Inhibition of thalamic nociceptive neurons follwing conditioning stimulation of the fornix

Abstract

Previously we found that conditioning stimulation applied to the mesencephalic periaqueductal gray matter (PAG) inhibited the response of thalamic neurons to nociceptive input in the lateral and medial pain pathways. The inhibitory system arising from the PAG exerted inhibitory effects on a large proportion of thalamic nociceptive neurons in the lateral pain pathway, while only on a small proportion of thalamic nociceptive neurons in the medial pain pathway. In the present experiment, we studied the effect of conditioning stimulation applied to the fornix (Fx) on the response of nociceptive neurons in the intralaminar nuclei and in the nucleus ventralis posteromedialis (VPM). Experiments were carried out on adult cats anesthetized with urethane and chloralose. Single neuron activities were recorded from the nucleus centralis lateralis (CL), the nucleus parafascicularis (Pf) and the VPM. We studied the effect of conditioning Fx stimulation on neurons that respond to stimulation of the greater splanchnic nerve, greater occipital nerve, and/or tooth pulp. We obtained 43 CL and 38 Pf nociceptive neurons. They usually respond to heavy pressure applied to deep tissues rather than skin. In 13 CL and 11 Pf neurons, conditioning Fx stimulation at an intensity of less than 1mA inhibited the response to peripheral input and/or to electrical stimulation of the mesencephalic reticular formation (MRF). Intravenous naloxone (1mg/kg) did not antagonize inhibition of the response of nociceptive CL and Pf neurons to peripheral input and/or MRF stimulation. A total of 20 tooth pulp neurons that responded to tooth pulp afferent input were recorded from the shell region of the VPM. The response to tooth pulp stimulation or trigeminothalamic tract stimulation was not inhibited in any of them by the conditioning Fx stimulation. The results suggest that nociceptive neurons in the intralaminar nuclei are inhibited following conditioning stimulation of the Fx, and that this inhibition is not mediated by opiate receptors. This inhibitory system arising from the Fx acts mainly at the thalamic level of the medial pain pathway.