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The Journal of Neurophysiology Vol. 85 No. 1 January 2001, pp. 1-9
Copyright ©2001 by the American Physiological Society
Department of Anatomy and Neurobiology, Program in Molecular, Cellular and Integrative Neuroscience, Colorado State University, Fort Collins, Colorado 80523
Smith, Bret N. and
F. Edward Dudek.
Short- and Long-Term Changes in CA1 Network Excitability After
Kainate Treatment in Rats. J. Neurophysiol. 85: 1-9, 2001. Neuron loss, axon sprouting, and the
formation of new synaptic circuits have been hypothesized to contribute
to seizures in temporal lobe epilepsy (TLE). Using the kainate-treated
rat, we examined how alterations in the density of CA1 pyramidal cells and interneurons, and subsequent sprouting of CA1 pyramidal cell axons,
were temporally associated with functional changes in the network
properties of the CA1 area. Control rats were compared with animals
during the first week after kainate treatment versus several weeks
after treatment. The density of CA1 pyramidal cells and putative
inhibitory neurons in stratum oriens was reduced within 8 days after
kainate treatment. Axon branching of CA1 pyramidal cells was
similar between controls and animals examined in the first week after
kainate treatment but was increased several weeks after kainate
treatment. Stimulation of afferent fibers in brain slices containing
the isolated CA1 region produced graded responses in slices from
controls and kainate-treated rats tested <8 days after treatment. In
contrast, synchronous all-or-none bursts of spikes at low stimulus
intensity (i.e., "network bursts") were only observed in the CA1
several weeks after kainate treatment. In the presence of bicuculline,
the duration of evoked bursts was significantly longer in CA1 pyramidal
cells weeks after kainate treatment than from controls or those
examined in the first week posttreatment. Spontaneous network bursts
were also observed in the isolated CA1 several weeks after kainate
treatment in bicuculline-treated slices. The data suggest that the
early loss of neurons directly associated with kainate-induced status
epilepticus is followed by increased axon sprouting and new recurrent
excitatory circuits in CA1 pyramidal cells. These changes characterize
the transition from the initial acute effects of the kainate-induced
insult to the eventual development of all-or-none epileptiform
discharges in the CA1 area.
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