AXONAL SPROUTING IN LAYER-V PYRAMIDAL NEURONS OF CHRONICALLY INJURED CEREBRAL-CORTEX

We performed experiments to determine whether axonal sprouting occurs in neurons of chronic neocortical epileptogenic lesions. Partially iso lated somatosensory cortical islands with intact pial blood supply wer e prepared in mature rats. Neocortical slices from these lesions, stud ied 6-39 d later, generated spontaneous and/or evoked epileptiform fie ld potentials (Prince and Tseng, 1993) during which neurons displayed prolonged polyphasic excitatory and inhibitory synaptic potentials/cur rents. Single electrophysiologically characterized layer V pyramidal n eurons in control and epileptogenic slices were filled with biocytin u sing sharp and patch-electrode techniques, their axonal arbors reconst ructed and compared quantitatively. Neurons in injured cortex had a 56 % increase in total axonal length, a 64% increase in the number of axo nal collaterals and more than a doubling (115% increase) of the number of axonal swellings. The presumed boutons were smaller and more close ly spaced than those of control cells. In some neurons the main descen ding axon had hypertrophic segments from which branches arose. These h ighly significant changes were most marked in the perisomatic region o f layer V. The axonal sprouting was associated with a decrease in soma tic area but no significant change in dendritic arbors. Results sugges t that a significant degree of axonal reorganization takes place in th e chronically injured cortex where it might be an adaptive mechanism f or recovery of function after injury, or might be maladaptive and play an important role in the generation of epileptiform events by increas ing the numbers and density of synaptic contacts between neurons.