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Effects of acute and repeated restraint stress on endocannabinoid content in the amygdala, ventral striatum, and medial prefrontal cortex in mice.
Neuropharmacology. 2008 Jan; 54(1):108-16.N

Abstract

Endocannabinoid signaling has been implicated in habituation to repeated stress. The hypothesis that repeated exposures to stress alters endocannabinoid signaling in the limbic circuit was tested by restraining male mice for 30 min/day for 1, 7, or 10 days and measuring brain endocannabinoid content. Amygdalar N-arachidonylethanolamine was decreased after 1, 7, and 10 restraint episodes; 2-arachidonylglycerol was increased after the 10th restraint. A similar pattern occurred in the medial prefrontal cortex (mPFC): N-arachidonylethanolamine was decreased after the 7th and 10th restraints and 2-arachidonylglycerol was increased after the 10th restraint. In the ventral striatum, the pattern reversed: N-arachidonylethanolamine was increased after the 10th restraint and 2-arachidonylglycerol was decreased after the 7th restraint. Palmitoylethanolamide contents changed in parallel with N-arachidonylethanolamine in the amygdala and ventral striatum. A single restraint episode did not affect the activity of fatty acid amide hydrolase (FAAH) in any of the brain regions examined. After the 10th restraint, both V(max) and K(m) for N-arachidonylethanolamine were increased in the mPFC; while only the V(max) was increased in the amygdala. On the other hand, the V(max) of FAAH was decreased in ventral striatum after the 10th restraint. After the 10th restraint, the maximum velocity for 2-oleoylglycerol hydrolysis was increased in mPFC; no other changes in 2-oleoylglycerol hydrolysis occurred. Repeated exposure to restraint produced no changes in CB(1) receptor density in any of the areas examined. These studies are consistent with the hypothesis that stress exposure alters endocannabinoid signaling in the brain and that alterations in endocannabinoid signaling occur during habituation to stress.

Authors+Show Affiliations

Medical College of Wisconsin, Department of Pharmacology and Toxicology, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

17675104

Citation

Rademacher, David J., et al. "Effects of Acute and Repeated Restraint Stress On Endocannabinoid Content in the Amygdala, Ventral Striatum, and Medial Prefrontal Cortex in Mice." Neuropharmacology, vol. 54, no. 1, 2008, pp. 108-16.
Rademacher DJ, Meier SE, Shi L, et al. Effects of acute and repeated restraint stress on endocannabinoid content in the amygdala, ventral striatum, and medial prefrontal cortex in mice. Neuropharmacology. 2008;54(1):108-16.
Rademacher, D. J., Meier, S. E., Shi, L., Ho, W. S., Jarrahian, A., & Hillard, C. J. (2008). Effects of acute and repeated restraint stress on endocannabinoid content in the amygdala, ventral striatum, and medial prefrontal cortex in mice. Neuropharmacology, 54(1), 108-16.
Rademacher DJ, et al. Effects of Acute and Repeated Restraint Stress On Endocannabinoid Content in the Amygdala, Ventral Striatum, and Medial Prefrontal Cortex in Mice. Neuropharmacology. 2008;54(1):108-16. PubMed PMID: 17675104.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of acute and repeated restraint stress on endocannabinoid content in the amygdala, ventral striatum, and medial prefrontal cortex in mice. AU - Rademacher,David J, AU - Meier,Sarah E, AU - Shi,Leyu, AU - Ho,W-S Vanessa, AU - Jarrahian,Abbas, AU - Hillard,Cecilia J, Y1 - 2007/06/29/ PY - 2007/04/25/received PY - 2007/06/11/revised PY - 2007/06/13/accepted PY - 2007/8/7/pubmed PY - 2008/4/19/medline PY - 2007/8/7/entrez SP - 108 EP - 16 JF - Neuropharmacology JO - Neuropharmacology VL - 54 IS - 1 N2 - Endocannabinoid signaling has been implicated in habituation to repeated stress. The hypothesis that repeated exposures to stress alters endocannabinoid signaling in the limbic circuit was tested by restraining male mice for 30 min/day for 1, 7, or 10 days and measuring brain endocannabinoid content. Amygdalar N-arachidonylethanolamine was decreased after 1, 7, and 10 restraint episodes; 2-arachidonylglycerol was increased after the 10th restraint. A similar pattern occurred in the medial prefrontal cortex (mPFC): N-arachidonylethanolamine was decreased after the 7th and 10th restraints and 2-arachidonylglycerol was increased after the 10th restraint. In the ventral striatum, the pattern reversed: N-arachidonylethanolamine was increased after the 10th restraint and 2-arachidonylglycerol was decreased after the 7th restraint. Palmitoylethanolamide contents changed in parallel with N-arachidonylethanolamine in the amygdala and ventral striatum. A single restraint episode did not affect the activity of fatty acid amide hydrolase (FAAH) in any of the brain regions examined. After the 10th restraint, both V(max) and K(m) for N-arachidonylethanolamine were increased in the mPFC; while only the V(max) was increased in the amygdala. On the other hand, the V(max) of FAAH was decreased in ventral striatum after the 10th restraint. After the 10th restraint, the maximum velocity for 2-oleoylglycerol hydrolysis was increased in mPFC; no other changes in 2-oleoylglycerol hydrolysis occurred. Repeated exposure to restraint produced no changes in CB(1) receptor density in any of the areas examined. These studies are consistent with the hypothesis that stress exposure alters endocannabinoid signaling in the brain and that alterations in endocannabinoid signaling occur during habituation to stress. SN - 0028-3908 UR - https://www.unboundmedicine.com/medline/citation/17675104/Effects_of_acute_and_repeated_restraint_stress_on_endocannabinoid_content_in_the_amygdala_ventral_striatum_and_medial_prefrontal_cortex_in_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0028-3908(07)00186-4 DB - PRIME DP - Unbound Medicine ER -