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The Journal of Neurophysiology Vol. 81 No. 5 May 1999, pp. 2243-2252
Copyright ©1999 by the American Physiological Society
1Institute for Developmental Neuroscience, Vanderbilt University, Nashville, Tennessee 37203; and 2Division of Neurosurgery, UCLA School of Medicine, Los Angeles, California 90095
Friedberg, Marc H.,
Stefan M. Lee, and
Ford F. Ebner.
Modulation of Receptive Field Properties of Thalamic
Somatosensory Neurons by the Depth of Anesthesia. J. Neurophysiol. 81: 2243-2252, 1999.
Modulation of receptive field properties of thalamic somatosensory
neurons by the depth of anesthesia. The dominant frequency of
electrocorticographic (ECoG) recordings was used to determine the depth
of halothane or urethan anesthesia while recording extracellular single-unit responses from thalamic ventral posterior medial (VPM) neurons. A piezoelectric stimulator was used to deflect individual whiskers to assess the peak onset latency, magnitude, probability of
response, and receptive field (RF) size. There was a predictable increase in the dominant ECoG frequency from deep stage IV to light
stage III-1 anesthetic levels. There was no detectable frequency at
stage IV, a 1- to 2-Hz dominant frequency at stage III-4, 3-4 Hz at
stage III-3, 5-7 Hz at stage III-2, and a dual 6- and 10- to 13-Hz
pattern at stage III-1. Reflexes and other physical signs showed a
correlation with depth of anesthesia but exhibited too much overlap
between stages to be used as a criterion for any single stage. RF size
and peak onset latency of VPM neurons to whisker stimulations increased
between stage III-4 and III-1. A dramatic increase in RF size and
response latency occurred at the transition from stage III-3 (RF size
~2 whiskers, latency ~7 ms) to stage III-2 (RF size ~6 whiskers,
latency ~11 ms). Response probability and magnitude decreased from
stage III-4 to stage III-3 and III-2. No responses were ever evoked in
VPM cells by vibrissa movement at stage IV. These changes in VPM
responses as a function of anesthetic depth were seen only when the
nucleus principalis (PrV) and nucleus interpolaris (SpVi)
trigeminothalamic pathways were both intact. Eliminating SpVi inputs to
VPM, either by cutting the primary trigeminal afferent fibers to SpVi
or cutting axons projecting from SpVi to VPM, immediately reduced the
RF size to fewer than three whiskers. In addition, the predictable changes in VPM response probability, response magnitude, and peak onset
latency at different anesthetic depths were all absent after SpVi
pathway interruption. We conclude that 1) the PrV input
mediates the near "one-to-one" correspondence between a neuronal
response in VPM and a single mystacial whisker, 2) in
contrast, the SpVi input to VPM is primarily responsible for the RF
properties of VPM neurons at light levels of anesthesia and presumably
in the awake animal, and 3) alterations in VPM responses
produced by changing the depth of anesthesia are due to its selective
influence on the properties mediated by SpVi inputs at the level of the thalamus.
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