Endocrine and other responses to acute administration of cannabinoid compounds to non-stressed male calves.
There is an abundance of cannabinoid (CB) receptors for derivatives of cannabis plants in the brain and throughout the body, and several naturally occurring arachidonic acid derivatives can activate these receptors. The specific objective of this study was to activate these CB receptors in castrated male calves through administration of several CB agonists and to measure immediate changes in concentrations of several serum hormones, respiration rate, and sensitivity to pain. The rationale for the study was that exogenous activation of CB receptors might reveal whether the endogenous CB system (consisting of receptors and endogenous ligands) plays a role in the stress response of animals and specifically whether the activated CB system might be part of a coping mechanism to combat stress. Intravenous administration of three CB agonists (anandamide, methanandamide and WIN 55212-2) to nine castrated male calves under non-stress conditions provoked immediate increases of serum cortisol and respiration rate as well as rapidly caused hypoalgesia to cutaneous pain and thermal stimuli. Although anandamide and methanandamide did not affect serum prolactin, administration of another CB agonist (WIN 55212-2) did increase serum prolactin abruptly. None of the CB agonists affected serum growth hormone. In summary, many of the changes following administration of CB agonists were similar to a stress response in this species, but there were some agonist-specific differences, notably regarding prolactin secretion, as well as differences between calves and observations made in other species. Although CB receptors in calves may be activated by endogenous ligands during exposure to some stressors, the present results are also consistent with this CB system being part of a coping mechanism that helps animals deal with imposed stressors.
Zenor
B N
BN
Department of Animal Sciences, Purdue University, West Lafayette, IN 47907, USA.
Weesner
G D
GD
Malven
P V
PV
D000276:Adjuvants, Immunologic / Q000008:administration & dosage; D000818:Animals; D001095:Arachidonic Acids / Q000008:administration & dosage; D001522:Behavior, Animal / Q000187:drug effects; D048588:Benzoxazines; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002186:Cannabinoids / Q000494:pharmacology; D002417:Cattle; D063388:Endocannabinoids; D013006:Growth Hormone / Q000097:blood; D006854:Hydrocortisone / Q000097:blood; D007275:Injections, Intravenous; D008297:Male; D009025:Morpholines / Q000494:pharmacology; D009281:Naphthalenes / Q000494:pharmacology; D010146:Pain / Q000139:chemically induced; D053284:Polyunsaturated Alkamides; D011388:Prolactin / Q000097:blood; D043882:Receptors, Cannabinoid; D011955:Receptors, Drug / Q000502:physiology*; D013315:Stress, Psychological / Q000503:physiopathology*
D000276:Adjuvants, Immunologic; D001095:Arachidonic Acids; D048588:Benzoxazines; D002121:Calcium Channel Blockers; D002186:Cannabinoids; D063388:Endocannabinoids; D009025:Morpholines; D009281:Naphthalenes; D053284:Polyunsaturated Alkamides; D043882:Receptors, Cannabinoid; D011955:Receptors, Drug; C088155:methanandamide; C070417:(3R)-((2,3-dihydro-5-methyl-3-((4-morpholinyl)methyl)pyrrolo-(1,2,3-de)-1,4-benzoxazin-6-yl)(1-naphthalenyl))methanone; D011388:Prolactin; D013006:Growth Hormone; C078814:anandamide; D006854:Hydrocortisone