title: Neurons in amygdala mediate ear pinna vasoconstriction elicited by unconditioned salient stimuli in conscious rabbits.
abstract: We determined whether functional integrity of neurons in the amygdala is necessary for sudden episodes of cutaneous vasoconstriction that occur when the conscious animal detects a salient alerting stimulus. To inhibit neuronal function, muscimol (5 nmol in 300 nl), a long acting and potent GABA-A receptor agonist that hyperpolarizes neurons, was injected bilaterally into the amygdala or into a more dorsal control site in conscious rabbits. Cutaneous blood flow was measured in the ear pinna flow using an ultrasonic Doppler probe chronically implanted around the central ear artery. Ear flow responses to salient unconditioned alerting stimuli (fur touch, slight cage movement. removal of drape covering cage) were examined before and after injection of the muscimol, and the effects compared with effects of muscimol on the ear flow response to more nociceptive stimuli, including ear pinch. Muscimol injections into the dorsal control site did not significantly alter alerting-related episodes of ear pinna vasoconstriction. Muscimol injections into the amygdala almost completely abolished ear vasoconstriction elicited by fur touch (0/5 positive responses), drape removal (0/7 positive responses) and cage movement (0/7 positive responses). Muscimol injections into the amygdala reduced the mean ear flow coefficient of variation for a 15 min observation period from 47+/-5 before injection to 15+/-33% after injection (P<0.01, n=7 rabbits). Muscimol injections into the amygdala did not alter the vigorous ear pinna vasoconstriction elicited by ear pinch (7/7 positive responses). Our results indicate that neuronal function in the amygdala, probably the central nucleus of the amygdala, is necessary for the occurrence of ear pinna vasoconstriction episodes elicited by unconditioned salient stimuli but not for the occurrence of corresponding vasoconstriction elicited by nociceptive stimuli.
authors.affiliation: Department of Physiology and Medicine, Flinders University, Bedford Park SA, Australia.
authors.forename: Y H
authors.initials: YH
authors.lastname: Yu
authors.forename: W W
authors.initials: WW
authors.lastname: Blessing
mesh_terms: D000679:Amygdala / Q000166:cytology* / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D001007:Anxiety / Q000503:physiopathology; D001288:Attention / Q000502:physiology; D003213:Conditioning, Psychological / Q000502:physiology; D003243:Consciousness / Q000502:physiology; D004431:Ear, External / Q000098:blood supply*; D005557:Formaldehyde; D018755:GABA Agonists / Q000494:pharmacology; D006339:Heart Rate / Q000502:physiology; D008297:Male; D008845:Microinjections; D009118:Muscimol / Q000494:pharmacology; D009305:Nasopharynx / Q000294:innervation; D009474:Neurons / Q000502:physiology*; D009619:Nociceptors / Q000502:physiology; D009812:Odorants; D010812:Physical Stimulation; D011817:Rabbits; D012018:Reflex / Q000502:physiology; D012039:Regional Blood Flow / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology*
chemical_list: D018755:GABA Agonists; D005557:Formaldehyde; D009118:Muscimol