title: An in vitro electrophysiological and Co2+-uptake study on the effect of infraorbital nerve transection on the cortical and thalamic neuronal activity.
abstract: Changes of neuronal membrane characteristics in somatosensory barrel cortex and barreloid thalamus were investigated in rats following unilateral transection of the infraorbital nerve. Kainate induced Co2+-uptake method and image analysis were used to assess the Ca2+ permeability of non-NMDA (N-methyl-D-aspartate) glutamate receptors. Changes in some biophysical parameters of the affected cortical neurons were also investigated by intracellular recording in slice experiments. The altered neuronal activity was measured on days 1, 5 and 14 after surgery. Kainate induced Co2+ uptake increased markedly reflecting enhanced Ca2+ permeability of alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionate/kainate (AMPA/KAIN)-type receptors. Changes were more pronounced in the cortex than in the thalamus and peaked on the first day following nerve transection. After that, parameters gradually returned to the normal level. However, a small enhancement was still detectable in the cortex at the end of the 2-week-long observation period. In parallel with the increased Co2+-uptake, moderate membrane potential changes, stronger spiking activity and enhanced excitability were characteristic for cortical neurons. The observed alterations in neuronal characteristics underlie the reorganization and regeneration processes following injuries or surgeries. We can conclude that immediate change of the receptive field in the barrel cortex following unilateral nerve transection is based on changes in biophysical parameters of the neurons. Altered peripheral activation evokes changes in the neuronal activity, thus providing opportunity for a quick synaptic rearrangement. AMPA/KAIN-type glutamate receptors have a decisive role in the regulation of these processes. This kind of synaptic plasticity is more significant in the cortex than in the thalamus.
authors.affiliation: Department of Physiology and Neurobiology, Eötvös Loránd University, 1088, Budapest, Hungary. vilagildi@ludens.elte.hu
authors.forename: I
authors.initials: I
authors.lastname: Világi
authors.forename: J
authors.initials: J
authors.lastname: Dóczi
authors.forename: D
authors.initials: D
authors.lastname: Kirilly
authors.forename: I
authors.initials: I
authors.lastname: Banczerowski-Pelyhe
authors.forename: J
authors.initials: J
authors.lastname: Takács
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000344:Afferent Pathways; D000818:Animals; D003035:Cobalt / Q000493:pharmacokinetics*; D003714:Denervation; D004594:Electrophysiology; D005260:Female; D008297:Male; D008442:Maxillary Nerve / Q000166:cytology* / Q000601:surgery; D009473:Neuronal Plasticity / Q000502:physiology; D009474:Neurons / Q000737:chemistry / Q000502:physiology; D009924:Organ Culture Techniques; D051381:Rats; D017207:Rats, Sprague-Dawley; D018091:Receptors, AMPA / Q000502:physiology; D018092:Kainic Acid Receptors / Q000502:physiology; D013003:Somatosensory Cortex / Q000166:cytology* / Q000502:physiology; D020651:Ventral Thalamic Nuclei / Q000166:cytology* / Q000502:physiology; D014738:Vibrissae / Q000294:innervation
chemical_list: D003035:Cobalt; D018091:Receptors, AMPA; D018092:Kainic Acid Receptors