Modulation of Receptive Field Properties of Thalamic Somatosensory Neurons by the Depth of Anesthesia

Abstract

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 approximately 2 whiskers, latency approximately 7 ms) to stage III-2 (RF size approximately 6 whiskers, latency approximately 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.

A New Thalamic Pathway of Vibrissal Information Modulated by the Motor Cortex

“…Although it has been well demonstrated that the receptive field size of VPM neurons depends on the depth of anesthesia (Friedberg et al, 1999;Aguilar and Castro-Alamancos, 2005), this dependence seems to apply primarily to the more numerous relay cells forming the core of the barreloids, because cells within the head and tail compartments maintained a large receptive field despite the deep level of anesthesia used in our experiments. One should also note that, because barreloids form curved, obliquely oriented rods with respect to the vertical, different ratios of mono-whisker and multiwhisker cells can be obtained, depending on the location of microelectrode descents and on the extent to which the entire thickness of the VPM is explored.…”

Cross-Sensory Modulation of Primary Sensory Cortex Is Developmentally Regulated by Early Sensory Experience

“…Body temperature was maintained at 37°C with a feedback-actuated heating pad (Harvard Apparatus). Supplementary injections (10% of the initial dose) were given as needed to maintain the anesthesia at stage III-3 (Friedberg et al, 1999). After making a small opening in the dura mater, microelectrodes were advanced in columnar penetrations perpendicular to the cortical surface.…”

I.v. cocaine induces rapid, transient excitation of striatal neurons via its action on peripheral neural elements: Single-cell, iontophoretic study in awake and anesthetized rats

“…With the exception of the monoamine-containing cells (Einhorn et al, 1988; Pitts and Marwah, 1987), single-unit studies with iv COC delivery in anesthetized animals are limited and focused on slow drug-induced changes in discharge rate or neuronal responses to afferent inputs (Jimenes-Rivera and Waterhouse, 1991;Waterhouse et al, 1991). Urethane was chosen because this drug, compared to other general anesthetics, minimally inhibits brain metabolism, neuronal activity and responses to sensory stimuli (Buzsaki et al 1983;Friedberg et al 1999). Therefore, by comparing data obtained in the same animals in two preparations we were able to clarify the role of an animal's activity state in determining striatal neuronal responses to both somatosensory stimuli and COC.…”