TY - JOUR
T1 - Footshock-induced analgesia
T2 - Its opioid nature depends on the strain of rat
AU - Urca, Gideon
AU - Segev, Shlomo
AU - Sarne, Yosef
PY - 1985/3/11
Y1 - 1985/3/11
N2 - Previous studies have indicated that stressful footshock can induce both opioid, naloxone-sensitive, and non-opioid, naloxone-insensitive forms of analgesia, depending on stimulation parameters used with 30 min of intermittent footshock (3 mA, 1 s on, 5 s off) producing opioid analgesia and 3 min of continuous shock (3 mA) producing non-opioid analgesia. Using a local strain of Charles River (CR)-derived rats were conducted a parametric investigation of footshock-induced analgesia applying both AC and DC scrambled shock ranging from 1 to 4 mA, continuous shock of 1, 3 and 5 min in duration and intermittent shock lasting 1, 3, 5, 10, 20, 30 and 80 min. All shock parameters produced potent analgesia. In no case did 10 mg/kg of naloxone block this analgesia. Varying the dose of the antagonist (0.1-10 mg/kg) and testing the animals at different points in the diurnal cycle did not result in the emergence of naloxone-sensitive anangesia. Based on the assumption that non-opioid systems may mask the activity of opioid analgesia systems, we attempted to either enhance opioid analgesia by: (1) preventing enkephalin degradation by the use of d-phenylalanine; (2) increasing the entry of blood-borne opioids into the brain by the use of DMSO; and (3) the attenuation of non-opioid analgesia by the use of reserpine. In no case did a naloxone-sensitive component of analgesia emerge. To test whether the animals possess an intact opioid analgesia system, both electrical stimulation of, and injection of opiates into the periaqueductal gray (PAG) were examined. Both procedures produced analgesia which was reversed by naloxone. Finally, 7 additional strains of rats were tested for the effects of naloxone on analgesia produced by 30 min of intermittent footshock. Naloxone attenuation of analgesia was observed consistently in only 2 of the 8 strains tested. Based on these and other data, we propose that both opioid and non-opioid analgesia systems are coactivated by footshock, and that their predominance is determined by genetic factors.
AB - Previous studies have indicated that stressful footshock can induce both opioid, naloxone-sensitive, and non-opioid, naloxone-insensitive forms of analgesia, depending on stimulation parameters used with 30 min of intermittent footshock (3 mA, 1 s on, 5 s off) producing opioid analgesia and 3 min of continuous shock (3 mA) producing non-opioid analgesia. Using a local strain of Charles River (CR)-derived rats were conducted a parametric investigation of footshock-induced analgesia applying both AC and DC scrambled shock ranging from 1 to 4 mA, continuous shock of 1, 3 and 5 min in duration and intermittent shock lasting 1, 3, 5, 10, 20, 30 and 80 min. All shock parameters produced potent analgesia. In no case did 10 mg/kg of naloxone block this analgesia. Varying the dose of the antagonist (0.1-10 mg/kg) and testing the animals at different points in the diurnal cycle did not result in the emergence of naloxone-sensitive anangesia. Based on the assumption that non-opioid systems may mask the activity of opioid analgesia systems, we attempted to either enhance opioid analgesia by: (1) preventing enkephalin degradation by the use of d-phenylalanine; (2) increasing the entry of blood-borne opioids into the brain by the use of DMSO; and (3) the attenuation of non-opioid analgesia by the use of reserpine. In no case did a naloxone-sensitive component of analgesia emerge. To test whether the animals possess an intact opioid analgesia system, both electrical stimulation of, and injection of opiates into the periaqueductal gray (PAG) were examined. Both procedures produced analgesia which was reversed by naloxone. Finally, 7 additional strains of rats were tested for the effects of naloxone on analgesia produced by 30 min of intermittent footshock. Naloxone attenuation of analgesia was observed consistently in only 2 of the 8 strains tested. Based on these and other data, we propose that both opioid and non-opioid analgesia systems are coactivated by footshock, and that their predominance is determined by genetic factors.
KW - enkephalin
KW - footshock analgesia
KW - naloxone
UR - http://www.scopus.com/inward/record.url?scp=0021987732&partnerID=8YFLogxK
U2 - 10.1016/0006-8993(85)90516-5
DO - 10.1016/0006-8993(85)90516-5
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AN - SCOPUS:0021987732
SN - 0006-8993
VL - 329
SP - 109
EP - 116
JO - Brain Research
JF - Brain Research
IS - 1-2
ER -