| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Physiology and Biophysics, Dalhousie University, Halifax, Nova Scotia B3H 4H7, Canada
Submitted 22 November 2002; accepted in final form 21 February 2003
 |
ABSTRACT |
|---|
|
|
|
INTRODUCTION |
|---|
|
;
Kaas 1991). This
"reorganization" is seen clearly after digit amputation when the
denervated portion of somatosensory (S1) cortex becomes responsive to
stimulation of an adjacent digit (Kelahan
and Doetsch 1984; Merzenich et
al. 1984; Rasmusson
1982). The raccoon has been useful for studying this issue because
of its highly developed somatosensory system
(Welker and Seidenstein 1959),
which allows precise delineation of the denervated areas. The site of the
plastic changes has not been conclusively identified; there is clear evidence
for subcortical reorganization (Rasmusson
1996; Rasmusson and Northgrave
1997), which would provide the denervated cortex with novel inputs
as well as for physiological changes in corticocortical connections
(Zarzecki et al. 1993). In the
raccoon, the starting point of reorganization, i.e., the state of the system
immediately after digit amputation, is paradoxically a strong inhibition when
adjacent digits are stimulated (Rasmusson
and Turnbull 1983; Rasmusson
et al. 1992), but the response changes to excitation several
months after denervation (Kelahan and
Doetsch 1984; Rasmusson
1982; Rasmusson and Turnbull
1983; Rasmusson et al.
1992). To determine the mechanisms for denervation-induced
plasticity, it is essential to clarify the interactions between peripheral and
corticocortical inputs in the intact animal.
One traditional method for studying the interaction between two inputs is
the conditioning-test pulse paradigm in which facilitatory or inhibitory
effects can be seen in the response to the test stimulus as a result of a
preceding conditioning pulse delivered to another pathway
(Gardner and Costanzo 1980).
The present study used this paradigm to determine if S1 cortical neurons that
receive peripheral input from one digit (the "on-focus" digit) are
influenced by an adjacent cortical area that receives input from an
"off-focus" digit. Initial studies showed this to be primarily
inhibitory. Consequently, additional neurons were tested after
microiontophoretic administration of specific GABAA and
GABAB receptor antagonists (gabazine and CGP 55845) to determine
the contribution of these two receptor subtypes to this corticocortical
inhibition.
|
|
METHODS |
|---|
|
Each animal was initially sedated with ketamine hydrochloride (10–20
mg/kg im, MTC Pharmaceuticals, Cambridge, ON) and then given iso-florane (5%
in oxygen) so that an intravenous catheter could be inserted into a vein in
the left forearm. The animal was subsequently maintained in an anesthetic,
areflexic state with 
-chloralose (intravenous, 5% in propylene glycol;
Sigma, St. Louis, MO). Injections of a corticosteroid (0.5 ml, 100 mg/ml,
Solu-Delta Cortef, Upjohn; Orangeville, Ontario, Canada) were given before
opening the skull and 2–3 h later (1 ml iv) to minimize cerebral edema.
Body temperature was monitored and maintained near 37°C using a
negative-feedback system comprised of a rectal probe and an electric heating
pad (Harvard Apparatus, Saint Laurent, Quebec, Canada). End tidal
CO2 was monitored (CWE, Ardmore, PA) and lactated Ringer solution
was delivered (intravenous) continuously throughout the experiment.
The animal was mounted and positioned in a Kopf stereotaxic frame. The skull was exposed and a craniotomy was made over the left S1 cortex, exposing the cortical representations of the fourth digit, fifth digit, and palm. A well was created around the craniotomy using dental impression compound (Kerr, Romulus, MI) and filled with warmed Elliot's solution (Abbott, Montreal, Quebec, Canada). The dura mater was cut and reflected to expose the brain.
Recording procedure
Recording and drug application were performed with five-barrel glass
micropipettes (A-M Systems, Carlsborg, WA). The center barrel was filled with
a fine (7 µm) carbon-fiber before being pulled on a vertical Narishige
microelectrode puller. The tapered end of the pipette was broken off,
resulting in a total tip diameter of 
20–40 µm. The carbon fiber
was then chemically etched (Armstrong-James
and Millar 1979). The other end of this barrel was filled with 3 M
NaCl for extracellular recording. The impedance of the carbon fiber-containing
recording electrode was between 1 and 5 M
at 1 kHz. The output signal
was amplified (10,000–50,000 times), band-pass filtered (0.2–5.0
kHz), and passed through a Humbug noise eliminator (Quest Scientific, North
Vancouver, British Columbia, Canada). The resulting signal was monitored with
an audio speaker and displayed on a storage oscilloscope.
The other barrels of the micropipette contained NaCl (0.9%) for current balancing, CGP 55845 (20 mM, pH 5.2), and gabazine (SR-95531, 20 mM, pH 3.3, Sigma). Both drugs were dissolved in 0.9% NaCl. Each barrel was filled immediately before recording using a syringe and Microfil needle (WPI, Sarasota, FL). Drug ejection and retaining currents were controlled by a Neurophore apparatus (Medical Systems, Greenvale, NY). A holding current (–15 nA) was applied to each drug barrel to prevent leakage of drugs. The ejection currents were normally +40 nA for both CGP 55845 and gabazine and were applied for 5 min.
The micropipette was advanced in 10-µm steps using an Inchworm microdrive (Burleigh, Fishers, NY) until suitable neuronal activity was isolated. The location of each electrode penetration was marked on a photograph of the cortex. The neuron's receptive field was determined by exploring the skin with a glass probe or von Frey hair monofilaments (Touch-Test Sensory Evaluator, North Coast Medical, San Jose, CA) and drawn on a photograph of the forepaw.
Testing procedure
The test stimulus was applied electrically to the digit containing the neuron's receptive field through a pair of Teflon-coated silver wire electrodes inserted under the glabrous skin of the distal pad of the digit. The strength of this test pulse was set to produce a response from the cortical neuron on virtually every trial and ranged between 100 and 600 µA.
The adjacent cortical area (e.g., digit 4 representation when recording
from a neuron in digit 5 cortex) was first identified using the recording
electrode as receiving inputs from the adjacent digit. This is rapidly done in
the raccoon using the sulcal patterns as landmarks
(Rasmusson 1982;
Welker and Seidenstein 1959).
The conditioning stimulus was delivered to this adjacent area through a
concentric bipolar electrode. The depth of the electrode was 0.5 mm below
the surface and strength of the stimulation electrode was adjusted to evoke a
consistent response from the recorded neuron (30–100 µA). Both the
conditioning and test pulses were delivered from the computer-controlled
Master 8 stimulator (AMPI, Jerusalem, Israel) and were 0.2 ms in duration. The
response of each cell was recorded before and after each drug administration
using the same stimulation parameters.
Recordings and the timing of stimuli were controlled using Data-Wave
interface and software (Thornton, CO). The sampling rate was 20 kHz.
Individual spikes were recorded and saved after discrimination on the basis of
amplitude and duration. Data were collected in 350-ms trials in which the
conditioning pulse (cortex) was delivered at the beginning of the trial and
the test pulse (digit) was delivered after an interval of 5, 25, 50, 100, or
200 ms. Control trials were also collected with stimulation of the digit
alone. The interval between trials was 2 s. The sequence of interstimulus
intervals (ISIs) was randomized initially and then remained the same for all
animals. Thirty trials were obtained at each interval for each neuron;
therefore the time necessary to collect a complete data set was 7 min.
The response for each ISI was counted as the number of spikes from 10 to 50 ms
after the digit stimulation and expressed as a percent of the response to
digit stimulation alone. In those cases where the conditioning stimulus
produced a response after 10 ms, this response was measured in the 50-, 100-,
and 200-ms trials and subtracted from the response at 5- and 25-ms trials
where it might have interfered with the test response
(Gardner and Costanzo 1980).
Changes in background activity (i.e., in the absence of peripheral
stimulation) were also monitored and recorded over several minutes before,
during, and after drug administration. In those neurons that had a spontaneous
rate >2 s–1, the responses to skin stimulation
were corrected for the spontaneous activity.
Comparisons were made between groups and before and after drug treatment using repeated-measures ANOVA and t-test (Stat-View, SAS Institute, Cary, NC). All error values in the figures and text are SE.
|
|
RESULTS |
|---|
|
The effects of conditioning stimulation on peripheral inputs (Fig. 1) was primarily inhibitory at longer intervals (50, 100, and 200 ms), whereas at 5 and 25 ms, about half of the neurons showed an increase in responsiveness. The mean responses (Fig. 2A) revealed an overall facilitation of the response at 5 ms and an inhibition at each of the later intervals. While the maximum inhibition occurred at 50 ms, it was still quite strong at 200 ms. The difference between intervals was statistically significant [repeated-measures ANOVA, F(4,240) = 7.74, P < 0.001]. The four longer intervals were significantly less than test alone values (t = 2.16, P = 0.03–6.26, P < 0.001), indicating a significant inhibitory effect, but the increase at 5 ms was not statistically significant (t = 1.58, P = 0.12) because of the bimodal distribution at this interval.
|
|
Effect of GABAB receptor blockade
A total of 57 neurons were studied before and after administration of the GABAB receptor antagonist. CGP 55845 did not have an effect on either the spontaneous activity (1.61 and 1.69 s–1 before and after the drug; paired t = 0.23, P = 0.82) or the response to the peripheral (test) stimulation alone (mean total spikes = 62.1 and 64.8, before and after the drug; paired t = 0.49; P = 0.63).
The effect of blocking GABAB receptors on the response following conditioning-test pairing is shown for a representative neuron in Fig. 3. This cell was inhibited at the four longer intervals and this inhibition was largely reversed by CGP 55845. The overall effect of CGP 55845 on all 57 neurons tested is shown in Fig. 2B. The asterisks in Fig. 2B indicate statistical differences between pre and post drug responses (repeated-measures ANOVA and paired t-test, P < 0.001) and were significant at all intervals except 5 ms. In addition, the means at the 3 short intervals were statistically >100% (t = 3.6, 2.3, and 2.2, P < 0.05), indicating that CGP 55845 revealed a significant facilitation at these intervals.
|
Effect of GABAA receptor blockade
The GABAA receptor antagonist, gabazine, was tested on 19 neurons that were mainly inhibited prior to the drug administration. Gabazine did not significantly affect the spontaneous activity of these neurons (predrug: 2.24 s–1, after gabazine: 2.65 s–1; paired t = 0.69, P = 0.50). Gabazine appeared to produce an increase in the response to the test stimulus alone (from 88.9 to 99.2 spikes), but this was not statistically significant (t = 0.91, P = 0.38). Gabazine produced an overall reduction in inhibition (Fig. 4) that was statistically different from predrug levels at ISIs of 5 and 100 ms [F(1,18 = 6.21 and 5.0, P < 0.05]. The response after gabazine was also not significantly different from the test alone response (100%), although the response at 200 ms approached significance (P = 0.059).
|
|
|
DISCUSSION |
|---|
|
) and
between distinct areas such as sensory and motor cortex in the cat
(Sakamoto et al. 1987). It is
therefore possible that corticocortical connections between digit
representational areas within S1 cortex are modified during the reorganization
that follows digit amputation. The present study examined corticocortical
interactions in the intact animal by recording a cortical neuron's responses
to stimulation of its major digit input (the test pulse) after conditioning
stimulation of an adjacent cortical region. The responses at different
conditioning-test pulse intervals ranging from 5 to 200 ms revealed the
direction and time course of corticocortical influences. The results show that inhibitory modulation of adjacent digit areas of S1 cortex is much more prevalent than excitatory modulation (Fig. 1). Only about half of the neurons showed an increase in response to peripheral stimulation at any interval tested, whereas almost all showed a decrease at one or more intervals. A pattern consisting of inhibition alone at one or more intervals was the most common, whereas about one-third of the neurons showed an excitatory-inhibitory pattern. Facilitation was most frequently seen at the shortest interval tested (5 ms) and rarely seen at intervals >25 ms. In most of the neurons that were facilitated, the facilitation was followed by inhibition. This could be a feedback inhibition following the firing of the recorded neuron or feedforward activation of inhibitory neurons in parallel with the excitatory connections.
These results indicate that some neurons in a digit representational area
of S1 cortex can be excited via an adjacent cortical area, but this
facilitation is relatively short lasting. The ISIs used here do not take into
account the different conduction times for the two pathways. The time for
corticocortical transmission over 2–5 mm would be on the order of
5–10 ms, whereas the latency following peripheral stimulation is
15–20 ms (Smits et al.
1991). Therefore it would be expected that if both cortex and skin
were stimulated at the same time, the corticocortical input would arrive
10 ms earlier than the peripheral input. Anatomical evidence indicates
that there are no monosynaptic connections between digit areas in raccoon S1
cortex (Doetsch et al. 1988;
Herron and Johnson 1987),
although there are extensive projections to and from the sulcal regions
separating the digit areas that could provide a pathway for polysynaptic
connections. The short latency of the strong facilitation seen here suggests
that the number of intervening synapses is small. Nearly all neurons, however,
can be inhibited from an adjacent digit area either with or without a
preceding facilitation, and this inhibitory influence often lasted 
200 ms.
This likely results from activation of inhibitory interneurons near the site
of recording.
The only physiological study on corticocortical connections within raccoon
S1 cortex (Smits et al. 1991)
examined possible projections from an area just anterior to the digit
representation called the "heterogeneous" zone by Johnson et al.
(1982). This region contains
neurons with multidigit receptive fields as well as joint, skin, and possibly
muscle inputs, and Smits et al. found evidence of many excitatory projections
back into the glabrous skin representation. In contrast, the regions examined
in the present study are both glabrous skin representations in which the
neurons have small receptive fields restricted to a single digit. The
dominance of inhibitory connections between adjacent glabrous digit
representations seen here may contribute to tactile localization and
acuity.
Contribution of GABAA and GABAB receptors to corticocortical inhibition
Microiontophoretic administration of GABAA and GABAB
receptor antagonists was used to determine the contribution of these two
receptor subtypes to the inhibitory modulation. The selectivity of gabazine
and CGP 55845 for GABAA and GABAB receptors,
respectively, and their reversibility have been demonstrated repeatedly over
the last 20 years (e.g., Bittiger et al.
1993; Wermuth and
Biziére 1986). However, direct comparison of the
effectiveness of the two drugs in reversing corticocortical inhibition is
problematic using the microiontophoretic technique since the exact
concentration of the drug present at any synapse depends on many variables in
addition to amount present in the pipette. Consequently, we used a prolonged
administration of the drug (5 min) that should saturate the relevant receptors
within the area of diffusion. We have found that the same duration and
concentration of CGP 55845 can produce changes in receptive-field size in this
preparation (Chowdhury and Rasmusson
2002a,b).
With this technique, we found that GABAB receptor blockade produced
a reversal of inhibition at all intervals and in fact revealed greater
facilitation at short intervals. The GABAA antagonist, on the other
hand, produced complete reversal at the shortest interval and 50%
reversal at longer intervals.
CGP 55845 is a highly specific GABAB antagonist
(Bittiger et al. 1993) and has
been shown to produce receptive-field enlargement in raccoon cortex
(Chowdhury and Rasmusson
2002a). The almost complete elimination of inhibitory modulation
produced by CGP 55845 in the present study indicates that GABAB
receptors play a major role in the corticocortical inhibition.
GABAB receptors are present presynaptically, where they act to
suppress GABA and glutamate release (Dutar
and Nicoll 1988; Waldmeier et
al. 1994; Zilberter et al.
1999). In addition, presynaptic GABAB receptors
contribute to paired-pulse suppression
(Chowdhury and Matsunami 2002;
Chowdhury et al. 1996;
Zilberter et al. 1999).
Blockade of the GABAB autoreceptors on GABAergic terminals in the
present experiment should increase GABA release and consequently should lead
to greater inhibition via GABAA receptors, but this was not
observed. Blockade of GABAB heteroreceptors on glutamate terminals,
on the other hand, should facilitate the release of glutamate by
thalamocortical and intrinsic excitatory neurons and could account for the
switch from inhibition to facilitation that was seen in many cells after CGP
55845.
GABAB receptors are also present postsynaptically. These
metabotropic receptors produce a postsynaptic hyperpolarization with slower
onset but much longer duration than GABAA receptor activation
(Connors et al. 1988). The
block of inhibitory modulation at long intervals in the present study is
consistent with the time course of a postsynaptic GABAB-mediated
hyperpolarization.
Gabazine was used to block GABAA receptors because it has higher
affinity for the receptor than bicuculline and is less likely to induce
seizure activity (Heaulme et al.
1986). In addition, bicuculline methiodide has been described as
having some non-GABAergic effects in the brain
(Seutin et al. 1997).
Inhibitory postsynaptic potentials associated with GABAA receptors
have a peak effect within 5 ms and a duration of 30 ms
(Connors et al. 1988;
Krnjevic and Schwartz 1967;
Salin and Prince 1996). In the
present study, the complete reversal of inhibition at the 5-ms ISI by gabazine
is consistent with a GABAA component to this early inhibition. As
mentioned earlier, this could be due to excitation of local interneurons by
the corticocortical pathways or feedback inhibition following the excitation
of other cells. The smaller reduction in inhibition at longer intervals by
gabazine suggests there may also be slow or multisynaptic corticocortical
pathways that end on local interneurons, but the large variability at these
data points makes it difficult to judge their importance.
Previous studies in the raccoon have demonstrated an increase in
receptive-field size after both GABAA and GABAB receptor
blockade (Chowdhury and Rasmusson
2002a; Tremere et al.
2001). It might be expected that this would also yield an increase
in spontaneous activity and in the evoked response to the peripheral stimulus
alone. While this was seen in some neurons, overall the effect was not
significant for either CGP 55845 or gabazine. This may be due to the fact that
receptive-field expansion is largely a reflection of changes in threshold at
the edges of the receptive field, whereas the present study used a constant
stimulus at one site.
The overall results of the present study are consistent with several
possible pathways. The finding that one or both GABA antagonists reversed
inhibition in most of the neurons indicates that the GABAergic neurons are
acting directly on the neuron that was being recorded or presynaptically on
its inputs. Differences between neurons in the amount of reversal of
inhibition could be due to the location of the GABAergic receptors on the
neuron relative to the micropipette. In addition, the inhibition that remained
in some neurons could be occurring earlier in the polyneuronal circuit
(Bindman et al. 1988) at a site
that is too far from the site of microiontophoresis to be affected by these
drugs.
Possible relevance to injury-induced reorganization
Immediately after digit amputation, neurons in S1 cortex of the raccoon
show predominantly inhibition from stimulation of adjacent digits
(Rasmusson and Turnbull 1983).
This inhibition is consistent with the largely inhibitory connections from the
adjacent digit representational area of S1 revealed in the present study. The
relative predominance of inhibitory corticocortical connections in the raccoon
may account for some of the differences that have been observed between it and
other species (Byrne and Calford
1991; Calford and Tweedale
1988; Li et al.
1994). Evidence in many models shows that the cortical GABAergic
circuits are gradually downregulated after the removal of sensory input
(Jones 2000); this would allow
any weak excitatory inputs greater opportunity to be strengthened. The
existence of some short-latency excitatory corticocortical connections
provides one potential pathway that could be gradually strengthened during the
process of long-term reorganization.
|
|
DISCLOSURES |
|---|
|
|
|
ACKNOWLEDGMENTS |
|---|
|
|
|
FOOTNOTES |
|---|
Address for reprint requests: D. D. Rasmusson, Department of Physiology and Biophysics, 5859 University Avenue, Dalhousie University, Halifax, Nova Scotia, Canada B3H 4H7 (E-mail: rasmus{at}dal.ca).
|
|
REFERENCES |
|---|
|
Bindman LJ,
Murphy KPSJ, and Pockett S. Postsynaptic control of the induction of
long-term changes in efficacy of transmission at neocortical synapses in
slices of rat brain. J Neurophysiol
60: 1053–1065,
1988.
Bittiger H, Froestl W, Mickel S, and Olpe HR. GABAB receptor antagonists: from synthesis to therapeutic applications. Trends Pharmacol Sci 14: 391–394, 1993.[Medline]
Byrne J and Calford M. Short-term expansion of receptive fields in rat primary somatosensory cortex after hindpaw digit denervation. Brain Res 565: 218–224, 1991.[Web of Science][Medline]
Calford MB and Tweedale R. Immediate and chronic changes in responses of somatosensory cortex in adult flying-fox after digit amputation. Nature 332: 446–448, 1988.[Medline]
Chowdhury SA, Kawashima T, Konishi T, Niwa M, and Matsunami K. Study of paired-pulse inhibition of transcallosal response in the pyramidal tract neuron in vivo. Eur J Pharmacol 314: 313–317, 1996.[Web of Science][Medline]
Chowdhury SA and Matsunami K. GABA-B-related activity in processing of transcallosal response in cat motor cortex. J Neurosci Res 68: 489–495, 2002.[Web of Science][Medline]
Chowdhury SA and Rasmusson DD. Comparison of receptive field expansion produced by GABAB and GABAA receptor antagonists in raccoon primary somatosensory cortex. Exp Brain Res 144: 114–121, 2002a.[Web of Science][Medline]
Chowdhury SA and Rasmusson DD. Effect of GABAB receptor blockade on receptive fields of raccoon somatosensory cortical neurons during reorganization. Exp Brain Res 145: 150–157, 2002b.[Web of Science][Medline]
Connors BW,
Malenka RC, and Silva LR. Two inhibitory postsynaptic potentials, and
GABAa and GABAb receptor-mediated responses in neocortex of rat and cat.
J Physiol 406:
443–468, 1988.
Doetsch GS, Standage GP, Johnston KW, and Lin C-S. Intracortical connections of two functional subdivisions of the somatosensory forepaw cerebral cortex of the raccoon. J Neurosci 8: 1887–1900, 1988.[Abstract]
Dutar P and Nicoll RA. A physiological role for GABAB receptors in the central nervous system. Nature 332: 156–158, 1988.[Medline]
Gardner EP and
Costanzo RM. Temporal integration of multiple-point stimuli in primary
somatosensory cortical receptive fields of alert monkeys. J
Neurophysiol 43:
444–468, 1980.
Heaulme M, Chambon JP, Leyris R, Molimard JC, Wermuth CG, and Biziere K. Biochemical characterization of the interaction of three pyridazinyl-GABA derivatives with the GABAA receptor site. Brain Res 384: 224–231, 1986.[Web of Science][Medline]
Herron P and Johnson JI. Organization of intracortical and commissural connections in somatosensory cortical areas I and II in the raccoon. J Comp Neurol 257: 359–371, 1987.[Web of Science][Medline]
Johnson JI, Ostapoff E-M, and Warach S. The anterior border zones of primary somatic sensory (SI) neocortex and their relation to cerebral convolutions, shown by micromapping of peripheral projections to the region of the fourth forepaw digit representation in raccoons. Neuroscience 7: 915–936, 1982.[Web of Science][Medline]
Jones EG. Cortical and subcortical contributions to activity-dependent plasticity in primate somatosensory cortex. Annu Rev Neurosci 23: 1–37, 2000.[Web of Science][Medline]
Kaas J. Plasticity of sensory and motor maps in adult mammals. Annu Rev Neurosci 14: 137–167, 1991.[Web of Science][Medline]
Kelahan AM and Doetsch GS. Time-dependent changes in the functional organization of somatosensory cerebral cortex following digit amputation in adult raccoons. Somatosens Res 2: 49–81, 1984.[Web of Science][Medline]
Krnjevic K and
Schwartz S. The action of 
-aminobutyric acid on cortical neurones.
Exp Brain Res 3:
320–336, 1967.[Web of Science][Medline]
Lee SM, Weisskopf MG, and Ebner FF. Horizontal long-term potentiation of responses in rat somatosensory cortex. Brain Res 544: 303–310, 1991.[Web of Science][Medline]
Li CX, Waters RS, Oladehin A, Johnson EF, McCandlish CA, and Dykes RW. Large unresponsive zones appear in cat somatosensory cortex immediately after ulnar nerve cut. Can J Neurol Sci 21: 233–247, 1994.[Web of Science][Medline]
Merzenich MM, Nelson RJ, Stryker MP, Cynader MS, Schoppmann A, and Zook JM. Somatosensory cortical map changes following digit amputation in adult monkeys. J Comp Neurol 224: 591–605, 1984.[Web of Science][Medline]
Rasmusson DD. Reorganization of raccoon somatosensory cortex following removal of the fifth digit. J Comp Neurol 205: 313–326, 1982.[Web of Science][Medline]
Rasmusson DD. Changes in the response properties of neurons
in the ventroposterior lateral thalamic nucleus of the raccoon after
peripheral deafferentation. J Neurophysiol
75: 2441–2450,
1996.
Rasmusson DD and Northgrave SA. Reorganization of the raccoon cuneate nucleus after
peripheral denervation. J Neurophysiol
78: 2924–2936,
1997.
Rasmusson DD and Turnbull BG. Immediate effects of digit amputation on SI cortex in the raccoon: unmasking of inhibitory sites. Brain Res 288: 368–370, 1983.[Web of Science][Medline]
Rasmusson DD, Webster HH, and Dykes RW. Neuronal response properties within subregions of raccoon somatosensory cortex one week after digit amputation. Somatosens Mot Res 9: 279–289, 1992.[Web of Science][Medline]
Sakamoto T, Porter LL, and Asanuma H. Long-lasting potentiation of synaptic potentials in the motor cortex produced by stimulation of the sensory cortex in the cat: a basis of motor learning. Brain Res 413: 360–364, 1987.[Web of Science][Medline]
Salin PA and
Prince DA. Electrophysiological mapping of GABAA
receptor-mediated inhibition in adult rat somatosensory cortex. J
Neurophysiol 75:
1589–1600, 1996.
Seutin V, Scuvee-Moreau J, and Dresse A. Evidence for a non-GABAergic action of quaternary salts of bicuculline on dopaminergic neurons. Neuropharmacology 36: 1653–1657, 1997.[Web of Science][Medline]
Smits E, Gordon
D, Witte S, Rasmusson DD, and Zarzecki P. Synaptic potentials evoked by
convergent somatosensory and corticocortical inputs in raccoon somatosensory
cortex: substrates for plasticity. J Neurophysiol
66: 688–695,
1991.
Tremere L, Hicks TP, and Rasmusson DD. Expansion of receptive fields in raccoon somatosensory cortex in vivo by GABAA receptor antagonism: implications for cortical reorganization. Exp Brain Res 135: 447–455, 2001.
Waldmeier PC, Wicki P, Feldtrauer JJ, Mickel SJ, Bittiger H, and Baumann PA. GABA and glutamate release affected by GABAB receptor antagonists with similar potency: no evidence for pharmacologically different presynaptic receptors. Br J Pharmacol 113: 1515–1521, 1994.[Web of Science]
Welker WI and Seidenstein S. Somatic sensory representation in the cerebral cortex of the raccoon (Procyon lotor). J Comp Neurol 111: 469–501, 1959.[Web of Science][Medline]
Wermuth CG and Biziére K. Pyridazinyl-GABA derivatives: a new class of synthetic GABA-A antagonists. Trends Pharmacol Sci 7: 421–424, 1986.
Zarzecki P,
Witte S, Smits E, Gordon DC, Kirchberger P, and Rasmusson DD.
Synaptic mechanisms of cortical representational plasticity: somatosensory and
corticocortical EPSPs in reorganized raccoon SI cortex. J
Neurophysiol 69:
1422–1432, 1993.
Zilberter Y, Kaiser KMM, and Sakmann B. Dendritic GABA release depresses excitatory transmission between layer 2/3 pyramidal and bitufted neurons in rat neocortex. Neuron 24: 978–988, 1999.
This article has been cited by other articles:
|
|
 |
|
  M. David-Jurgens and H. R. Dinse Effects of Aging on Paired-Pulse Behavior of Rat Somatosensory Cortical Neurons Cereb Cortex, September 10, 2009; (2009) bhp185v1. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. P. Pluto, N. L. Chiaia, R. W. Rhoades, and R. D. Lane Reducing Contralateral SI Activity Reveals Hindlimb Receptive Fields in the SI Forelimb-Stump Representation of Neonatally Amputated Rats J Neurophysiol, September 1, 2005; 94(3): 1727 - 1732. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Fierro, F. Brighina, G. Vitello, A. Piazza, S. Scalia, G. Giglia, O. Daniele, and A. Pascual-Leone Modulatory effects of low- and high-frequency repetitive transcranial magnetic stimulation on visual cortex of healthy subjects undergoing light deprivation J. Physiol., June 1, 2005; 565(2): 659 - 665. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. T. Porter and D. Nieves Presynaptic GABAB Receptors Modulate Thalamic Excitation of Inhibitory and Excitatory Neurons in the Mouse Barrel Cortex J Neurophysiol, November 1, 2004; 92(5): 2762 - 2770. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. P. Pluto, R. D. Lane, and R. W. Rhoades Local GABA Receptor Blockade Reveals Hindlimb Responses in the SI Forelimb-Stump Representation of Neonatally Amputated Rats J Neurophysiol, July 1, 2004; 92(1): 372 - 379. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
TOP
ABSTRACT
INTRODUCTION
) and after (
) administration of
gabazine. *, difference between gabazine and predrug, P <
0.05.