The administration of Delta(9)-tetrahydrocannabinol (Delta(9)-THC) and synthetic cannabinoids stimulates acetylcholine (ACh) release in the rat prefrontal cortex (PFCx) and hippocampus as estimated by brain microdialysis. The present study was aimed at assessing whether the ability of Delta(9)-THC to stimulate ACh release is dependent upon opioid and dopamine (DA) receptors. Administration of the mu opioid receptor antagonists naloxone and naltrexone prevented the Delta(9)-THC-induced release of ACh in the PFCx and hippocampus. Similarly, bilateral infusion in the ventral tegmental area (VTA). 24 h before Delta(9)-THC, of the pseudo-irreversible mu(1), antagonist naloxonazine completely prevented the increase of ACh release by Delta(9)-THC. Pre-treatment with the D, receptor antagonist SCH 39166 reduced Delta(9)-THC-induced ACh release both in the PFCx and in the hippocampus. Since A9-THC has been shown to increase DA release in the nucleus accumbens (NAc) shell via a mu(1)-opioid receptor mediated mechanism located in the VTA (Tanda, G., Pontieri, F.E., Di Chiara, G., 1997. Cannabinoid and heroin activation of mesolimbic dopamine transmission by a common mu(1) opioid receptor mechanism. Science 276, 2048-2050.), we hypothesize that Delta(9)-THC-induced stimulation of ACh release in the PFCx and hippocampus is related to stimulation of endogenous opioids release in the VTA with secondary activation of DA neurons projecting to the NAc shell. (c) 2005 Elsevier Ltd. All rights reserved.

Modulation of Delta(9)-THC-induced increase of cortical and hippocampal acetylcholine release by micro opioid and D(1) dopamine receptors

PISANU, AUGUSTA;ACQUAS, ELIO MARIA GIOACHINO;FENU, SANDRO;DI CHIARA, GAETANO
2006-01-01

Abstract

The administration of Delta(9)-tetrahydrocannabinol (Delta(9)-THC) and synthetic cannabinoids stimulates acetylcholine (ACh) release in the rat prefrontal cortex (PFCx) and hippocampus as estimated by brain microdialysis. The present study was aimed at assessing whether the ability of Delta(9)-THC to stimulate ACh release is dependent upon opioid and dopamine (DA) receptors. Administration of the mu opioid receptor antagonists naloxone and naltrexone prevented the Delta(9)-THC-induced release of ACh in the PFCx and hippocampus. Similarly, bilateral infusion in the ventral tegmental area (VTA). 24 h before Delta(9)-THC, of the pseudo-irreversible mu(1), antagonist naloxonazine completely prevented the increase of ACh release by Delta(9)-THC. Pre-treatment with the D, receptor antagonist SCH 39166 reduced Delta(9)-THC-induced ACh release both in the PFCx and in the hippocampus. Since A9-THC has been shown to increase DA release in the nucleus accumbens (NAc) shell via a mu(1)-opioid receptor mediated mechanism located in the VTA (Tanda, G., Pontieri, F.E., Di Chiara, G., 1997. Cannabinoid and heroin activation of mesolimbic dopamine transmission by a common mu(1) opioid receptor mechanism. Science 276, 2048-2050.), we hypothesize that Delta(9)-THC-induced stimulation of ACh release in the PFCx and hippocampus is related to stimulation of endogenous opioids release in the VTA with secondary activation of DA neurons projecting to the NAc shell. (c) 2005 Elsevier Ltd. All rights reserved.
2006
Delta(9)-tetrahydrocannabinol, Microdialysis, Prefrontal cortex, Hippocampus, D-1 dopamine receptors, Mu(1)-opioid receptors, Cannabinoid CB1, Behavioral sensitization, Nucleus accumbens, Squirrel monkeys, Spatial memory, Knockout mice, Spinal cord, In vivo, Rat, Delta(9)-tetrahydrocannabinol
File in questo prodotto:
File Dimensione Formato  
Pisanu et al Neuropharmacology 2006.pdf

Solo gestori archivio

Tipologia: versione editoriale
Dimensione 494.21 kB
Formato Adobe PDF
494.21 kB Adobe PDF   Visualizza/Apri   Richiedi una copia

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11584/18791
Citazioni
  • ???jsp.display-item.citation.pmc??? 11
  • Scopus 39
  • ???jsp.display-item.citation.isi??? 32
social impact