PMID- 10482810
OWN - NLM
STAT- MEDLINE
DCOM- 19991020
LR  - 20190614
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 839
IP  - 1
DP  - 1999 Aug 21
TI  - Opioid and cannabinoid receptor-mediated regulation of the increase in 
      adrenocorticotropin hormone and corticosterone plasma concentrations induced by 
      central administration of delta(9)-tetrahydrocannabinol in rats.
PG  - 173-9
AB  - The purpose of this study was to investigate the cannabinoid and opioid mediated 
      regulation on the effects of central Delta(9)-tetrahydrocannabinol (Delta(9)-THC) 
      administration on hypothalamus-pituitary-adrenal (HPA) axis activity in the male 
      rat. Intracerebroventricular (i.c.v.) administration of delta(9)-THC (25, 50, 100 
      microg/rat) markedly increased plasma adrenocorticotropin hormone (ACTH) and 
      corticosterone concentrations. Time course effect studies revealed that both 
      hormones secretion peaked at 60 min after Delta(9)-THC i.c.v. administration (50 
      microg/rat), decreased gradually and returned to baseline levels by 480 min. The 
      i.c.v. administration of the specific cannabinoid receptor antagonist SR-141716A 
      (3 microg/rat) significantly attenuated the increase of both hormones secretion 
      induced by Delta(9)-THC (50 microg/rat). Nevertheless, higher doses (12.5 and 50 
      microg/rat) of this compound increased both ACTH and corticosterone plasma 
      concentrations. Subcutaneous (s.c.) administration with the opiate receptor 
      antagonist naloxone (0.3 mg/kg) was without effect but significantly diminished 
      the increase of both hormones secretion induced by Delta(9)-THC (50 microg/rat). 
      Taken together, these results indicate that opiate and cannabinoid receptors are 
      involved in the activation of the HPA axis induced by Delta(9)-THC. Furthermore, 
      the increase of ACTH and corticosterone secretion after the administration of 
      higher doses of SR-141716A than those required to block such activation, suggests 
      that endogenous cannabinoids are tonically inhibiting the release of both 
      hormones or that this agonist-like activity may be part of an uncharacterized 
      action of this compound not mediated by cannabinoid receptors.
FAU - Manzanares, J
AU  - Manzanares J
AD  - Departamento de Farmacologia, Facultad de Farmacia, Universidad Complutense, 
      28040, Madrid, Spain. jorgemr@eucmax.sim.ucm.es
FAU - Corchero, J
AU  - Corchero J
FAU - Fuentes, J A
AU  - Fuentes JA
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 (Narcotic Antagonists)
RN  - 0 (Piperidines)
RN  - 0 (Psychotropic Drugs)
RN  - 0 (Pyrazoles)
RN  - 0 (Receptors, Cannabinoid)
RN  - 0 (Receptors, Drug)
RN  - 0 (Receptors, Opioid)
RN  - 36B82AMQ7N (Naloxone)
RN  - 7J8897W37S (Dronabinol)
RN  - 9002-60-2 (Adrenocorticotropic Hormone)
RN  - RML78EN3XE (Rimonabant)
RN  - W980KJ009P (Corticosterone)
SB  - IM
MH  - Adrenocorticotropic Hormone/*blood
MH  - Analysis of Variance
MH  - Animals
MH  - Corticosterone/*blood
MH  - Dronabinol/antagonists & inhibitors/*pharmacology
MH  - Injections, Intraventricular
MH  - Male
MH  - Naloxone/pharmacology
MH  - Narcotic Antagonists/pharmacology
MH  - Piperidines/pharmacology
MH  - Pituitary-Adrenal System/drug effects
MH  - Psychotropic Drugs/*pharmacology
MH  - Pyrazoles/pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Cannabinoid
MH  - Receptors, Drug/*physiology
MH  - Receptors, Opioid/*physiology
MH  - Rimonabant
EDAT- 1999/09/14 00:00
MHDA- 1999/09/14 00:01
CRDT- 1999/09/14 00:00
PHST- 1999/09/14 00:00 [pubmed]
PHST- 1999/09/14 00:01 [medline]
PHST- 1999/09/14 00:00 [entrez]
AID - S0006-8993(99)01756-4 [pii]
AID - 10.1016/s0006-8993(99)01756-4 [doi]
PST - ppublish
SO  - Brain Res. 1999 Aug 21;839(1):173-9. doi: 10.1016/s0006-8993(99)01756-4.