Activation of the primary motor cortex by somatosensory stimulation in adult rats is mediated mainly by associational connections from the somatosensory cortex

Neuroscience. 1999 May;90(2):353-61. doi: 10.1016/s0306-4522(98)00451-5.


In anaesthetized adult rats, facial nerve injury causes a disinhibition of the interhemispheric connections between homotopic representation fields in the primary motor cortex with a latency of 4 min (Toldi et al., 1996, Neurosci Lett. 203, 179-182). One possible explanation for the induction of such rapid changes is an alteration of the somatosensory input to the motor cortex. To test this hypothesis, unit activity in primary motor cortex was recorded during electrical stimulation of trigeminal afferents in the contralateral whisker-pad. About one-third of all recorded primary motor cortex neurons responded with latencies shorter than in the ventrolateral and posterior nuclei of the thalamus. Responses failed at stimulation frequencies > or = 10 Hz and after elimination or inactivation of the somatosensory cortex. Within primary motor cortex, the activatable neurons displayed a bilaminar distribution and were identified as pyramidal neurons by neurobiotin labelling. The results suggest that trigeminal afferents participate in modulation of the activity of primary motor cortex output neurons via primary somatosensory cortex-to-primary motor cortex associational connections, even under anaesthesia.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Afferent Pathways / physiology
  • Animals
  • Electric Stimulation
  • Evoked Potentials / drug effects
  • Evoked Potentials / physiology
  • Female
  • Functional Laterality
  • Lidocaine / pharmacology
  • Male
  • Motor Cortex / physiology*
  • Neurons / drug effects
  • Neurons / physiology*
  • Pyramidal Cells / physiology
  • Rats
  • Rats, Sprague-Dawley
  • Reaction Time
  • Somatosensory Cortex / physiology*
  • Vibrissae / innervation


  • Lidocaine