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The Journal of Neurophysiology Vol. 87 No. 3 March 2002, pp. 1175-1185
Copyright ©2002 by the American Physiological Society
Department of Cell Biology and Anatomy and the Neuroscience Center of Excellence, Louisiana State Health Sciences Center, New Orleans, Louisiana 70112
Lo, Fu-Sun,
Jokubas Ziburkus, and
William Guido.
Synaptic Mechanisms Regulating the Activation of a
Ca2+-Mediated Plateau Potential in Developing Relay Cells
of the LGN. J. Neurophysiol. 87: 1175-1185, 2002. Using intracellular recordings in an
isolated (in vitro) rat brain stem preparation, we examined the
synaptic responses of developing relay neurons in the dorsal lateral
geniculate nucleus (LGN). In newborn rats, strong stimulation of the
optic tract (OT) evoked excitatory postsynaptic potentials (EPSPs) that
gave rise to a sustained (300-1,300 ms), slow-decaying (<0.01 mV/s), depolarization (25-40 mV). Riding atop this response was a train of
spikes of variable amplitude. We refer to this synaptically evoked
event as a plateau potential. Pharmacology experiments indicate the plateau potential was mediated by the activation of
high-threshold L-type Ca2+ channels. Synaptic
activation of the plateau potential relied on
N-methyl-D-aspartate (NMDA) receptor-mediated
activity and the spatial and/or temporal summation of retinally evoked
EPSPs. Inhibitory postsynaptic responses (IPSPs) did not prevent the expression of the plateau potential. However,
GABAA receptor activity modulated the intensity
of optic tract stimulation needed to evoke the plateau potential, while
GABAB receptor activity affected its duration.
Expression of the plateau potential was developmentally regulated,
showing a much higher incidence at P1-2 (90%) than at P19-20 (1%).
This was in part due to the fact that developing relay cells show a
greater degree of spatial summation than their mature counterparts,
receiving input from as many as 7-12 retinal ganglion cells. Early
spontaneous retinal activity is also likely to trigger the plateau
potential. Repetitive stimulation of optic tract in a manner that
approximated the high-frequency discharge of retinal ganglion cells led
to a massive temporal summation of EPSPs and the activation of a
sustained depolarization (>1 min) that was blocked by L-type
Ca2+ channel antagonists. These age-related
changes in Ca2+ signaling may contribute to the
activity-dependent refinement of retinogeniculate connections.
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