Tags

Type your tag names separated by a space and hit enter

Modulation of Delta(9)-THC-induced increase of cortical and hippocampal acetylcholine release by micro opioid and D(1) dopamine receptors.
Neuropharmacology. 2006 May; 50(6):661-70.N

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 micro 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), 24h before Delta(9)-THC, of the pseudo-irreversible micro(1) antagonist naloxonazine completely prevented the increase of ACh release by Delta(9)-THC. Pre-treatment with the D(1) receptor antagonist SCH 39,166 reduced Delta(9)-THC-induced ACh release both in the PFCx and in the hippocampus. Since Delta(9)-THC has been shown to increase DA release in the nucleus accumbens (NAc) shell via a micro(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 micro(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.

Authors+Show Affiliations

Department of Toxicology, Cagliari, Italy.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16427098

Citation

Pisanu, A, et al. "Modulation of Delta(9)-THC-induced Increase of Cortical and Hippocampal Acetylcholine Release By Micro Opioid and D(1) Dopamine Receptors." Neuropharmacology, vol. 50, no. 6, 2006, pp. 661-70.
Pisanu A, Acquas E, Fenu S, et al. Modulation of Delta(9)-THC-induced increase of cortical and hippocampal acetylcholine release by micro opioid and D(1) dopamine receptors. Neuropharmacology. 2006;50(6):661-70.
Pisanu, A., Acquas, E., Fenu, S., & Di Chiara, G. (2006). Modulation of Delta(9)-THC-induced increase of cortical and hippocampal acetylcholine release by micro opioid and D(1) dopamine receptors. Neuropharmacology, 50(6), 661-70.
Pisanu A, et al. Modulation of Delta(9)-THC-induced Increase of Cortical and Hippocampal Acetylcholine Release By Micro Opioid and D(1) Dopamine Receptors. Neuropharmacology. 2006;50(6):661-70. PubMed PMID: 16427098.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Modulation of Delta(9)-THC-induced increase of cortical and hippocampal acetylcholine release by micro opioid and D(1) dopamine receptors. AU - Pisanu,A, AU - Acquas,E, AU - Fenu,S, AU - Di Chiara,G, Y1 - 2006/01/19/ PY - 2005/08/10/received PY - 2005/11/08/revised PY - 2005/11/21/accepted PY - 2006/1/24/pubmed PY - 2006/7/14/medline PY - 2006/1/24/entrez SP - 661 EP - 70 JF - Neuropharmacology JO - Neuropharmacology VL - 50 IS - 6 N2 - 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 micro 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), 24h before Delta(9)-THC, of the pseudo-irreversible micro(1) antagonist naloxonazine completely prevented the increase of ACh release by Delta(9)-THC. Pre-treatment with the D(1) receptor antagonist SCH 39,166 reduced Delta(9)-THC-induced ACh release both in the PFCx and in the hippocampus. Since Delta(9)-THC has been shown to increase DA release in the nucleus accumbens (NAc) shell via a micro(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 micro(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. SN - 0028-3908 UR - https://www.unboundmedicine.com/medline/citation/16427098/Modulation_of_Delta_9__THC_induced_increase_of_cortical_and_hippocampal_acetylcholine_release_by_micro_opioid_and_D_1__dopamine_receptors_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0028-3908(05)00397-7 DB - PRIME DP - Unbound Medicine ER -