Somatosensory neurons in partially deafferented rat hindlimb granular cortex subsequent to transection of the sciatic nerve: effects of glutamate and acetylcholine.
The effects of drugs administered iontophoretically were studied on 302 neurons isolated from partially deafferented hindlimb granular cortex of the rat and were compared to a previously studied sample from normal granular cortex. The proportions of cells affected by glutamate and acetylcholine (ACh) were not markedly different after partial deafferentation, but the cells were more readily depolarized by glutamate and their responses to a fixed dose of glutamate were larger. Fewer cells were excited strongly by ACh (up to the point of depolarization block) and the amplitudes of responses to test pulses of ACh were reduced in infragranular layers after partial deafferentation. Fifteen cells (5.9%) were inhibited by ACh administration, whereas in normal cortex this value was less than 1%. Fewer receptive fields were uncovered by glutamate after partial deafferentation, but more receptive fields were enlarged by this substance after nerve transection. These data were interpreted to mean that the cells from deafferented cortex had fewer excitatory inputs and as well, were apparently under a comparatively weaker degree of inhibitory control after deafferentation. The administration of ACh uncovered fewer somatic inputs than in normal animals. Responses were enhanced by ACh less frequently, and repeated treatments with ACh often led to a reduction in the effectiveness of the afferent stimulus. Increases in neuronal thresholds for somatic stimuli also were observed. The laminar distribution of the effects of ACh was similar to the distribution observed in normal animals. The responses to iontophoretically administered ACh and its agonists appeared to be mediated through both nicotinic and muscarinic receptor processes after partial deafferentation. Often the time course of the effects of ACh was abnormal, being characterized by oscillations between silence and very high rates of discharge with a period of 6-12 s. These observations are consistent with the hypothesis that after a major deafferentation (i) there is a reduction of the inhibitory controls normally present in the somatosensory cortex, and (ii) neuronal responses to ACh are modified in partially deafferented cortex. The magnitude of the responses of cells to ACh in the supragranular layers are larger after deafferentation whereas the magnitude of responses in the infragranular layers are reduced by this procedure. These changes may be related to changes induced by deafferentation in the distribution of receptors and/or in their pharmacological properties.
D000109:Acetylcholine / Q000494:pharmacology*; D000344:Afferent Pathways / Q000502:physiology; D000818:Animals; D004558:Electric Stimulation; D005971:Glutamates / Q000494:pharmacology*; D018698:Glutamic Acid; D006614:Hindlimb / Q000294:innervation; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D012016:Reference Values; D012584:Sciatic Nerve / Q000502:physiology*; D013003:Somatosensory Cortex / Q000187:drug effects / Q000502:physiology*
D005971:Glutamates; D018698:Glutamic Acid; D000109:Acetylcholine