 10.1016/0006-8993(95)01557-4 [doi]
PST - ppublish
SO  - Brain Res. 1996 Apr 9;715(1-2):86-97. doi: 10.1016/0006-8993(95)01557-4.