Modulation of Postsynaptic Responses of Nociceptor-Activated Neurons of the Cat Somatosensory Cortex by Stimulation of the Substantia Nigra

Abstract

We studied the effect of electrical stimulation of the substantia nigra (SN) on postsynaptic processes evoked in neurons of the somatosensory cortex of the cat by stimulation of nociceptive (intense stimulation of the dental pulp) and non-nociceptive (moderate, in strength, stimulations of the n. infraorbitalis and ventroposteromedial nucleus, VPM, of the thalamus) afferent inputs. The intracellularly recorded 7 cells activated exclusively by stimulation of dental nociceptors and 10 cells activated by both nociceptive and non-nociceptive afferent volleys (nociceptive and convergent cortical neurons, respectively) were examined in detail. Complexes EPSP-action potential-long-lasting IPSP (up to 200-300 msec) developed in neurons of both groups after stimulations of both nociceptive afferents and the thalamic VPM. Conditioning stimulation of the SN preceding test stimulation of the dental pulp or VPM with intervals from 100 to 700 msec resulted in selective suppression of IPSPs; their amplitudes decreased by 40-60%. The maximum effect in both cases was observed at conditioning/test intervals of 300 to 700 msec. Under conditions of SN stimulation, the release of dopamine, by affecting receptors and secondary messengers, modulates postsynaptic activity in the cortical GABA-ergic system and decreases the amplitude of IPSPs induced by stimulations of both nociceptors (dental pulp) and low-threshold afferent inputs (VPM of the thalamus). This process can be mediated by both pre-synaptic and post-synaptic mechanisms.

Dopaminergic modulation of receptive fields in rat sensorimotor cortex

“…Inhibitory postsynaptic potentials (IPSP) of S1 neurons activated by nociceptive pathways were reduced after stimulation of the substantia nigra (Labakhua et al, 2008). While this may not be mediated by a direct dopaminergic projection to S1, it emphasizes the role of the dopaminergic system in the regulation of SMC inhibition.…”