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Brain Research, 540 (1991) 106-112 © 1991 Elsevier Science Publishers B.V. 0006-8993/91/$03.50 ADONIS 000689939116495V

BRES 16495

Topographic analysis of field potentials in rat vibrissa/barrel cortex Shi D i 1'2 and D a n i e l S. Barth ~ l Department of Psychology, University of Colorado, Boulder, CO (U.S.A.)and 2Mental Health Institute, Belling Medical University (P.R. China)

(Accepted 30 October 1990) Key words: Evoked potential; Topographic analysis; Vibrissa; Somatosensory cortex

An 8 x 8 multichannei microelectrode array was used to simultaneously record epicortical field potentials, evoked by displacement of contralateral vibrissae, from a 4 x 4 mm2 area of vibrissa/barrel cortex in 4 rats. The epicortical responses began with early positive(P1)and negative (N1) sharp waves, followed by slower positive (P2) and negative (N2) waves. The potential complex systematically shifted toeation with vibrissa stimulated, in accordance with the known somatotopic anatomy of vibrissa/barrel cortex. Topographical distributions of potentials at the P1, N1, P2 and N2 peaks were approximately concentric, but had distinct spatial extents, suggesting that they were generated by different but overlapping neuronal subpopulations. We propose that the SEP in the vibrissa/barrel cortex is produced by both sequential and parallel processing of somatosensory information, and that all components of the epicortical SEP are generated only in primary somatosensory cortex of the rat. Applications and weaknesses of topographic analysis methods are discussed.

INTRODUCTION Somatosensory evoked potentials (SEP) in rat ~5"z7 and other species 2"3a°, including man 1't2-14'32, consist of a repeatable sequence of amplitude peaks that are characterized by their polarity and mean response latency. Neuroanatomical and functional correlates of peaks in extracellular macropotentials of the SEP complex are of interest because of insights they may provide about basic stages in the processing of somatosensory information in large neural systems a1'23. Recent topographical studies of human SEPs recorded at the scalp in response to stimulation of median nerve 11'17-19'23 have indicated that its waveform peaks are associated with distinct extracranial potential distributions, suggesting the existence of multiple intracranial sources responsible for the SEP complex. This hypothesis is further supported by studies demonstrating that experimental and clinical lesions of the central nervous system at different locations can have differential effects on the latency and amplitude of certain peaks in the SEP complex 10'11'17-19'23'24'26'27'33'36. While this work raises the possibility of multiple neuronal generators producing the somatosensory evoked response, in no species have the location and spatial extent of these multiple cortical regions been clearly identified. Rat vibrissa/barrel cortex provides a unique opportunity for such a study of the functional anatomy of the SEP

complex, due to its well established cytoarchitectonic organization and the direct one to one relationship between layer IV barrels and corresponding peripheral tactile sensory organs, the mystacial vibrissae. In the classical studies of Woolsey and LeMessurier in rat 38 and Woolsey in mouse 37, epicortical SEP mapped from vibrissa/barrel cortex showed a clear somatotopic cortical representation of the mystacial pad that was in close agreement with subsequent anatomical investigations 39. These findings were based on the vibrissa-evoked response complex as a whole and did not address the spatial and temporal characteristics of its different amplitude peaks. The objectives of the present study were to (1) define the characteristic amplitude peaks of epicortical SEP in vibrissa/barrel field; (2) identify the location and spatial extent of neural subpoputations producing the SEP complex, based on the topography of epicortical potentials at its amplitude peaks; and (3) determine if activity in these putative neural subpopulations, identified for the peaks of the SEP. are sufficient to explain the entire spatiotemporal pattern of the SEP complex. MATERIALS AND METHODS Animal preparation Four adult Sprague-Dawley rats (300-350 g) were anesthetized with a combination of ketamine HCI (66 mg/kg) and xylazine (13 mg/kg) followed by atropine sulphate (0.6 mg/kg). During subse-

Correspondence: Shi Di, Department of Psychology, Campus Box 345, University of Colorado at Boulder, Boulder, CO 80309-0345, U.S.A.

107 waveform peak. Regression weights across all latencies were assumed to represent the relative contribution over time of each subpopulation of neurons to the overall response complex.

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RESULTS A conventional drawing of the left mystacial pad is shown in Fig. 2A. Mystacial vibrissae are organized in 5 rows, labeled as A , B, C, D and E, with at least 5 large vibfissae in each row. Fig. 2C shows typical averaged I

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responses in rat # 1 , recorded simultaneously from all

Fig. 1. Cartoon depiction of the exposed right hemisphere of rat cortex with a rectangular array of 64 surface electrodes (0.5 mm interelectrode distance) centered on the approximate location of the vibrissa/barrel cortex. The electrode array covers 4 x 4 mm2 of cortical surface.

electrodes of the 8 x 8 micro-array. The response, evoked by displacement of contralateral vibrissa C1

quent experimentation, anesthetic levels were maintained so that the corneal reflex could barely be elicited. A unilateral craniotomy exposed a region over the parieto-temporal cortex in the right hemisphere. The dura was removed and exposed cortex covered with saline throughout the experiment. Normal body temperature was maintained using a regulated heating pad.

Stimulation Each of 25 large vibrissae in the left mystacial pad (5 in each row) were stimulated individually. The method of stimulation was similar to that described in a previous report s. The vibrissae were cut to a length of approximately 12 mm and attached to the tip of a balsa wood probe. The probe was driven by a laboratory-built stimulator which used a small audio speaker to transform computer-controlled electrical square wave pulses into vertical mechanical movements up to few millimeters. In the present study, brief (0.3 ms duration; 1 s interstimulus interval) monophasic pulses were used to produce vibrissal displacements of approximately 0.2 mm excursion in the dorsoventral direction. This stimulation setting produced highly repeatable evoked cortical responses. Field potential recording and analysis Mapping of field potentials on the cortical surface was performed with a specially designed epicortical electrode array. The array consisted of 64 platinum electrodes (tip diameter: 100/~m) configured in an 8 x 8 electrode square with interelectrode distances of 0.5 mm, covering a 4 x 4 mm2 area at the approximate location of the vibrissa/barrel cortex in the right hemisphere (Fig. 1). Recordings were referred to a Ag/AgC1 ball electrode mounted in a burr-hole drilled in the frontal bone. The surface field potentials were simultaneously amplified (Grass 12A5 amplifiers; 0.1-100 Hz bandpass), digitally sampled (250 Hz; 400 ms) and averaged responses (n = 50) stored on disk for further analysis. Topographical analysis of the SEP was similar to that described in a previous study on auditory evoked potentials in the rat 5. Four characteristic amplitude peaks were first visually identified and the spatial distributions of epicortical potentials associated with each selected peak then determined. Digital high-pass (15 Hz) filtering was used in this procedure to highlight the spatial patterns of the early fast waves, while the slow waves were analyzed without filtering. Multiple linear regression9 was used to determine the relationship between selected spatial patterns and the overall response complex. This analysis resulted set of 4 time series of regression coefficients, reflecting the weighted contributions of the selected spatial patterns at all latencies of the original unfiltered data. A physiological interpretation of multiple regression in this application is that the 4 spatial patterns represented surface potentials produced by subpopulations of neurons active at each

(indicated by the upper right circle in Fig. 2A), were largest in the middle left region of the recording array (highlighted with a box in Fig. 2C), and progressively diminished in amplitude over approximately 2 m m of cortical surface in all directions. A t the locus of greatest amplitude, the response complex consisted of 4 distinct response peaks (Fig. 2B). It began with a rapid positive (P1)-negative (N1) wave sequence, with average peak latencies of 8 ms and 16 ms, respectively. These fast components were followed by positive (P2) and negative (N2) slow waves with average peak latencies of approximately 32 ms and 80 ms. The rapid positive-negative waves appeared highly restricted within a 1 m m 2 area and were detected by only a few adjacent electrodes in the array, while the slow waves were more widely distributed throughout a 2-3 m m 2 area and detected by most of the electrodes. Fig. 2D shows the topography of averaged evoked potentials from the same animal, produced by stimulation of another vibrissa (D3; lower left circle in Fig. 2A). The response complex was quite similar to that resulting from stimulation of vibrissa C1, with a focal biphasic sharp wave, followed by a widely distributed positive-negative slow wave complex. The morphology and timing of both the rapid and slow waveforms in the cortical area of maximum response amplitude were consistently reproduced by stimulation of any of the 25 vibrissa in this animal, and in the other 3 animals studied. The major difference between the two conditions in the present example was a spatial shift of the response complex, from the middle left region of the electrode array during C1 stimulation, to the lower right region during D3 stimulation. Thus, a rostroventral shift in the stimulus locus on the mystacial pad resulted in a corresponding shift in cortical response of the contralateral evoked potential primarily in the rostrolateral direction, following the known somatotopic a n a t o m y of vibrissa/barrel cortex. Spatial patterns of the 4 identified waveform peaks are more clearly shown in isopotential maps (Fig. 3A). The patterns were approximately concentric with similar orientation and shape. The m a j o r difference between

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Fig. 2. Epicortical field potential profiles produced by vibrissa displacement in rat #1. A: a schematic drawing of rat left mystacial pad, the 5 rows of vibrissae are indicated by letters A-E, and the 5 large vibrissae in each row are numbered in ascending order in the caudalrostral direction. B: enlarged SEP responses to stimulation of vibrissae C1 and D3 are superimposed. The typical response consisted of sharp positive (P1)-negative (N1) waves at - 8 ms and -16 ms poststimulus peak latency, respectively, followed by a slower positive (P2)--negative (N2) waveform at -30 ms and - 8 0 ms. C: typical averaged responses to C1 (upper right circle in A) stimulation were largest in the tower left region of the recording array (box), and decreased rapidly in amplitude over approximately 2 mm of cortical surface in all directions. D: averaged responses to D3 (lower left circle in A) stimulation were very similar to that resulting from stimulation of vibrissa C1, except that the response focus shifted from the middle left region of the recording array, as shown in C, to the lower right region, corresponding to the stimulation shift from C1 to D3. Orientation: rostral, right; caudal, left; medial, up; lateral, down.

latencies was the steepness of the potential gradient, the rate of decline in a m p l i t u d e from the maximum. The N1 had a steepest gradient with a highly restricted spatial distribution, while the gradient of the P1 was m o r e shallow with potentials distributed over twice the a r e a of the N1. T h e P2 was even m o r e widely distributed, with a shallow s m o o t h gradient, and the N2 had a similarly wide distribution but with a less organized p a t t e r n than the o t h e r peaks. Fig. 3B shows multiple regression coefficients for each of the r e p r e s e n t a t i v e spatial patterns, as a function of time. T h e coefficients were m a x i m u m at the latency of the p e a k they r e p r e s e n t e d , indicating that at this latency, the c o r r e s p o n d i n g spatial p a t t e r n of potentials m a d e a maximal contribution to the overall response complex. H o w e v e r , the coefficients also reflected substantial contributions of a given p e a k ' s t o p o g r a p h y at o t h e r latencies as well. Coefficients shown here for responses e v o k e d by d i s p l a c e m e n t of vibrissa D2 on rat # 1, were consistently

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Fig. 3. Multiple regression analysis of the 4 identified peaks of the SEP evoked by displacement of D2 on rat #1. A: potential distributions at the latency of each peak are depicted as normalized isopotential maps. The spatial patterns were approximately concentric with similar orientation and shape, but the potential gradient was different at each latency. B: multiple regression coefficients representing the contribution of each peak's spatial pattern to the overall SEP complex across all latencies. The regression coefficients were maximum at the latency of their respective peak because this was the latency from which each spatial pattern wasinitialty derived. Yet, the coefficient also reflected contributions of a given peak's topography through the entire SEP period.

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100 ms Fig. 4. Enlargement of multiple regression coefficients. Superimposition of regression coefficients for responses evoked by displacement of each of 25 vibrissae in rat #1 (A), and superimposition of regression coefficients averaged across vibrissae for individual animals (B). Horizontal calibration: 100 ms; vertical calibration omitted to emphasize statistical nature of results.

reproduced at all vibrissae in this animal (Fig. 4A). Thus, while the spatial patterns of epicortical potentials systematically shifted location with vibrissa stimulated, the regression coefficients remained quite consistent across vibrissae. The coefficient waveforms were also consistent across animals (Fig. 4B). In all animals, the weighted sum

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of all 4 spatial patterns over time was sufficient to explain over 96% of the variance of the original waveforms. Combinations of 3 patterns were capable of explaining up to 91%, combinations of 2 up to 86%, and single patterns up to 60% of the variance. Fig. 5A displays topographical distributions of just the

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Fig. 5. Topographical distributions of the SEE A: isopotential maps of the P1 peak evoked by stimulating 25 vibrissae in rat #1 are shown in 5 x 5 matrix. Maps of response to row A - E are displayed from bottom up, maps of response to vibrissae 1-5 in each row are displayed from the left to the right. B: dots represent response maxima from each map, highlighting the cortical representation pattern of peripheral vibrissae. The response maxima for vibrissae C1 and D3 are darkened, and correspond to their locations in the barrel cortex previously shown in Fig. 2. The epicortical responses systematically shifted location, approximating the spatial arrangement of stimulated vibrissae on the contralateral mystacial pad as shown in C. D: a schematic drawing of the layer IV barrel field in rat primary somatosensory cortex, adapted from succinic dehydrogenase stains study (Killackey, H.P., The somatosensory cortex of the rodent, Trends Neurosci., 6 (1983) 425-429). The topographical response pattern derived from the present study approximated the size, location, and orientation of the known barrel field of layer IV in rat somatosensory cortex.

110 P1 peak, evoked by stimulating a 5 x 5 vibrissae matrix in rat #1. The center points of each map are plotted in Fig. 5B. In this figure, the epicortical responses may be clearly seen to systematically shift location in approximate relation to the peripheral mystacial pad (Fig. 5C), as well as the characteristic somatotopic arrangement of layer IV barrels (Fig. 5D) and barrel-related functional columns devoted to separate vibrissae in rat primary somatosensory cortex. This vibrissa-dependent topology was also apparent for the N1 and P2 in all animals. However, the somatotopic arrangement of the N2 was poorly defined due to the variability of this component's spatial distribution. DISCUSSION Early somatosensory evoked potential studies of rat 38 and mouse 37 used a single electrode, sequentially placed on the SmI surface, to map the somatotopic representation of mystacial vibrissae in epicortical SEP. This work, supported by anatomical and physiological studies 34"39, established a direct correspondence between reconstructed somatotopic maps of epicortical SEP and the configurations of both underlying layer IV barrels and peripheral vibrissae. The present data, recorded simultaneously from the entire vibrissa/barrel field, confirm these findings and demonstrate a clear relationship between the known somatotopic anatomy of vibrissa/ barrel cortex and the spatial distribution and location of epicortically recorded SEP. More importantly, our data, when combined with spatiotemporal analysis, extend these early results by indicating that while the epicortical SEP complex evoked by displacement of a given vibrissa is centered on the expected location of a corresponding cortical barrel/ column, its sequential peaks are produced by different subpopulations of neurons having distinct topographical distributions within the barrel field. Thus, these findings generally support the conclusions of other studies concerned with the neurogenesis of somatosensory evoked responses in rat and other species, which used experimental manipulations such as electroconvulsive shock 24, pentobarbital anesthesia 25, concussion 26'27 and selective central nervous system ablation 1° to produce differential effects on certain SEP peaks, suggesting the presence of multiple neuronal generators underlying the SEP complex. Selective changes in peaks of the SEP waveform have also been noted in patients with cerebral lesions 32,36. There are 4 characteristic amplitude peaks within the first 300 ms of the epicortical SEP complex in rat vibrissalbarrel cortex. The earliest detectable signal is a brief positive sharp wave (P1) followed by a negative

sharp wave (N1). The compiex ends with a positive (P2)-negative (N2) slow wave sequence. Topographical maps depicting the potentials across the electrode array at each of these identified peaks, show large differences in the extent of vibrissa/barrel cortex active at different latencies of the SEP complex. Yet, at no latency are epicortical potentials restricted to the area of a single vibrissa/barrel column, estimated from 2-DG studies to be less than 500/~m diameter in the superficial cortical layers TM. This result could be anticipated from 2-DG studies 7'2° indicating that the cortical tissue activated by stimulation of a single vibrissa is beyond the boundaries of a single barrel/column, extending over parts of adjacent barrels/columns. These results also concur with data of single-unit studies 4,e'AS-16,28'29"3°'31`demonstrating that many neurons within a barrel/column responded in short latency to stimulation of more than one vibrissa. Spatial patterns of the initial P1 and Nt are consistently more localized than the later P2 and N2. The P1 and N1 recorded here are similar to the archetypal positive-negative wave sequence of sensory evoked potentials recorded in a number of different cortical areas and species 12'35. The P1 can typically be recorded only from a small area over the somatosensory cortex contralateral to the site of stimulation, and represents the first indication of cortical activity following the stimulus. In a previous study of the laminar evoked potentials of rat vibrissa/barrel cortex ( D i e t al. 1990), the initial positivity of the epicortical SEP resulted from depolarization of proximal apical dendrites of supragranular pyramidal cells, similar to the type A activation pattern described by Mitzdorf for cat visual cortex 22, a pattern of initial cortical response to specific thalamocortical afferents. Laminar potentials at the approximate latency of the epicortical N1 were the result of distal depolarization of apical dendrites from both supragranular and infragranular pyramidal cells. This laminar pattern was similar to the type C activation pattern of Mitzdorf, thought to result from less focal innervation of distal apical dendrites, primarily from axon collaterals of the supragranular cells. Thus, in this early study, a simple model was proposed, suggesting that the epicortical P1 is due to focal monosynaptic and disynaptic (via layer IV stellate cells) activation through specific thalamocortical afferents, and the N1 is the result of subsequent less focal polysynaptic activation through pyramidal axon collaterals. Yet, this simple model of a focal P1 followed by a less focal N1 does not fit the present topographical data. While the topography of the P1 is more focal than either the P2 or N2, it is not the most focal peak of the SEP complex, and is distributed over twice the epicortical area of the later N1 (Fig. 3). This phenomenon is consistently observed for all vibrissae and all animals recorded.

111 Furthermore, multiple regression coefficients representing the relative contribution over time of putative neuronal populations producing each of these wave peaks, indicate that the P1 and N1 are initiated almost simultaneously and simply peak at different times. Our results therefore suggest parallel activity in two distinct subpopulations of neurons within vibrissa/barrel cortex at the beginning of the SEP, a focal population giving rise to the N1, and a more distributed population giving rise to the P1. These findings are quite similar to a recent report from our laboratory (Barth and DIS), where the same methods were used to study the topography of auditory evoked potentials (AEP) in Area 4121 of rat neocortex. In this study of auditory cortex, the P1 also covered approximately twice the epicortical area of the N1. However, close inspection of the regression coefficients indicated that the earliest sign of the AEP complex was a very brief focal positivity (earlier than the P1) with the same location and distribution as the subsequent N1. Thus, the AEP began with a low amplitude focal positivity, consistent with a focal type A activation pattern, followed quickly by the more widespread large amplitude positivity of the P1, and then by a focal large amplitude N1. A similar pattern of initial focal positivity spreading rapidly to a more distributed positivity of the P1 peak may not have been discriminated in the SEP complex of the present study due to the fact that, in contrast to auditory cortex, the topographies of epicortical potentials in vibrissa/barrel cortex are approximately concentric and therefore almost completely overlapping in space. Failure to detect focal positivity initiating the SEP complex may therefore reflect a methodological weakness in the resolution of epicortical spatiotemporal analysis, rather than fundamental differences in the neurogenesis of somatosensory and auditory evoked potentials in the rat. Despite this difference at the beginning of the response complex, it is clear that in both somatosensory and auditory cortex, the epicortical P1 peak is produced by more distributed neural processing than the subsequent focal N1 peak, and is probably not exclusively the result of specific thalamocortical afferents. In contrast to the early sharp waves of the SEP, the slow P2 and N2 are both widely distributed on the surface of vibrissa/barrel cortex, and are more variable in amplitude and latency. Given their long latency and wide spatial distribution, these later slow waves may reflect integrative processing involving much of the barrel field, and are probably the result of both excitatory and inhibitory postsynaptic potentials. In epicortical evoked potential studies of the cat 1°'33, it was suggested that these longer latency SEP waveforms be categorized as associative responses, produced outside of primary so-

matosensory cortex. These conclusions were based on the cortical locations of long latency SEP components, and on the effects of localized primary somatosensory cortical ablation on their amplitude and waveshape. Our data do not support this conclusion. All components of the SEP were confined to the approximate dimensions and location of the SmI region, as functionally defined by systematic stimulation of each vibrissa. To further test this hypothesis, in one animal, the epicortical electrode array was placed in 3 additional quadrants posterior and inferior to the barrel field, resulting in a total of 256 recording sites covering 8 × 8 mm 2 of the right hemisphere. In none of these additional recording sites were components of the SEP detected. These findings are similar to the results of somatosensory evoked potentials recorded from human scalp 32'36, suggesting that both early and late components of SEP are generated only in the region of primary somatosensory cortex. In the present study, we have identified 4 characteristic amplitude peaks of the SEP complex, shown the topography of epicortical potentials at each of these peaks to differ, and used linear multiple regression to demonstrate that a weighted combination of the epicortical potential patterns derived from only these 4 isolated latencies was sufficient to explain over 96% of the total data variance in all animals. However, it should not be concluded that the putative subpopulations of cells producing each of the identified peaks of the SEP are unique. Indeed, the potential patterns for all of the peaks are concentric and overlapping, the main differences lying in the potential gradient across the cortical surface. Spatial overlap is particularly evident for the P2 and N2 peaks. In comparison to an earlier topographical study of rat auditory cortex 5, where the topographies of the P2 and N2 were spatially separated, the degree of spatial overlap of these peaks in the SEP complex renders them nearly indistinguishable in the present analysis. Nor was any attempt made to explore linear combinations of potential patterns selected at SEP latencies other than those of the 4 amplitude peaks. The fact that combinations of 3 and even 2 of the selected potential patterns could still explain a large percentage of the data variance reflects the degree of spatial overlap in these distributions. Yet, as previously noted 5, the percent of variance accounted for by a given pattern does not necessarily reflect the physiological significance of the SEP waveform it represents, since the primary factors governing a waveform's contribution to the total SEP variance are simply its duration and spatial extent. For these reasons, the uniqueness of the putative neuronal populations producing the SEP complex cannot be resolved with statistical arguments alone. In this light, topographical analysis of the SEP complex should lead to further experiments that

112 selectively activate or deactivate the hypothetical neuronal groups identified here, yielding confirmatory information about their existence and function during somato-

Acknowledgements. This research was supported by USPHS grant 1-R01-NS22575, NSF grant BNS-86-57764, Whitaker Foundation grant $880620.

sensory information processing in, the rat.

REFERENCES 1 Allison, T., Goff, W.R., Williamson, P.D. and Vangilder, J.C., On the neural origins of components of the human somatosensory evoked potentials. In: J.E. Desmedt (Ed.), Progress in Clinical Neurophysiology, Vol. 7, Karger, Basel, 1980, pp. 51-68. 2 Arezzo, J.C., Legatt, A.D. and Vaughan, H.G.J., Topography and intracranial sources of somatosensory evoked potentials in the monkey, I. Early components, Electroenceph. Ctin. Neurophysiol., 46 (1979) 155-172. 3 Arezzo, J.C., Vaughan, H.G.J. and Legatt, A.D., Topography and intracranial sources of somatosensory evoked potentials in the monkey, II. Cortical components, Electroenceph. Clin. Neurophysiol., 51 (198I) 1-18. 4 Axelrad, H., Verley, R. and Farkas, K., Responses evoked in mouse and rat SI cortex by vibrissa, Neurosci. Lea., 3 (1976) 265-274. 5 Barth, D.S. and Di, S., Three dimensional analysis of auditory evoked potentials in rat neocortex, J. Neurophysiol., 64 (1990) 1527-1536. 6 Chapin, J.K., Laminar differences in sizes, shapes, and responses profiles of cutaneous receptive fields in the rat SI cortex, Exp. Brain Res., 62 (1986) 549-559. 7 Chmielowska, J., Kossut, M. and Chmielowski, M., Single vibrissal cortical column in the mouse labeled with 2-deoxyglucose, Exp. Brain Res., 63 (1986) 607-619. 8 Di, S., Baumgartner, C. and Barth, D.S., Laminar analysis of extracellular field potentials in rat vibrissa/barrel cortex, J. Neurophysiol., 63 (1990) 832-840. 9 Dillon, W.R. and Goldstein, M., Multivariate Analysis, Wiley, New York, 1984. 10 Dong, W.K., Harkins, S.W. and Ashleman, B.T., Origins of cat somatosensory far-field and early near-field evoked potentials, Electroenceph. Clin. Neurophysiol., 53 (1982) 143-165. 11 Fagan, E.R., Taylor, M.J. and Logan, W.J., Somatosensory evoked potentials, Part I. A review of neural generators and special considerations in pediatrics, Pediatr. Neurol., 3(4) (1988) 189-196. 12 Goff, W.R., Allison, T. and Vaughan Jr., H.G., The functional neuroanatomy of event related potentials. In: E. Callaway, P. Tueting and S.H. Koslow (Eds.), Event-Related Brain Potentials in Man, Academic Press, New York, 1978. 13 Goff, G.D., Matsumiya, Y., Allison, T. and Goff, W.R., The scalp topography of human somatosensory and auditory evoked potentials, Electroenceph. Clin. Neurophysiol., 42 (1977) 57-76. 14 Goff, W.R., Williamson, P.D., Vangilder, J.C., Allison, T. and Fisher, T.C., Neural origins of long latency evoked potentials recorded from the depth and from the cortical surface of the brain in man. In: J.E. Desmedt (Ed.), Progress in Clinical Neurophysiology, Vol. 7, Karger, Basel, 1980, pp. 126~145. 15 Ito, M., Some quantitative aspects if vibrissa-driven neuronal responses in rat neocortex, 3". Neurophysiol., 46 (1981) 705-715. 16 Ito, M., Processing of vibrissa sensory information within the rat neocortex, J. Neurophysiol., 54 (1985) 479-490. 17 Jones, S.J. and Power, C.N., Scalp topography of human somatosensory evoked potentials: the effect of interfering tactile stimulation applied to the hand, Electroenceph. Clin. Neurophysiol., 58 (1984) 25-36. 18 Kakigi, R., Ipsilateral and contralateral SEP components following median nerve stimulation: effects of the interfering stimuli applied to the contralateral hand, Electroenceph. Clin. Neurophysiol., 64 (1986) 246-259.

19 Kakigi, R. and Shibasaki, H., Scalp topography of mechanically and electrically evoked somatosensory potentials in man, Electroenceph. Clin. Neurophysiol., 59 (1984) 44-56. 20 Kossut, M., Hand, P.J., Greenberg, J. and Hand, C.L., Single vibrissal cortical column in SI cortex of rat and its alterations in neonatal and adult vibrissa-deafferented animals: a quantitative 2DG study, J. Neurophysiol., 60 (1988) 829-852. 21 Krieg, W.J.S., Connections of the cerebral cortex I (The albino rat. A) Topography of the cortical areas, J. Comp. Neurol., 84 (1946) 221-275. 22 Mitzdorf, U., Current source-density method and application in cat cerebral cortex: investigation of evoked potentials and EEG phenomena, Physiol. Rev., 65 (1985) 37-100. 23 Rtmond, A., Handbook of Electroencephalography and Clinical Neurophysiology, Electrical Reactions of the Brain and Complementary Methods of Evaluation. Part A (Evoked Responses), Elsevier, Amsterdam, 1975. 24 Shaw, N.A., Effect of electroconvulsive shock on the somatosensory evoked potential in the rat, Exp. Neurol., 90 (1985) 566-579. 25 Shaw, N.A. and Cant, B.R., The effect of pentobarbital on central somatosensory conduction time in the rat, Electroenceph. Clin. Neurophysiol., 51 (1981) 674-677. 26 Shaw, N.A. and Cant, B.R., The effect of experimental concussion on somatosensory evoked potentials, Aust. J. Exp. Biol. Med. Sci., 62 (1984) 361-371. 27 Shaw, N.A., Somatosensory evoked potentials after experimental head injury in the awake rat, J. Neurol. Sci., 74 (1986) 257-270. 28 Simons, D.J., Response properties of vibrissa units in the rat SI somatosensory neoeortex, J. Neurophysiol., 41 (1978) 798-820. 29 Simons, D.J., Multi-whisker Stimulation and its effects on vibrissa units in rat SmI barrel cortex, Brain Research, 276 (1983) 178-182. 30 Simons, D.J. and Wollsey, T.A., Functional organization in mouse barrel cortex, Brain Research, 165 (1979) 327-332. 31 Simons, D.J., Temporal and spatial integration in the rat SI vibrissa cortex, J. NeurophysioL, 54 (1985) 615"635. 32 Stohr, P.E. and Goldring, S., Origin of somatosensory evoked scalp responses in man, J. Neurosurg., 31 (1969) t17-127. 33 Thompson, R.F., Johnson, R.H. and Hoopes, J.J,, Organization of auditory, somatic sensory and visualprojections to association fields of cerebral cortex in the cat, J. Neurophysiol., 26 (1963) 343-364. 34 Welker, C., Microelectrode delineation of fine grain somatotopic organization of SmI cerebral neocortex in albino rat, Brain Research, 26 (1971) 259-275. 35 Werner, G. and Whitsel, B.L., Functional organization of the somatosensory cortex. In: G. iggo (Ed.), Handbook of Sensory Physiology, Vol. 2 (Somatosensory System), Springer Verlag, Berlin, 1973, pp. 621-700. 36 Williamson, P.D., Goff, W.R. and Allison, T., Somato-sensory evoked responses in patients with unilateral cerebral lesions, Electroenceph. Clin. Neurophysiol., 28 (1970) 566-578. 37 Woolsey, T.A., Somatosensory, auditory, and visual cortical areas in the mouse, Johns Hopkins Med. J., 121 (1967) 91-i12. 38 Woolsey, C.N. and LeMessurier, D:H., The pattern of cutaneous representation in the rat's cerebral cortex, Fed. Proc. Am. Assoc. Exp. Biol., 7 (1948) 137-138. 39 Woolsey, T.A. and Van der Loos, H,, The structural organization of layer IV in the somatosensory region (SI) of mouse cerebral cortex, Brain Research, 17 (1970) 205-242.

barrel cortex.

An 8 x 8 multichannel microelectrode array was used to simultaneously record epicortical field potentials, evoked by displacement of contralateral vib...
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