School of Physiology and Pharmacology, The University of New South Wales, Sydney 2052, Australia
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ABSTRACT |
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Coleman, G. T., H. Q. Zhang, G. M. Murray, M. K. Zachariah, and M. J. Rowe. Organization of somatosensory areas I and II in marsupial cerebral cortex: parallel processing in the possum sensory cortex. Controversy exists over the organization of mammalian thalamocortical somatosensory networks. An issue of particular contention is whether the primary and secondary somatosensory areas of cortex (SI and SII) are organized in a parallel or serial scheme for processing tactile information. The current experiments were conducted in the anesthetized brush-tail possum (Trichosurus vulpecula) to determine which organizational scheme operates in marsupials, which have taken a quite different evolutionary path from the placental species studied in this respect. The effect of rapid reversible inactivation of SI, achieved by localized cortical cooling, was examined on both evoked potential and single neuron responses in SII. SI inactivation was without effect on the amplitude, latency, and time course of SII-evoked potentials, indicating that the transient inputs responsible for the SII-evoked potential reach SII directly from the thalamus rather than traversing an indirect serial route via SI. Tactile responsiveness was examined quantitatively before, during, and after SI inactivation in 16 SII neurons. Fourteen were unchanged in their responsiveness, and two showed some reduction, an effect probably attributable to the loss of a facilitatory influence exerted by SI on a small proportion of SII neurons. The temporal precision and pattern of SII responses to dynamic forms of mechanical stimuli were unaffected, and temporal dispersion in the SII response bursts was unchanged in association with SI inactivation. In conclusion, the results establish that, within this marsupial species, tactile inputs can reach SII directly from the thalamus and are not dependent on a serially organized path through SI. A predominantly parallel organizational scheme for SI and SII operates in this representative of the marsupial order, as it does in a range of placental mammals including the cat and rabbit, the tree shrew and prosimian galago, and at least one primate representative, the marmoset monkey.
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INTRODUCTION |
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In most mammals, each sensory system, whether
somatosensory, visual, or auditory, is characterized by multiple
representations within the cerebral cortex. For the tactile system, two
of the principal cortical processing regions are somatosensory area I (SI) and area II (SII), (for reviews see Burton 1986;
Felleman and Van Essen 1991
; Johnson
1990
; Jones 1986
; Kaas 1987
;
Rowe 1990a
). It is probable that corresponding areas are
present in marsupials as SI and SII were identified in the possum
(Adey and Kerr 1954
; Haight and Neylon
1978
) and the opossum (Beck et al. 1996
;
Lende 1963a
,b
, 1969
; Pubols 1977
;
Pubols et al. 1976
) although the forelimb area is
substantially smaller in SII than in SI.
As both SI and SII receive direct anatomic projections from the
ventroposterior (VP) nucleus of the thalamus in both primate and
nonprimate placental mammals (for review see Jones 1985)
and in marsupials (Haight and Neylon 1978
; Pubols
1968
), it was usually assumed that the cortical mechanisms in
tactile sensation depend on parallel, distributed processing
(Mountcastle 1978
; Rowe 1990a
). Direct
evidence in support of the parallel processing hypothesis was obtained
in a diverse range of placental mammals, including cat (Burton
and Robinson 1987
; Mackie et al. 1996
;
Manzoni et al. 1979
; Turman et al. 1992
),
rabbit (Murray et al. 1992
), tree shrew, and the
prosimian galago (Garraghty et al. 1991
), as SI inactivation in these species has little effect on SII tactile responsiveness. In contrast, it was found that in simian primates SII
responsiveness is abolished by surgical ablation of SI (Burton et al. 1990
; Garraghty et al. 1990
; Pons
et al. 1987
, 1992
). This dependency of SII
responsiveness on SI provided evidence for a serial scheme in which
tactile information is conveyed from the thalamus to SI and then to SII
via intracortical connections (Garraghty et al. 1990
;
Pons et al. 1987
, 1992
). These findings in support of a
serial processing scheme led to the hypothesis that there are
fundamental differences between simian primates and other eutherian
mammals in the organization of thalamocortical systems for tactile
processing (Garraghty et al. 1991
; Mackie et al.
1996
; Murray et al. 1992
; Turman et al.
1992
). However, our recent re-investigation of SI-SII
organization in the marmoset, with localized cooling for SI
inactivation, demonstrated a substantial direct thalamic input to SII,
indicating a parallel organization of SI and SII in this primate
species (Rowe et al. 1996
; Zhang et al.
1996
). This study extends the analysis of parallel versus
serial processing in SI and SII to the brush-tail possum,
Trichosurus vulpecula, a representative of the marsupial
order that has taken a divergent evolutionary path from placental
mammals ~100 million years ago in the Cretaceous period (Rowe
1990a
). The aim was to determine whether there was evidence for
parallel organization of SI and SII at this early stage of mammalian
evolution (see DISCUSSION). The study was reported in
abstract form (Coleman et al. 1997
).
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METHODS |
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Eighteen experiments were performed on the brush-tail possum,
T. vulpecula. In four, examining principally the effect of
SI inactivation on SII-evoked potentials, anesthesia was induced with
either ketamine (20-60 mg/kg) and xylazine (2-6 mg/kg) or Saffan
(alfaxalone and alfadolone acetate; Glaxo; 18 mg/kg), and maintained
with chloralose (20 mg/kg iv initial dose and as needed). In the
remainder, 4 were with ketamine and xylazine anesthesia (doses as
described previously) and maintained with pentobarbitone (~2-4 mg
kg1 h
1 iv), and 10 were with initial Saffan
anesthesia (18 mg/kg im) and maintenance with pentobarbitone (1 mg
kg
1 h-1 iv) and ventilation mixture of
halothane (~1-2%), N2O (~80%), and oxygen (20%).
Experiments were terminated by pentobarbitone overdose and were
approved by the university animal ethics committee (Approval No. ACE
94/77) and accorded with the Australian Code of Practice for the Care
and Use of Animals for Scientific Purposes.
Rectal temperature for this marsupial was maintained at ~36°C. The femoral artery and vein were cannulated, and a tracheal cannula was inserted. A unilateral craniotomy was performed to expose the somatosensory cortical areas. A paraffin pool (36°C) was created to prevent the cortex from drying. The distal forelimb contralateral to the craniotomy was fixed in a perspex trough to allow reliable placement of the mechanical stimulator on the receptive fields of cortical neurons.
Mapping of distal limb representations in SI and SII
The distal forelimb areas within SI and SII were mapped by surface recording of evoked potentials with a ball electrode. Areas of representation were identified from short-latency (<15 ms) positive-going evoked potentials generated by brief taps (3- to 5-ms duration; 400-µm amplitude) to the central palmar surface of the contralateral forelimb.
Inactivation of the SI hand area by cooling
A cylindrical silver block (5- to 7-mm diam) fitted with a
Peltier device and a thermistor was placed over the SI hand area of
cortex. The temperature at the block face was held at 36-37°C but
could be lowered within 1-2 min to <10°C and restored equally rapidly to the control temperature. The effectiveness of this procedure
for rapid reversible inactivation of localized regions of somatosensory
cortex was established by Brooks (1983) and in our earlier studies
(Mackie et al. 1996
; Murray et al. 1992
;
Turman et al. 1992
, 1995
; Zhang et al.
1996
).
Evoked potentials were recorded simultaneously from SI, with an
electrode in the face of the cooling block and with a second electrode
from the forelimb representation within SII. Evoked potentials were
averaged (20-40 successive responses) by a laboratory computer.
Inactivation of the SI area was judged to have taken place when the SI
evoked potential was abolished (usually at 10°C). The effect of SI
inactivation on SII responsiveness was evaluated by recording evoked
potential and single neuron responses within SII.
Recording and stimulation procedures for single neuron studies
Conventional extracellular recording was carried out from
individual tactile-sensitive neurons within the SII hand area
(Zhang et al. 1996). Receptive fields of
tactile-sensitive SII neurons were delineated by gentle tapping with a
small probe or with von Frey hairs. Quantified mechanical stimuli
generated by a servo-controlled mechanical stimulator (Zhang et
al. 1996
) were delivered with circular probes (2- to 4-mm diam)
at a rate of one per 8-10 s to allow recovery of skin position.
Individual SII neurons were tested for responsiveness to static skin
displacement or trains of either sinusoidal vibration or rectangular
pulses. The effect of SI inactivation on SII neurons was evaluated
wherever possible by comparison of responsiveness during inactivation
with both pre- and postinactivation controls. For each neuron, the
comparison was based on statistical analysis involving one-way ANOVA,
and the source of differences was identified by contrast analysis
(Duncan test; P < 0.05 for significance) (Snedecor
and Cochran 1989).
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RESULTS |
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Identification of distal forelimb regions of SI and SII in the possum
Two spatially separate representations of the contralateral
hand, within the SI and SII areas identified by Adey and Kerr (1954),
were found by evoked potential mapping. The SI hand area, typically
5-7 mm in anteroposterior extent and 4-5 mm in mediolateral extent,
was in the medial region of cortex (Fig.
1).
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The SII representation of the contralateral hand was in the lateral
margin of the parietal cortex (Fig. 1) just above sulcus (Haight and Neylon 1978
). Its size was consistently
smaller than its SI counterpart and rarely larger than 2-3 mm across
its broadest dimension. The representation of the contralateral face (Adey and Kerr 1954
) created a discontinuity between the
SI and SII hand representations, with an average separation of ~8 mm between the nearest boundaries of the SI and SII hand areas, enabling cooling-induced inactivation of SI to be achieved without direct spread
of cooling causing significant disruption to neural activity within the
SII hand area (see Turman et al. 1992
).
Inactivation of the SI hand area by localized cooling
As the temperature of the SI block face was reduced in a series of
5-6°C steps from 36°C, there was a progressive reduction in
amplitude of the SI-evoked potential and an increase in latency to its
positive peak (Fig. 2). The attenuation
of the SI response was apparent once the temperature fell to ~25°C,
with marked reduction and slowing by 16°C. In all 10 experiments in
which the effectiveness of cooling was evaluated in this stepwise
manner, the SI-evoked potential was abolished by cooling to 5-10°C.
In some experiments, there was a small residual positive-going SI
response apparent at short latency at these low temperatures (e.g., at
5 and 11°C in Fig. 2), almost certainly attributable to activity in
the thalamocortical input fibers (see Turman et al.
1992; Zhang et al. 1996
). With stepwise
rewarming to 36°C there was progressive recovery of the SI response
(Fig. 2), confirming the reversibility of the procedure in the possum
as in placental mammals (Turman et al. 1992
;
Zhang et al. 1996
).
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Effect of SI inactivation on evoked potentials recorded from SII
Inactivation of the SI hand area was without effect on the amplitude, latency, and time course of SII-evoked potentials in the 13 experiments where this was examined. This is illustrated for two experiments (Figs. 2 and 3A) where, despite the marked delay and attenuation of the SI response as the SI temperature fell and the abolition of the SI response at 5-10°C, there was no change in the SII response. This was confirmed in Fig. 3, B and C, by the quantified plots of peak amplitude and onset latency for the SII-evoked response in association with the decline and disappearance of the SI-evoked potential. Furthermore, the time course of the SII evoked potential appears unchanged (Figs. 2 and 3) despite the marked delay in the time course of the attenuated SI response at the lower SI temperatures. Further evidence that the SII-evoked potential is generated by direct thalamic input rather than by signals traversing an indirect serial route via SI comes from the absence of any significant difference in onset latencies of the simultaneously recorded SI- and SII-evoked potentials (13.6 ± 1.7 ms (SD) and 13.0 ± 1.8 ms (SD), respectively; P = 0.41; n = 15). In these 15 experiments onset latencies were the same in 1 case and marginally shorter for SI in 5 cases and for SII in 9 cases.
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Effect of SI inactivation on responsiveness of individual SII neurons
As the evoked potential is generated by an abrupt transient input, it may take place before contributions can be made to the SII response over a putative indirect serial path via SI. It was therefore necessary to examine the effects of SI inactivation on the responses of single SII neurons to maintained tactile stimuli that would allow any contributions coming over an indirect path to be manifest.
Quantitative single-neuron analysis was completed for 16 SII neurons with tactile receptive fields on the distal forelimb. In none was there an abolition of responsiveness in association with SI inactivation. In all but 2 of 16 SII neurons tested statistically for an effect of SI inactivation on responsiveness there was no evidence of any consistent effect. The failure of SI inactivation to alter responsiveness of SII neurons to tactile stimuli is shown for two neurons in Fig. 4. The graphs in Fig. 4, A and B, plot the response level to a fixed stimulus as a function of time during the stepwise cooling of SI leading to complete inactivation at 5-6°C. They also show the subsequent recovery of SI transmission as the SI temperature was restored in a similar stepwise sequence.
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In Fig. 4A, the mean response (± SD) of the SII neuron to a train of mechanical pulses was 5.7 ± 1.0 imp/s (n = 23) during the period of SI inactivation (SI at 5°C), a response level that was unchanged (i.e., P > 0.05) from the pre- and postcooling control levels of 5.7 ± 0.9 imp/s (n = 10) and 5.8 ± 1.1 imp/s (n = 20), respectively, obtained when the SI surface temperature was 37°C. In Fig. 4B, the response level, plotted for another SII neuron, was again unchanged by SI inactivation. The mean response when SI was inactivated (at 5-6°C) was 6.9 ± 2.1 imp/s (n = 16), which was not significantly different from the pre- and postcooling levels of 6.9 ± 4.6 imp/s (n = 11) and 6.3 ± 1.3 imp/s (n = 10) respectively.
All 16 SII neurons tested failed to display a maintained response to static indentations of the skin and were purely dynamically sensitive. They were activated by abrupt mechanical perturbations in the form of low-frequency rectangular pulse trains. The traces in Fig. 5A show an SII neuron responding with a spike burst to the ON and OFF phases of the rectangular mechanical pulses in both pre- and postcooling control circumstances (SI at 37°C) and where SI was inactivated (7°C). The graph in Fig. 5B plots the response level to successive repetitions of the stimulus while two SI inactivation sequences took place. Although the neuron displayed considerable moment-to-moment variability in responsiveness and some drift in response level over time, there was no consistent change in association with SI inactivation. This was apparent from the statistical tests where the mean (± SD) precooling control response (11.2 ± 4.4 imp/s; n = 20) was not significantly different from the level during the first period of SI inactivation (12.3 ± 8.4 imp/s; n = 14). Although the postcooling control response was statistically higher than that during the first inactivation period, it was also statistically higher than the precooling control, reflecting the upward drift in response level over the first ~10 min of sampling. During the later sampling period there was a downward drift in responsiveness that gave a statistical difference between response levels in the second inactivation period and its immediately preceding control segment but not between this second inactivation period and its postcooling control (see Fig. 5 legend). The data emphasize the importance of reversible inactivation that permits repetition of the inactivation to test for the consistency of effects. In cases such as Fig. 5 there is insufficient consistency to accept a systematic effect of SI inactivation on SII responsiveness.
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In only 2 of 16 SII neurons was there any evidence for an effect of SI inactivation on responsiveness. Data for the more convincing of these two cases is illustrated in Fig. 6 where three repetitions of the inactivation procedure produced a fall in response level. Although there was considerable moment-to-moment fluctuation in response level, the statistical tests, comparing the response level during each inactivation segment with the immediately preceding and succeeding control levels, revealed a significant change (P < 0.05) in four of the six comparisons (see Fig. 6 legend).
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Effect of SI inactivation on temporal patterning in the SII responses to repetitive mechanical stimuli
We also examined the effect of SI inactivation on the pattern of SII responses to the repetitive mechanical stimuli. This pattern of activity could change with SI inactivation if inputs to SII were mediated via both direct and indirect (via SI) paths from the thalamus. The peristimulus time histograms in Fig. 7, constructed before (A), during (B), and after (C) SI inactivation from the responses of an SII neuron to mechanical pulse stimuli, show no evidence in association with SI inactivation of a change in response level or in the temporal distribution of impulse activity to the onset and offset phases of the rectangular pulses.
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More precise evaluation of the timing of the response to the mechanical
stimuli was achieved by constructing cycle histograms (Fig.
8), which show the probability of spike
occurrence at different points throughout the cycle period of the
mechanical pulse train. Impulse traces in Fig. 8,
A-C, show a burst of spikes at the onset and
offset phases of each mechanical pulse. However, the cycle histograms
show that the timing relations of these spike bursts are unchanged in
Fig. 8B when SI was inactivated (5°C) compared with the
control distributions in A and C and that the
dispersion in the bursts is also unchanged by SI inactivation. The
expanded spike waveforms verify that the identical SII unit was studied before (SI at 37°C), during (SI at 5°C), and after (SI at 37°C) SI inactivation. The absence of any prolongation in the SII spike waveform when SI was at 5°C also confirms that there was no spread of
cooling to the SII recording site (see Zhang et al.
1996).
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DISCUSSION |
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Effect of SI inactivation on SII-evoked potential responses
As SII evoked potentials were unaffected by SI inactivation, one
may conclude that this feature of SII responsiveness, based as it is on
a synchronous afferent volley generated by a brief tap stimulus, cannot
be dependent on inputs that traverse an indirect serial path from the
thalamus via SI. If thalamocortical organization in the possum
conformed to a strict serial scheme, the prolongation of the SI-evoked
potential and its increase in latency, in the course of SI cooling,
must lead to a comparable delay and prolongation of the SII-evoked
potential. As this was not observed, the inputs responsible for this
transient SII response presumably transverse a direct path from the
thalamus to SII. The almost identical onset latencies for the SI- and
SII-evoked potentials also suggest that the inputs project directly to
each area over parallel pathways. Furthermore, as there was no effect
of SI inactivation on the late components of the SII-evoked potential
(e.g., Fig. 2), there was no evidence for the SII response being
generated by both a direct (thalamic) and an indirect (via SI) source
of input. In these respects the evoked potential results for the possum
are similar to those obtained in the cat, rabbit, and marmoset monkey (Murray et al. 1992; Turman et al. 1992
;
Zhang et al. 1996
).
Effect of SI inactivation on responsiveness of individual SII neurons
Quantitative single neuron analysis established that SII responses
to skin stimulation are mediated via a direct projection from the
thalamus independent of SI. Even for the neurons (2/16) that displayed
some fall in response in association with SI inactivation, it is
probable that the reduction was not attributable to loss of a component
of the peripherally generated input that traversed an indirect route
from the thalamus to SII via SI. Instead it may reflect the loss of a
background facilitatory influence that arises in SI and is mediated via
the intracortical path from SI to SII, in agreement with our earlier
observations in placental mammals (Murray et al. 1992;
Turman et al. 1992
, 1995
; Zhang et al.
1996
). It should also be emphasized that the small fall in responsiveness in these two SII neurons cannot be attributed to direct
spread of cooling from the SI cooling site as the separation of the SII
recording site from the cooling block was substantial (>8 mm) (see
Turman et al. 1992
).
Thalamocortical connectivity and the organization of the SI and SII areas in the possum
Much controversy over how SI and SII are organized in placental
mammals has persisted despite the recognition that, in all placental
species examined, there are direct anatomic projections from the
thalamus to both SI and SII, an anatomic arrangement that would suggest
a parallel organization. In the case of the possum, Haight and Neylon
(1978) established that the SI area coincides with the anatomic
projection field of the VP thalamic nucleus. Although their tracer
studies identified a projection of VP neurons to SII, the incidence of
these SII-related neurons was rather sparse, a finding that could be
taken as evidence that the principal path for tactile inputs to SII
might be via an indirect route from VP via SI. However, the current
findings provide little support for this interpretation and confirm
that tactile information traverses a direct path from the thalamus to
SII. The sparse distribution of SII-related VP neurons in the possum
probably reflects the small size of the SII forelimb area
vis-à-vis its SI counterpart in marsupials (Adey and Kerr
1954
; Beck et al. 1996
; Lende 1963a
,b
, 1969
; Pubols 1977
; Pubols et al.
1976
). Nevertheless, the finding of SII-related cells in VP,
although sparse, establishes an anatomic substrate for a direct
thalamocortical input to SII that is consistent with the present findings.
Parallel organization of SI and SII in different species
Earlier studies from our laboratory and elsewhere demonstrated
parallel organization of SI and SII in a diverse range of nonprimate placental mammals (Burton and Robinson 1987;
Garraghty et al. 1991
; Manzoni et al.
1979
; Murray et al. 1992
; Turman et al.
1992
, 1995
). In each of these species, SI inactivation had
little effect on tactile responsiveness within SII. In contrast, in the
macaque and marmoset monkeys SII responsiveness was abolished when SI was inactivated by surgical ablation, a result indicative of a serial
scheme of processing (Garraghty et al. 1990
; Pons
et al. 1987
, 1992
), which led to the hypothesis that there are
fundamental differences between simian primates and other placental
mammals in the organization of thalamocortical systems for tactile
processing (Garraghty et al. 1991
; Murray et al.
1992
; Turman et al. 1992
). However, a recent
reinvestigation of the serial-parallel processing issue for SI and SII
in the marmoset monkey with localized cortical cooling for reversible
inactivation of SI (Rowe et al. 1996
; Zhang et
al. 1996
) demonstrated a very substantial, perhaps exclusive, parallel organization of SI and SII for tactile processing, indicating that the serial processing scheme is not necessarily an attribute of
all primate species. Furthermore, the finding that SII responsiveness in the marsupial, T. vulpecula, survives SI inactivation
demonstrates that the predominantly parallel organizational scheme also
operates in mammals of the marsupial order that diverged from the
placental line in the Cretaceous period, ~140-70 million years ago
(Rowe 1990a
). The current finding strengthens the case
for parallel organization of SI and SII being a common ancestral
feature at this early stage of mammalian evolution and therefore
suggests that, in a phylogenetic sense, parallel processing is a very
old strategy. An alternative interpretation would be that the parallel organization of SI and SII is sufficiently advantageous as a design strategy, that it has emerged independently as an example of parallel evolution in the separate placental and marsupial lines of mammalian evolution.
Although the parallel scheme appears to be the dominant organizational
mode for SI and SII in most mammalian species in which systematic study
was undertaken (Burton and Robinson 1987;
Garraghty et al. 1991
; Manzoni et al.
1979
; Murray et al. 1992
; Pons et al.
1987
, 1992
; Rowe et al. 1996
; Turman et
al. 1992
, 1995
; Zhang et al. 1996
), including a
variety of nonprimate placental mammals, the marmoset monkey, and now a
marsupial representative, there is also the report of serial
organization of SI and SII in the Old World simian primate, the macaque
monkey (Pons et al. 1987
,1992
). The possible existence
within the mammalian orders of both organizational modes therefore
raises the issue of what advantages or disadvantages might be conferred
on the animal by each of these organizational schemes. One advantage
the parallel scheme could confer is an element of built-in redundancy,
providing a more "fail-safe" mode of operation for the sensory
system and making the system less susceptible to local disruptions.
However, it must be emphasized that parallel organization of SI and SII
need not mean redundancy in design of the processing network. First,
quantitative aspects of processing may differ somewhat in SI and SII
even where the same peripheral source of input is conveyed to both SI
and SII (Ferrington and Rowe 1980
; Fisher et al.
1983
). Second, the output connections of SI and SII are not
identical (Burton 1986
; Friedman et al.
1986
; Kaas 1993
), and therefore even identical
information processed in the two areas may be utilized for different
perceptual or sensorimotor purposes. Thus parallel SI and SII
processing sites may constitute dual-purpose systems, in contrast to a
strict serial system in which both SI and SII constitute different
stages of a single, hierarchically organized network. Furthermore, the simultaneity of their processing may serve to minimize "reaction times" for the animal. In contrast, a serial scheme may add temporal delays and extend "reaction time." A further disadvantage of a multistage serial processing scheme may be that some aspects of information processing, in particular, those that rely on temporal precision in impulse signaling, may be degraded as successive synaptic
junctions are traversed in the processing path (e.g., see
Ferrington and Rowe 1980
; Rowe 1990b
).
However, as possible compensation for these putative disadvantages, the serial processing scheme may allow more scope than the largely simultaneous parallel processing model for a time-dependent modulation or gating of sensory inputs at successive stages of the processing network.
Finally, it must be emphasized that, in view of our recent demonstration that a parallel organization of SI and SII does operate in the marmoset monkey, it may be important to re-investigate, with the same reversible-inactivation procedure, the issue of serial and parallel processing in SI and SII of the macaque monkey, in case the surgical ablation procedure for SI inactivation may have induced effects that confounded the interpretation of results in this primate species.
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ACKNOWLEDGMENTS |
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The authors acknowledge the technical assistance of C. Riordan and H. Bahramali, and the National Parks and Wildlife Service of New South Wales for permission to conduct studies on the possum.
This work was supported by the Australian Research Council and the National Health and Medical Research Council of Australia.
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FOOTNOTES |
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Address for reprint requests: M. J. Rowe, School of Physiology and Pharmacology, University of New South Wales, Sydney, N.S.W. 2052, Australia.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 5 October 1998; accepted in final form 25 January 1999.
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REFERENCES |
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