Modulation of Synaptic Processes in Cortical Neurons in Response to Painful Stimulation and Analgesia

Abstract

We studied effects of electrical stimulation of the substantia nigra (SN), locus coeruleus (LC), raphe nuclei (RN), substantia innominata (SIn), nucleus caudatus (NC) and central grey (CG) on postsynaptic processes evoked in neurons of the cat somatosensory cortex by excitation of nociceptive and non-nociceptive afferent inputs (intense stimulation of the dental pulp and moderate stimulation of the thalamic ventroposteromedial nucleus, VPMN, respectively). We analyzed intracellularly recorded activity of cortical cells activated exclusively by stimulation of nociceptors and cells activated by both nociceptive and non-nociceptive influences ("nociceptive" and "convergent" neurons). In neurons of both groups, stimulation of both nociceptive afferents and thalamic VPMN resulted in the development of successions of EPSP-action potential (AP) or their series-IPSP (IPSP duration 200-300 msec). Conditioning electrical stimulation of the above-mentioned nuclei induced suppression of synaptic reactions that occur in cortical neurons in response to stimulation of nociceptive inputs. The maximum decrease in the amplitude of the IPSP was observed at test intervals of 600 to 800 msec when stimulated nuclei containing biogenic amines and 100-150 msec at conditioning electrical stimulation of cholinergic structures. We observed certain parallelism between conditioning influent ions of CG activation and effects of systemic injections of morphine. Discusses is the physiological significance of presumebly dendritic action potentials observed in our experiments. Decrease in the amplitude or complete postsynaptic inhibition of IPSP in cortical neurons under different treatments associate with the occurrence of convulsive epileptic activity, and at the painful action with analgesic effect. Discussed are the mechanisms for modulatory influences exerted by conditioning stimulation of SN, LC, RN, NC, SIn and CG on the somatosensory neurons, activated upon excitation of high-threshold (nociceptive) afferent inputs. Such modulation is probably based on changes developing in both pre and post-synaptic intracortical mechanisms.