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Journal of Neuroscience, Vol 15, 8234-8245, Copyright © 1995 by Society for Neuroscience
Axonal sprouting in layer V pyramidal neurons of chronically injured cerebral cortex
P Salin, GF Tseng, S Hoffman, I Parada and DA Prince
Department of Pharmacology, University of California San Francisco 94143-0450, USA.
We performed experiments to determine whether axonal sprouting occurs in
neurons of chronic neocortical epileptogenic lesions. Partially isolated
somatosensory cortical islands with intact pial blood supply were prepared
in mature rats. Neocortical slices from these lesions, studied 6-39 d
later, generated spontaneous and/or evoked epileptiform field potentials
(Prince and Tseng, 1993) during which neurons displayed prolonged
polyphasic excitatory and inhibitory synaptic potentials/currents. Single
electrophysiologically characterized layer V pyramidal neurons in control
and epileptogenic slices were filled with biocytin using sharp and
patch-electrode techniques, their axonal arbors reconstructed and compared
quantitatively. Neurons in injured cortex had a 56% increase in total
axonal length, a 64% increase in the number of axonal collaterals and more
than a doubling (115% increase) of the number of axonal swellings. The
presumed boutons were smaller and more closely spaced than those of control
cells. In some neurons the main descending axon had hypertrophic segments
from which branches arose. These highly significant changes were most
marked in the perisomatic region of layer V. The axonal sprouting was
associated with a decrease in somatic area but no significant change in
dendritic arbors. Results suggest that a significant degree of axonal
reorganization takes place in the chronically injured cortex where it might
be an adaptive mechanism for recovery of function after injury, or might be
maladaptive and play an important role in the generation of epileptiform
events by increasing the numbers and density of synaptic contacts between
neurons.
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