| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Anatomy and Neurobiology, Medical College of Ohio, Toledo, Ohio
Submitted 2 March 2005; accepted in final form 24 March 2005
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
60% of sites that were stump/hindlimb responsive during GRB. These findings indicate that activity in the contralateral SI contributes to the suppression of reorganized hindlimb receptive fields in neonatally amputated rats. |
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
). Results from previous studies suggest that these hindlimb inputs originate in the SI hindlimb representation in the same hemisphere and are transmitted to SI forelimb-stump neurons via a polysynaptic circuit through the intervening dysgranular cortex (Lane et al. 1999; Stojic et al. 2001). Hindlimb responses can be revealed when GRB is induced globally by topical application or locally by injection at the recording site, suggesting that the GABA receptors of interest are located on hindlimb responsive forelimb-stump neurons and/or on axons of other cells carrying hindlimb information into the deafferented region (Pluto et al. 2004). Because inhibitory interneurons typically have relatively short axons that synapse locally, it is likely that the GABAergic neurons that suppress hindlimb responses are themselves located within the SI forelimb-stump area. As GABA release by interneurons is usually triggered by excitatory inputs to these cells (McBain and Fisahn 2001), we attempted here to modulate the hindlimb suppression, independent of GRB, by reducing excitatory input to SI GABAergic neurons.
One source of excitatory input to SI GABAergic neurons is the contralateral SI via the corpus callosum. Callosal fibers make predominantly excitatory connections between homotopic regions of SI (Koralek and Killackey 1990), terminating on both pyramidal and inhibitory neurons (Carr and Sesack 1998). Callosal axons are thus capable of exerting monosynaptic excitation and/or disynaptic inhibition at postsynaptic targets in the opposite hemisphere (Kawaguchi 1992; Vogt and Gorman 1982). Callosal connections in SI appear to modulate inhibition and cutaneous receptive fields (Clarey et al. 1996; Rema and Ebner 2003; Shuler et al. 2001; Swadlow 2003). In this study, the contralateral SI forelimb region was reversibly inactivated with lidocaine in an attempt to weaken disynaptic inhibition and thereby reveal hindlimb receptive fields in the SI forelimb-stump representation independent of the use of GABA receptor antagonists.
|
METHODS |
|---|
|
TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
Neonatal forelimb removal
Neonatal forelimb amputations were carried out using methods previously described (Lane et al. 1995). Within 12 h of birth, rat pups were anesthetized by hypothermia until immobile. The left forelimb was amputated at the proximal humerus with iridectomy scissors, and the brachial artery was sealed by electrocautery. The region was infiltrated with 0.7% bupivicaine, and the skin was closed with cyanoacrylate adhesive. The pups were re-warmed, returned to their mother, and allowed to reach 
60 days of age before being used in terminal recording experiments. These rats grew and behaved normally and showed no signs of pain; body weight was normal in these animals.
Receptive field mapping
Rats were anesthetized with 60 mg/kg ketamine hydrochloride and 15 mg/kg xylazine administered intraperitoneally and prepared for recordings as previously described (Lane et al. 1999). The trachea was cannulated, and the rat was placed on a thermoregulatory blanket and fixed in a stereotaxic device. Mechanical ventilation was set at 60–75 strokes/min (5–7 ml/stroke), and heart rate was monitored periodically. A state of light anesthesia was maintained by periodically testing the corneal reflex and administering 1g/kg urethan when needed; urethan was used because it maintains a long-lasting but relatively light level of anesthesia. The cisterna magna was opened to drain cerebral spinal fluid (to prevent herniation through the craniotomy), a midsagittal incision was made over the skull, and a craniotomy was performed over the cortex contralateral to the amputation. Warmed (37°C) neurobasal culture medium (Gibco-BRL) was applied periodically to prevent desiccation. A magnified (20 times) digital photograph of the exposed cortex was used to mark electrode penetrations with reference to the surface vasculature. Multi-unit responses were recorded with extracellular tungsten electrodes (1.0 M
). Electrode penetrations were spaced 250–300 µm apart, and activity was recorded at layer IV depth (600–800 µm). Light, cutaneous stimuli were delivered separately to the stump, whisker pad, lower jaw, trunk, and hindlimb by lightly tapping the body surface with a modified artist's brush. This type of stimulation could activate deeper proprioceptive receptors (e.g., muscle spindle, joint, Golgi tendon organs) in addition to superficial touch receptors (e.g., Meissner, Merkel, Pacinian, Ruffini). The cortical surface vasculature was used to determine electrode placement in the retesting of unit clusters at specific recording sites. At the end of the recording session, each animal was given a lethal dose of carbon dioxide and perfused with heparinized saline followed by 4% formaldehyde dissolved in sodium phosphate buffer (pH 7.4). The brains were postfixed overnight, removed, and cut on a freezing microtome at 50 µm. Horizontal cortical sections were processed for cytochrome oxidase histochemistry (Wong-Riley 1979).
GABA receptor blockade (GRB)
After mapping the SI forelimb-stump representation, 30 µl of a 50 µM bicuculline methiodide/saclofen hydrochloride (Research Biochemicals International) solution was applied topically to SI to induce GRB. The forelimb-stump region was remapped 10–15 min later, when increased neuronal bursting activity indicated that GRB had taken effect. The bursting pattern induced by GRB was used to monitor the level of receptor antagonism, and tactile stimuli were delivered between periods of intense bursting. All sites were retested during GRB (1 h); additional 30-µl drug applications were employed if needed. Evoked responses were considered significant if at least nine sets of action potentials were elicited in response to a train of 10 light taps delivered to the body surface at a frequency of 3 Hz. After each GRB mapping session, the cortical surface was flushed with fresh neurobasal medium and 60 min allowed for the drug to washout.
Lidocaine inactivation of the opposite SI forelimb region
In these experiments, the SI forelimb-stump region was first mapped under normal and GRB conditions to define the region and to identify stump/hindlimb responsive sites. The opposite SI forelimb representation was then mapped and a total of 15–25 µl 4% lidocaine (Roxane Laboratories) was injected at two central sites within the representation, 400 µm below the pial surface. Evoked responses at two to three sites across the lidocaine-treated SI forelimb area were monitored every 10 min to confirm that the area was inactivated. Evoked and spontaneous activity was also monitored at one to two sites in the adjacent SI hindlimb and vibrissae regions to confirm that only the SI forelimb region was inactivated. Sites within the forelimb-stump region that were stump/hindlimb responsive during GRB were retested during lidocaine inactivation. The effect of contralateral lidocaine inactivation on the spontaneous activity levels of SI forelimb-stump neurons was examined in four amputated rats. Spontaneous activity was quantified by counting the number of spikes with amplitudes greater than twice the level of background activity using the Corel Draw 4 program for off-line analysis of oscilloscope traces (3 10-s sweeps at each of 4 recording sites in each animal under normal conditions and during lidocaine treatment). These values were averaged and compared by dependent t-test. In another two amputated rats, the forelimb-stump area was mapped prior to GRB mapping, to determine if the lidocaine-revealed hindlimb responses were influenced by prior GRB treatment.
Data analysis
All SI forelimb-stump recording sites were classified as responsive to cutaneous stimulation of the stump only, stump/hindlimb, stump/face (vibrissae and/or lower jaw), or stump/trunk, under normal conditions, and during GRB. All sites that were stump/hindlimb responsive during GRB were again tested during lidocaine inactivation of the opposite SI forelimb region. Frequency data (% of total sites) were compared by one-way ANOVA to test for hindlimb responses under each condition. Specific comparisons of hindlimb response frequencies between two different conditions were analyzed by the dependent t-test. Spontaneous activity values (spikes/s) were compared by the dependent t-test. The accepted level of significance for all statistical tests was P < 0.05.
|
RESULTS |
|---|
|
TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
, 1999; Stojic et al. 2001).
|
After completing the map of the SI forelimb-stump region under normal conditions and during GRB to identify hindlimb responsive sites, the opposite (intact) SI forelimb representation was mapped and lidocaine was injected centrally in this region (Fig. 1, A–C). Recordings were conducted at granular and infragranular depths (600–1,000 µm) in the injected SI forelimb region to confirm that the activity of potential callosal efferent neurons was reduced. Within 3–4 min of lidocaine treatment, evoked and spontaneous activity was greatly diminished at several sites throughout the injected representation. In contrast, neuronal activity in the adjacent SI hindlimb and vibrissae representations was largely unaffected, indicating that inactivation was principally restricted to the SI forelimb region (Fig. 2).
|
|
Recordings in the SI forelimb-stump representation during lidocaine inactivation revealed hindlimb responses in 59.8% of those sites that were hindlimb responsive during GRB (Fig. 1D). Overall, hindlimb responses were found in 18.3 ± 5% of the total SI forelimb-stump sites during lidocaine inactivation. This value was significantly greater than the 3.3 ± 4% found during normal conditions (P = 0.0001) and significantly less than the 30.6 ± 7% found during GRB (P = 0.0001; Fig. 3 ).
In two amputated rats, lidocaine was injected and the SI forelimb-stump sites tested prior to GRB to determine whether residual effects of GABA antagonism contributed to the 18.3% of sites that exhibited hindlimb expression for the overall group data. In these animals, the percentage of hindlimb-expressing SI forelimb-stump sites (2 and 8% at baseline) increased to 12 and 17% during lidocaine inactivation, respectively. Subsequent GRB revealed 30% of sites as hindlimb responsive in both animals, and re-injection of lidocaine 1 h after GRB revealed hindlimb responses in 22 and 21% of sites, respectively (data not shown). These findings suggest that there was a minor enhancing effect of previous GRB on the ability of lidocaine treatment to reveal stump/hindlimb receptive fields. All lidocaine-revealed hindlimb responses in these rats were at sites that became hindlimb responsive during GRB, and the majority of these responses did not persist for >30 min even if supplemental injections (10 µl) were given.
In three normal rats, hindlimb responses were found in 3.7 ± 3% of sites initially, and in 12.7 ± 1% during GRB. These results are consistent with the previous finding in normal rats of hindlimb responses in 2.7% of sites under normal and in 11.7% during GRB conditions (Lane et al. 1997). In the normal rats studied here, contralateral lidocaine inactivation revealed hindlimb responses in 3.0 ± 3% of sites, indicating no significant effect of lidocaine treatment on hindlimb expression in the SI forelimb representation of normal rats.
Effects of contralateral lidocaine inactivation on spontaneous activity
The influence of inactivating the intact, contralateral SI forelimb representation on spontaneous activity in the SI forelimb-stump representation was examined in four amputated rats. On average, contralateral lidocaine inactivation significantly decreased the level of spontaneous activity at 16 multiunit SI forelimb-stump sites (4 per rat), from 6.9 at baseline to 2.9 spikes/s during lidocaine treatment (P = 0.0001; Fig. 4).
|
|
DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
Contralateral SI-mediated inhibition
GABAergic neurons, which are located in all layers of SI, receive excitatory asymmetric synaptic contacts from a number of sources (Keller and White 1986; 1987; Swadlow 1995). One source of excitatory input to inhibitory interneurons is callosal projection neurons that interconnect the two SIs (Carr and Sesack 1998; Somogyi et al. 1983). A small number of callosal projection neurons are glutamic acid decarboxylase or GABA positive (Fabri and Manzoni 2004; Gonchar et al. 1995). These findings establish callosal SI connections as a potential substrate for modulating inhibition in SI. Recent functional and neuroimaging studies further suggest that transcallosal modulation is important for the integration of bilateral tactile information (Shuler et al. 2001; Werhahn et al. 2002; Wiest et al. 2004).
Although SI predominantly processes input from the contralateral body surface, a number of studies have described ipsilaterally evoked responses and have further shown that the opposite SI plays a regulatory role in their expression. For example, ipsilateral responses in the SI vibrissae barrel cortex of rats and mice were noted after a 4- to 5-ms delay but were abolished when the opposite SI was ablated (Pidoux and Verley 1979). In the rat SI hindlimb region, 51% of single units responded to stimulation of both the contralateral and ipsilateral hindlimbs. Under deeper anesthesia, however, 77% of these cells lost the ipsilateral receptive field, indicating that these responses are more likely to be expressed under relatively light anesthesia (Armstrong-James and George 1988). More recent work has demonstrated ipsilateral responses in the vibrissae barrel cortex and shown that these responses have a suppressive influence on subsequent contralateral responses. These responses and their suppressive effects are, however, abolished by muscimol inactivation of the opposite SI (Shuler et al. 2001). In cortical area 3b of the flying fox, cutaneous receptive fields on the digits immediately expanded when a small region of the opposite area 3b was cooled to 10°C (Clarey et al. 1996). Together these findings indicate that SI neurons are capable of processing bilateral sensory input, and suggest that the opposite hemisphere may provide a "tonic" inhibition in SI (Calford 2002).
It is not yet known whether the density and/or distribution of callosal projections are altered in neonatally amputated rats, although results from previous developmental sensory system studies suggest that this may be the case. The relatively exuberant callosal projections found during development compete with thalamocortical axons for cortical occupancy (Ivy and Killackey 1982; Lent et al. 1990). In the cat, >70% of callosal axons are eliminated from birth to adulthood, and this transition is influenced by visual experience (Innocenti et al. 1985; Koppel and Innocenti 1983). Normally, callosal projections in rat SI eventually distribute in a "complementary" pattern mostly to dysgranular areas of layer IV, where they are less dense than in the supra- and infra-granular layers (Hayama and Ogawa 1997; Olavarria et al. 1984). This pattern is altered, however, after either neonatal transection of the infraorbital nerve or removal of the dorsal thalamus (Koralek and Killackey 1990). The density and distribution of callosal projections was also abnormal in rats that had undergone neonatal spinal overhemisection to remove dorsal column input bilaterally (Remple et al. 2004). Similarly, callosal terminals were altered in the deafferented visual cortex of hamsters that sustained neonatal enucleation (Fish et al. 1991; Rhoades and Dellacroce 1980), or transection of the optic radiations (Rhoades et al. 1987). These findings raise the possibility that there is an abnormal distribution of callosal fibers in neonatally amputated rats due to the large-scale disruption of thalamocortical input to the SI forelimb-stump area. The observation that contralateral lidocaine inactivation does not enhance the expression of hindlimb receptive fields in the SI forelimb region of normal rats further suggests that this circuit is altered by neonatal amputation. Neuronal tracer experiments are currently underway to examine the areal and laminar distribution of callosal projections in these animals.
It is worth noting that although both GRB and contralateral lidocaine inactivation are capable of revealing hindlimb receptive fields, these manipulations have opposite effects on spontaneous activity within the SI forelimb-stump representation. While GRB treatment increases, contralateral lidocaine injections decreases, the spontaneous firing rate of these neurons. A previous study demonstrated that GRB significantly increases the spontaneous firing rate of individual neurons in the SI forelimb-stump of neonatally amputated rats (Stojic et al. 2001). Other studies have also shown increased spontaneous firing rates of neurons in the visual and SI cortex as well as the dorsal column nuclei of the cat (Dykes and Craig 1998; Dykes et al. 1984; Sillito et al. 1981), and in slices of rat SI (Chagnac-Amitai and Connors 1989) after application of bicuculline. By blocking inhibition in SI, GRB increases the overall activity of neurons and allows weak or previously suppressed (i.e., hindlimb) inputs to be expressed. On the other hand, contralateral lidocaine inactivation reduced spontaneous activity. This finding is consistent with those of Clarey et al. (1996), who reported a decrease in spontaneous activity when the opposite sensory cortex was cooled. The decreased spontaneous activity that results from contralateral SI deactivation indicates that callosal input generally has a net excitatory effect (Kawaguchi 1992; Vogt and Gorman 1982), but the unmasking of hindlimb responses suggests that callosal inputs also provide one source of drive to the GABAergic neurons that normally suppress hindlimb receptive fields.
Hindlimb receptive fields were only expressed for 30 min after lidocaine injections, which is consistent with the transient (
30 min) expansion of receptive fields noted by Clarey et al. (1996). The transitory nature of this effect suggests that inhibitory function is reestablished when input from the opposite hemisphere is reduced for a sustained period of time (25–30 min). The reestablishment of inhibition could reflect an increase in other sources of input and/or in the sensitivity of SI GABAergic neurons to these inputs (Clarey et al. 1996). Together with the fact that lidocaine inactivation revealed hindlimb responses in only 60% of the sites that were stump/hindlimb responsive during GRB, it seems probable that other factors contribute to the modulation of GABAergic inhibition in SI (Fig. 5). This could include other brain regions such as SII, the ventroposterior thalamus (Porter et al. 2001; Staiger et al. 1996; Swadlow 1995), as well as peripheral C-fiber activity (Calford 2002). Alternatively, inhibitory SI neurons have a high level of basal activity during normal behavior (McCasland et al. 1997), and hence a portion of the selective inhibition of hindlimb receptive fields (Stojic et al. 2001) may not require continuous input from outside sources. The variety of form and function among GABAergic neurons (Beierlein et al. 2003; Markram et al. 2004; McBain and Fisahn 2001; Reyes et al. 1998; Swadlow et al. 1998; Tamas et al. 2003), the differential locations and roles of GABAA and GABAB receptors (Chowdhury and Rasmusson 2003), and the interplay between stimulus-driven and tonic inhibition (Mody 2005) support the concept that multiple factors are involved in modulating the expression of receptive fields in SI. Our results suggest that the suppression of hindlimb receptive fields in the SI forelimb-stump representation of neonatally amputated rats is mediated by a dynamic circuit with multiple inputs as well as the capacity to compensate or adjust for a loss of activity in one of these inputs.
|
|
GRANTS |
|---|
|
TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
|
ACKNOWLEDGMENTS |
|---|
|
TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
|
FOOTNOTES |
|---|
Address for reprint requests and other correspondence: C. P. Pluto, Dept. of Anatomy and Neurobiology, Medical Collegeo of Ohio, 3000 Arlington Ave., Toledo, OH 43614 (E-mail: cpluto{at}mco.edu)
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
Beierlein M, Gibson JR, and Connors BW. Two dynamically distinct inhibitory networks in layer 4 of the neocortex. J Neurophysiol 90: 2987–3000, 2003.
Calford MB. Dynamic representational plasticity in sensory cortex. Neuroscience 111: 709–738, 2002.[CrossRef][ISI][Medline]
Carr DB and Sesack SR. Callosal terminals in the rat prefrontal cortex: synaptic targets and association with GABA-immunoreactive structures. Synapse 29: 193–205, 1998.[CrossRef][ISI][Medline]
Chagnac-Amitai Y and Connors BW. Horizontal spread of synchronized activity in neocortex and its control by GABA-mediated inhibition. J Neurophysiol 61: 747–758, 1989.
Chowdhury SA and Rasmusson DD. Corticocortical inhibition of peripheral inputs within primary somatosensory cortex: the role of GABA(A) and GABA(B) receptors. J Neurophysiol 90: 851–856, 2003.
Clarey JC, Tweedale R, and Calford MB. Interhemispheric modulation of somatosensory receptive fields: evidence for plasticity in primary somatosensory cortex. Cereb Cortex 6: 196–206, 1996.
Dykes RW and Craig AD. Control of size and excitability of mechanosensory receptive fields in dorsal column nuclei by homolateral dorsal horn neurons. J Neurophysiol 80: 120–129, 1998.
Dykes RW, Landry P, Metherate R, and Hicks TP. Functional role of GABA in cat primary somatosensory cortex: shaping receptive fields of cortical neurons. J Neurophysiol 52: 1066–1093, 1984.
Fabri M and Manzoni T. Glutamic acid decarboxylase immunoreactivity in callosal projecting neurons of cat and rat somatic sensory areas. Neuroscience 123: 557–566, 2004.[CrossRef][ISI][Medline]
Fish SE, Rhoades RW, Bennett-Clarke CA, Figley B, and Mooney RD. Organization, development and enucleation-induced alterations in the visual callosal projection of the hamster: single axon tracing with Phaseolus vulgaris leucoagglutinin and Di-I. Eur J Neurosci 3: 1255–1270, 1991.[CrossRef][ISI][Medline]
Gonchar YA, Johnson PB, and Weinberg RJ. GABA-immunopositive neurons in rat neocortex with contralateral projections to S-I. Brain Res 697: 27–34, 1995.[CrossRef][ISI][Medline]
Hayama T and Ogawa H. Regional differences of callosal connections in the granular zones of the primary somatosensory cortex in rats. Brain Res Bull 43: 341–347, 1997.[CrossRef][ISI][Medline]
Innocenti GM, Frost DO, and Illes J. Maturation of visual callosal connections in visually deprived kittens: a challenging critical period. J Neurosci 5: 255–267, 1985.[Abstract]
Ivy GO and Killackey HP. Ontogenetic changes in the projections of neocortical neurons. J Neurosci 2: 735–743, 1982.[Abstract]
Kawaguchi Y. Receptor subtypes involved in callosally-induced postsynaptic potentials in rat frontal agranular cortex in vitro. Exp Brain Res 88: 33–40, 1992.[CrossRef][ISI][Medline]
Keller A and White EL. Distribution of glutamic acid decarboxylase-immunoreactive structures in the barrel region of mouse somatosensory cortex. Neurosci Lett 66: 245–250, 1986.[CrossRef][ISI][Medline]
Keller A and White EL. Synaptic organization of GABAergic neurons in the mouse SmI cortex. J Comp Neurol 262: 1–12, 1987.[CrossRef][ISI][Medline]
Koppel H and Innocenti GM. Is there a genuine exuberancy of callosal projections in development? A quantitative electron microscopic study in the cat. Neurosci Lett 41: 33–40, 1983.[CrossRef][ISI][Medline]
Koralek KA and Killackey HP. Callosal projections in rat somatosensory cortex are altered by early removal of afferent input. Proc Natl Acad Sci USA 87: 1396–1400, 1990.
Lane RD, Bennett-Clarke CA, Chiaia NL, Killackey HP, and Rhoades RW. Lesion-induced reorganization in the brainstem is not completely expressed in somatosensory cortex. Proc Natl Acad Sci USA 92: 4264–4268, 1995.
Lane RD, Killackey HP, and Rhoades RW. Blockade of GABAergic inhibition reveals reordered cortical somatotopic maps in rats that sustained neonatal forelimb removal. J Neurophysiol 77: 2723–2735, 1997.
Lane RD, Stojic RS, Killackey HP, and Rhoades RW. Source of inappropriate receptive fields in cortical somatotopic maps from rats that sustained neonatal forelimb removal. J Neurophysiol 81: 625–633, 1999.
Lent R, Hedin-Pereira C, Menezes JR, and Jhaveri S. Neurogenesis and development of callosal and intracortical connections in the hamster. Neuroscience 38: 21–37, 1990.[CrossRef][ISI][Medline]
Markram H, Toledo-Rodriguez M, Wang Y, Gupta A, Silberberg G, and Wu C. Interneurons of the neocortical inhibitory system. Nat Rev Neurosci 5: 793–807, 2004.[CrossRef][ISI][Medline]
McBain CJ and Fisahn A. Interneurons unbound. Nat Rev Neurosci 2: 11–23, 2001.[ISI][Medline]
McCasland JS, Hibbard LS, Rhoades RW, and Woolsey TA. Activation of a wide-spread network of inhibitory neurons in barrel cortex. Somatosens Mot Res 14: 138–147, 1997.[CrossRef][ISI][Medline]
Mody I. Aspects of the homeostaic plasticity of GABAA receptor- mediated inhibition. J Physiol 562: 37–46, 2005.
Olavarria J, Van Sluyters RC, and Killackey HP. Evidence for the complementary organization of callosal and thalamic connections within rat somatosensory cortex. Brain Res 291: 364–368, 1984.[CrossRef][ISI][Medline]
Pidoux B and Verley R. Projections on the cortical somatic I barrel subfield from ipsilateral vibrissae in adult rodents. Electroencephalogr Clin Neurophysiol 46: 715–726, 1979.[CrossRef][ISI][Medline]
Pluto CP, Lane RD, and Rhoades RW. Local GABA receptor blockade reveals hindlimb responses in the SI forelimb-stump representation of neonatally amputated rats. J Neurophysiol 92: 372–379, 2004.
Porter JT, Johnson CK, and Agmon A. Diverse types of interneurons generate thalamus-evoked feedforward inhibition in the mouse barrel cortex. J Neurosci 21: 2699–2710, 2001.
Rema V and Ebner FF. Lesions of mature barrel field cortex interfere with sensory processing and plasticity in connected areas of the contralateral hemisphere. J Neurosci 23: 10378–10387, 2003.
Remple MS, Jain N, Diener PS, and Kaas JH. Bilateral effects of spinal overhemisections on the development of the somatosensory system in rats. J Comp Neurol 475: 604–619, 2004.[CrossRef][ISI][Medline]
Reyes A, Lujan R, Rozov A, Burnashev N, Somogyi P, and Sakmann B. Target-cell-specific facilitation and depression in neocortical circuits. Nat Neurosci 1: 279–285, 1998.[CrossRef][ISI][Medline]
Rhoades RW and Dellacroce DD. Neonatal enucleation induces an asymmetric pattern of visual callosal connections in hamsters. Brain Res 202: 189–195, 1980.[CrossRef][ISI][Medline]
Rhoades RW, Fish SE, Mooney RD, and Chiaia NL. Distribution of visual callosal projection neurons in hamsters subjected to transection of the optic radiations on the day of birth. Brain Res 429: 217–232, 1987.[Medline]
Shuler MG, Krupa DJ, and Nicolelis MA. Bilateral integration of whisker information in the primary somatosensory cortex of rats. J Neurosci 21: 5251–5261, 2001.
Sillito AM, Kemp JA, and Blakemore C. The role of GABAergic inhibition in the cortical effects of monocular deprivation. Nature 291: 318–320, 1981.[CrossRef][Medline]
Somogyi P, Kisvarday ZF, Martin KA, and Whitteridge D. Synaptic connections of morphologically identified and physiologically characterized large basket cells in the striate cortex of cat. Neuroscience 10: 261–294, 1983.[CrossRef][ISI][Medline]
Staiger JF, Zilles K, and Freund TF. Distribution of GABAergic elements postsynaptic to ventroposteromedial thalamic projections in layer IV of rat barrel cortex. Eur J Neurosci 8: 2273–2285, 1996.[CrossRef][ISI][Medline]
Stojic AS, Lane RD, Killackey HP, and Rhoades RW. Suppression of hindlimb inputs to S-I forelimb-stump representation of rats with neonatal forelimb removal: GABA receptor blockade and single-cell responses. J Neurophysiol 83: 3377–3387, 2000.
Stojic AS, Lane RD, and Rhoades RW. Intracortical pathway involving dysgranular cortex conveys hindlimb inputs to S-I forelimb-stump representation of neonatally amputated rats. J Neurophysiol 85: 407–413, 2001.
Swadlow HA. Influence of VPM afferents on putative inhibitory interneurons in S1 of the awake rabbit: evidence from cross-correlation, microstimulation, and latencies to peripheral sensory stimulation. J Neurophysiol 73: 1584–1599, 1995.
Swadlow HA. Fast-spike interneurons and feedforward inhibition in awake sensory neocortex. Cereb Cortex 13: 25–32, 2003.
Swadlow HA, Beloozerova IN, and Sirota MG. Sharp, local synchrony among putative feed-forward inhibitory interneurons of rabbit somatosensory cortex. J Neurophysiol 79: 567–582, 1998.
Tamas G, Lorincz A, Simon A, and Szabadics J. Identified sources and targets of slow inhibition in the neocortex. Science 299: 1902–1905, 2003.
Vogt BA and Gorman AL. Responses of cortical neurons to stimulation of corpus callosum in vitro. J Neurophysiol 48: 1257–1273, 1982.
Werhahn KJ, Mortensen J, Kaelin-Lang A, Boroojerdi B, and Cohen LG. Cortical excitability changes induced by deafferentation of the contralateral hemisphere. Brain 125: 1402–1413, 2002.
Wiest MC, Bentley N, and Nicolelis MA. Heterogeneous integration of bilateral whisker signals by neurons in primary somatosensory cortex of awake rats. J Neurophysiol Nov 24 [Epub ahead of print], 2004.
Wong-Riley M. Changes in the visual system of monocularly sutured or enucleated cats demonstratable with cytochrome oxidase histochemistry. Brain Res 160: 134–138, 1979.[CrossRef][ISI][Medline]
This article has been cited by other articles:
|
|
 |
|
  R. D. Lane, C. P. Pluto, C. L. Kenmuir, N. L. Chiaia, and R. D. Mooney Does Reorganization in the Cuneate Nucleus Following Neonatal Forelimb Amputation Influence Development of Anomalous Circuits Within the Somatosensory Cortex? J Neurophysiol, February 1, 2008; 99(2): 866 - 875. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Karayannis, I. Huerta-Ocampo, and M. Capogna GABAergic and Pyramidal Neurons of Deep Cortical Layers Directly Receive and Differently Integrate Callosal Input Cereb Cortex, May 1, 2007; 17(5): 1213 - 1226. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Glazewski, B. L. Benedetti, and A. L. Barth Ipsilateral Whiskers Suppress Experience-Dependent Plasticity in the Barrel Cortex J. Neurosci., April 4, 2007; 27(14): 3910 - 3920. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Tommerdahl, S. B. Simons, J. S. Chiu, O. Favorov, and B. L. Whitsel Ipsilateral input modifies the primary somatosensory cortex response to contralateral skin flutter. J. Neurosci., May 31, 2006; 26(22): 5970 - 5977. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Hlushchuk and R. Hari Transient Suppression of Ipsilateral Primary Somatosensory Cortex during Tactile Finger Stimulation J. Neurosci., May 24, 2006; 26(21): 5819 - 5824. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. A. Woolsey Should One Hand (Paw) Really Not Know What the Other Is Doing? Focus on "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): 1666 - 1667. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
