Dorsal root lesions block the expression of morphine withdrawal elicited from the rat spinal cord.
Evidence has been accumulating to indicate that the spinal cord plays an important role in the expression of several narcotic abstinence signs in the intact animal. One characteristic and reproducible withdrawal sign which can be elicited in both intact and spinal-transected dependent rats is the naloxone-induced increase in arterial blood pressure. Employing this model, this autonomic component of narcotic withdrawal was quantitated in dependent spinal (C1)-transected rats with intact dorsal roots and in those with surgical lesions of the dorsal roots from T3 to L4. The withdrawal-associated hypertension observed in animals with intact dorsal roots was abolished in the rats having the lesioned roots. The central spinal location of the opiate receptors mediating the naloxone response was confirmed by experiments demonstrating the failure of a selective peripherally acting narcotic antagonist to elicit a comparable withdrawal response. It was concluded that continuous afferent input and spinal opiate receptors are requirements for the expression of spinal narcotic withdrawal.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004195:Disease Models, Animal; D005727:Ganglia, Spinal / Q000503:physiopathology*; D008297:Male; D009020:Morphine / Q000008:administration & dosage*; D009270:Naloxone / Q000627:therapeutic use; D009433:Neural Inhibition; D009434:Neural Pathways / Q000503:physiopathology; D051381:Rats; D011919:Rats, Inbred Strains; D013375:Substance Withdrawal Syndrome / Q000503:physiopathology*; D013997:Time Factors
D009270:Naloxone; D009020:Morphine