Electrophysiologically recorded C-fiber reflexes in intact and acute decerebrate-spinal cats: Absence of nalckone facilitation in intact cats

A C-fiber reflex was obtained from stimulating and recording electrodes attached respectively to the superficial peroneal and posterior biceps semitendinosus nerves in intact cats. Naloxone in a dose dependent manner increased vocalizations produced by nerve stimulation, but it did not facilitate the C-fiber reflex in the intact cat. However, naloxone facilitated C-fiber reflexes in decerebrate-sptnal cats under identical stimulating and recording conditions as used in the Intact cat. It was concluded that naloxone causes Increased nociception to cutaneous nerve stimulation in intact cats but for naloxone to facilitate the C-fiber reflex, removal of supraspinal control is necessary. Many C-fiber afferents transmit nociception to the CNS (Bessou and Perl, 1969). Electrical stimulation of the superficial peroneal nerve that activates C fibers produces a segmental reflex in the unanesthetized decerebrate-splnal cat (Koll, Hasse, Schutz and Muhlberg, 1963). This C-fiber reflex is manifested by a long latency discharge recorded from an ipsilateral L₇ or S₁ ventral root. The C-fiber reflex is considered nociceptive because only intense stimulation evokes it and morphine depresses it in doses lower than those that depress other spinal reflexes (Koll et al., 1963). Low doses of the opiate antagonists naloxone and naltrexone consistently facilitate the C-fiber reflex (Bell and Martin, 1977). These results support the hypothesis that released endogenous opioids inhibit the C-fiber reflex. However, the facilitative effects of the opiate antagonists could be confined to the decerebrate-spinal preparation where invasive expert mental procedures (decerebration, dissection, etc.) may release endogenous opioids. Furthermore, eliminating supraspinal control may unmask the facultative effects of naloxone. Therefore, we examined the effect of naloxone on the C-fiber reflex of the intact cat.