Showing papers on "Somatosensory system published in 1996"

Activation of the primary visual cortex by Braille reading in blind subjects.

Abstract: Primary visual cortex receives visual input from the eyes through the lateral geniculate nuclei, but is not known to receive input from other sensory modalities. Its level of activity, both at rest and during auditory or tactile tasks, is higher in blind subjects than in normal controls, suggesting that it can subserve nonvisual functions; however, a direct effect of non-visual tasks on activation has not been demonstrated. To determine whether the visual cortex receives input from the somatosensory system we used positron emission tomography (PET) to measure activation during tactile discrimination tasks in normal subjects and in Braille readers blinded in early life. Blind subjects showed activation of primary and secondary visual cortical areas during tactile tasks, whereas normal controls showed deactivation. A simple tactile stimulus that did not require discrimination produced no activation of visual areas in either group. Thus in blind subjects, cortical areas normally reserved for vision may be activated by other sensory modalities.

Coding of peripersonal space in inferior premotor cortex (area F4).

Abstract: 1. We studied the functional properties of neurons in the caudal part of inferior area 6 (area F4) in awake monkeys. In agreement with previous reports, we found that the large majority (87%) of neurons responded to sensory stimuli. The responsive neurons fell into three categories: somatosensory neurons (30%); visual neurons (14%); and bimodal, visual and somatosensory neurons (56%). Both somatosensory and bimodal neurons typically responded to light touch of the skin. Their RFs were located on the face, neck, trunk, and arms. Approaching objects were the most effective visual stimuli. Visual RFs were mostly located in the space near the monkey (peripersonal space). Typically they extended in the space adjacent to the tactile RFs. 2. The coordinate system in which visual RFs were coded was studied in 110 neurons. In 94 neurons the RF location was independent of eye position, remaining in the same position in the peripersonal space regardless of eye deviation. The RF location with respect to the monkey was not modified by changing monkey position in the recording room. In 10 neurons the RF's location followed the eye movements, remaining in the same retinal position (retinocentric RFs). For the remaining six neurons the RF organization was not clear. We will refer to F4 neurons with RF independent of eye position as somatocentered neurons. 3. In most somatocentered neurons (43 of 60 neurons) the background level of activity and the response to visual stimuli were not modified by changes in eye position, whereas they were modulated in the remaining 17. It is important to note that eye deviations were constantly accompanied by a synergic increase of the activity of the ipsilateral neck muscles. It is not clear, therefore, whether the modulation of neuron discharge depended on eye position or was a consequence of changes in neck muscle activity. 4. The effect of stimulus velocity (20-80 cm/s) on neuron response intensity and RF extent in depth was studied in 34 somatocentered neurons. The results showed that in most neurons the increase of stimulus velocity produced an expansion in depth of the RF. 5. We conclude that space is coded differently in areas that control somatic and eye movements. We suggest that space coding in different cortical areas depends on the computational necessity of the effectors they control.

A primate genesis model of focal dystonia and repetitive strain injury I. Learning-induced dedifferentiation of the representation of the hand in the primary somatosensory cortex in adult monkeys

Abstract: In this study we tested a neuroplasticity/learning origins hypothesis for repetitive strain injuries (RSIs), including occupationally induced focal dystonia.Repetitive movements produced in a specific form and in an appropriate behavioral context cause a degradation of the sensory feedback information controlling fine motor movements, resulting in the ``learned99 genesis of RSIs. Two adult New World owl monkeys were trained at a behavioral task that required them to maintain an attended grasp on a hand grip that repetitively and rapidly (20 msec) opened and closed over short distances. The monkeys completed 300 behavioral trials per day (1,100 to 3,000 movement events) with an accuracy of 80 to 90%. A movement control disorder was recorded in both monkeys. Training was continued until the performance accuracy dropped to below 50%. We subsequently conducted an electrophysiologic mapping study of the representations of the hand within the primary somatosensory (SI) cortical zone. The hand representation in the true primary somatosensory cortical field, SI area 3b, was found to be markedly degraded in these monkeys, as characterized by (1) a dedifferentiation of cortical representations of the skin of the hand manifested by receptive fields that were 10 to 20 times larger than normal, (2) the emergence of many receptive fields that covered the entire glabrous surface of individual digits or that extended across the surfaces of two or more digits, (3) a breakdown of the normally sharply segregated area 3b representations of volar glabrous and dorsal hairy skin of the hand, and (4) a breakdown of the local shifted-overlap receptive field topography of area 3b, with many digital receptive fields overlapping the fields of neurons sampled in cortical penetrations up to more than four times farther apart than normal. Thus, rapid, repetitive, highly stereotypic movements applied in a learning context can actively degrade cortical representations of sensory information guiding fine motor hand movements. This cortical plasticity/learning-based dedifferentiation of sensory feedback information from the hand contributes to the genesis of occupationally derived repetitive strain injuries, including focal dystonia of the hand. Successful treatment of patients with RSI will plausibly require learning-based restoration of differentiated representations of sensory feedback information from the hand. NEUROLOGY 1996;47: 508-520

Mice with disrupted GM2/GD2 synthase gene lack complex gangliosides but exhibit only subtle defects in their nervous system

Abstract: Gangliosides, sialic acid-containing glycosphingolipids, are abundant in the vertebrate (mammalian) nervous system. Their composition is spatially and developmentally regulated, and gangliosides have been widely believed to lay essential roles in establishment of the nervous system, especially in neuritogenesis and synaptogenesis. However, this has never been tested directly. Here we report the generation of mice with a disrupted beta 1,4-N-acetylgalactosaminyltransferase (GM2/GD2 synthase; EC 2.4.1.92) gene. The mice lacked all complex gangliosides. Nevertheless, they did not show any major histological defects in their nervous systems or in gross behavior. Just a slight reduction in the neural conduction velocity from the tibial nerve to the somatosensory cortex, but not to the lumbar spine, was detected. These findings suggest that complex gangliosides are required in neuronal functions but not in the morphogenesis and organogenesis of the brain. The higher levels of GM3 and GD3 expressed in the brains of these mutant mice may be able to compensate for the lack of complex gangliosides.

Spontaneous GABAA receptor-mediated inhibitory currents in adult rat somatosensory cortex.

Abstract: 1. Spontaneous inhibitory synaptic currents (sIPSCs) were studied with whole cell voltage-clamp recordings from 131 pyramidal cells in adult rat somatosensory cortical slices. Neurons were intracel...

Targeted deletion of the mouse POU domain gene Brn-3a causes a selective loss of neurons in the brainstem and trigeminal ganglion, uncoordinated limb movement, and impaired suckling

Abstract: The Brn-3 subfamily of POU domain genes are expressed in sensory neurons and in select brainstem nuclei. Earlier work has shown that targeted deletion of the Brn-3b and Brn-3c genes produce, respectively, defects in the retina and in the inner ear. We show herein that targeted deletion of the Brn-3a gene results in defective suckling and in uncoordinated limb and trunk movements, leading to early postnatal death. Brn-3a (-/-) mice show a loss of neurons in the trigeminal ganglia, the medial habenula, the red nucleus, and the caudal region of the inferior olivary nucleus but not in the retina and dorsal root ganglia. In the trigeminal and dorsal root ganglia, but not in the retina, there is a marked decrease in the frequency of neurons expressing Brn-3b and Brn-3c, suggesting that Brn-3a positively regulates Brn-3b and Brn-3c expression in somatosensory neurons. Thus, Brn-3a exerts its major developmental effects in somatosensory neurons and in brainstem nuclei involved in motor control. The pheno-types of Brn-3a, Brn-3b, and Brn-3c mutant mice indicate that individual Brn-3 genes have evolved to control development in the auditory, visual, or somatosensory systems and that despite differences between these systems in transduction mechanisms, sensory organ structures, and central information processing, there may be fundamental homologies in the genetic regulatory events that control their development.

Glutamate receptor blockade at cortical synapses disrupts development of thalamocortical and columnar organization in somatosensory cortex.

Abstract: The segregation of thalamocortical inputs into eye-specific stripes in the developing cat or monkey visual cortex is prevented by manipulations that perturb or abolish neural activity in the visual pathway. Such findings show that proper development of the functional organization of visual cortex is dependent on normal patterns of neural activity. The generalisation of this conclusion to other sensory cortices has been questioned by findings that the segregation of thalamocortical afferents into a somatotopic barrel pattern in developing rodent primary somatosensory cortex (S1) is not prevented by activity blockade. We show that a temporary block of N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors in rat S1 during the critical period for barrel development disrupts the topographic refinement of thalamocortical connectivity and columnar organization. These effects are evident well after the blockade is ineffective and thus may be permanent. Our findings show that neural activity and specifically the activation of postsynaptic cortical neurons has a prominent role in establishing the primary sensory map in S1, as well as the topographic organization of higher order synaptic connections.

P2Y1 purinergic receptors in sensory neurons: contribution to touch-induced impulse generation.

Abstract: Somatic sensation requires the conversion of physical stimuli into the depolarization of distal nerve endings. A single cRNA derived from sensory neurons renders Xenopus laevis oocytes mechanosensitive and is found to encode a P2Y1 purinergic receptor. P2Y1 mRNA is concentrated in large-fiber dorsal root ganglion neurons. In contrast, P2X3 mRNA is localized to small-fiber sensory neurons and produces less mechanosensitivity in oocytes. The frequency of touch-induced action potentials from frog sensory nerve fibers is increased by the presence of P2 receptor agonists at the peripheral nerve ending and is decreased by the presence of P2 antagonists. P2X-selective agents do not have these effects. The release of ATP into the extracellular space and the activation of peripheral P2Y1 receptors appear to participate in the generation of sensory action potentials by light touch.

Mnemonic neuronal activity in somatosensory cortex

Abstract: Single-unit activity was recorded from the hand areas of the somatosensory cortex of monkeys trained to perform a haptic delayed matching to sample task with objects of identical dimensions but different surface features. During the memory retention period of the task (delay), many units showed sustained firing frequency change, either excitation or inhibition. In some cases, firing during that period was significantly higher after one sample object than after another. These observations indicate the participation of somatosensory neurons not only in the perception but in the short-term memory of tactile stimuli. Neurons most directly implicated in tactile memory are (i) those with object-selective delay activity, (ii) those with nondifferential delay activity but without activity related to preparation for movement, and (iii) those with delay activity in the haptic-haptic delayed matching task but no such activity in a control visuo-haptic delayed matching task. The results indicate that cells in early stages of cortical somatosensory processing participate in haptic short-term memory.

Associative pairing of tactile stimulation induces somatosensory cortical reorganization in rats and humans.

Abstract: We used a protocol of associative (Hebbian) pairing of tactile stimulation (APTS) to evoke cortical plastic changes Reversible reorganization of the adult rat paw representations in somatosensory cortex (SI) induced by a few hours of APTS included selective enlargement of the areas of cortical neurones representing the stimulated skin fields and of the corresponding receptive fields (RFs) Late, presumably NMDA receptor-mediated response components were enhanced, indicating an involvement of glutamatergic synapses A control protocol of identical stimulus pattern applied to only a single skin site revealed no changes of RFs, indicating that co-activation is crucial for induction Using an analogous APTS protocol in humans revealed an increase of spatial discrimination performance indicating that fast plastic processes based on co-activation patterns act on a cortical and perceptual level

Altered Sensory Processing in the Somatosensory Cortex of the Mouse Mutant Barrelless

Abstract: Mice homozygous for the barrelless ( brl ) mutation, mapped here to chromosome 11, lack barrel-shaped arrays of cell clusters termed “barrels” in the primary somatosensory cortex. Deoxyglucose uptake demonstrated that the topology of the cortical whisker representation is nevertheless preserved. Anterograde tracers revealed a lack of spatial segregation of thalamic afferents into individual barrel territories, and single-cell recordings demonstrated a lack of temporal discrimination of center from surround information. Thus, structural segregation of thalamic inputs is not essential to generate topological order in the somatosensory cortex, but it is required for discrete spatiotemporal relay of sensory information to the cortex.

NMDA receptors and plasticity in adult primate somatosensory cortex

Abstract: Topographic maps in adult primate somatosensory cortex are capable of dramatic reorganizations after peripheral nerve injuries. In the present experiments, we have deprived a circumscribed portion of the hand map in somatosensory cortex of our adult squirrel monkeys by transecting the median nerve to one hand, and evaluated the hypothesis that N-methyl-d-aspartate (NMDA) glutamatergic receptors are necessary for the reorganization that follows within four weeks. In one monkey, we confirm previous results demonstrating that the deprived cortex has regained responsiveness in its expanse four weeks after median nerve transection. However, in three monkeys in which NMDA receptors were concurrently blocked, most of the deprived cortex remained unresponsive. Thus, much of the cortical "recovery" that typically follows peripheral nerve injury in adult monkeys is apparently dependent on NMDA receptors and may well be due to Hebbian-like changes in synaptic strength. Perhaps the elimination of the normally dominant inputs to "median nerve cortex" permits the gradual strengthening of correlations between the activity of the formally impotent presynaptic and deprived postsynaptic elements. These enhanced correlations may also have been made possible by reductions in intracortical inhibition as a necessary but not sufficient condition.

Significance of the second somatosensory cortex in sensorimotor integration : enhancement of sensory responses during finger movements

Abstract: THE functional significance of the second somatosensory cortex (SII) is poorly understood. However, lesion and cortical stimulation studies indicate that SII may be involved in sensory aspects of tactile learning and in movement control. In the present study, we explored a possible role of SII in sensorimotor integration in humans using a multichannel magnetometer. Somatosensory evoked fields (SEFs) from SII to electrical stimulation of left and right median nerves were recorded in six healthy volunteers during rest and in different test conditions. Continuous cutaneous stimulation of the right hand or face reduced the SEFs to both left and right median nerve stimulation. Right-sided finger movements increased the SEFs to right, but not left, median nerve stimulation. The responses were equally enhanced by simple finger flexion movement and by a complex finger sequence. The suppression of SEFs by competing cutaneous inputs from different areas of the body indicates that the neurones underlying the responses receive inputs from large, bilateral receptive fields. The enhancement of sensory reactions to signals from the actively moving limb but not to those from the opposite limb indicates a spatial tuning of the SII neurones to behaviourally relevant input channels, also suggesting that SII is important for the integration of sensory information to motor programmes.

Regulation of alpha7 nicotinic acetylcholine receptors in the developing rat somatosensory cortex by thalamocortical afferents.

Abstract: Distributions of alpha7 nicotinic acetylcholine receptor (nAChR) mRNA and [125]alpha-bungarotoxin (alpha-BTX) binding sites in the developing rat somatosensory cortex were characterized in relation to acetylcholinesterase (AChE) histochemical staining of thalamocortical terminals to investigate the role of this receptor in cortical development. Using quantitative in situ hybridization and receptor autoradiography, elevated levels of mRNA and binding-site expression were first detected at post-natal day 1 (P1) in deep and superficial layers, just beneath the AChE-stained thalamocortical terminals. Onset of expression occurred approximately 1 d after ingrowth of AChE-stained thalamocortical afferents. By P5, mRNA and binding-site expression exhibited a disjunctive, barrel-like pattern in layer IV and, more clearly, in layer VI. The mRNA and binding-site expressions peaked at approximately 1 week postnatal and then declined to adult levels. Unilateral electrolytic or cytochemical lesions placed in the thalamic ventrobasal complex at P0 (just as thalamocortical afferents are innervating the cortex) and at P6 (when the somatotopic map is well established) resulted in a marked reduction of alpha7 nAChR mRNA and [125]alpha-BTX binding-site levels in layers IV and VI, indicating their regulation by thalamocortical afferents. With P6 lesions, this reduction was observed as early as 6 hr postlesion. These results suggest that alpha7 nAChRs are localized primarily on cortical cells in rat somatosensory cortex and provide further evidence for thalamocortical influence on cortical ontogeny. These data also suggest a role for cholinergic systems during a critical period of cortical synaptogenesis.

Effects of somatosensory and parallel-fiber stimulation on neurons in dorsal cochlear nucleus

Abstract: 1. Single units and evoked potentials were recorded in the dorsal cochlear nucleus (DCN) of paralyzed decerebrate cats in response to electrical stimulation at two sites: 1) in the somatosensory do...

Spatiotemporal properties of short-term plasticity sensorimotor thalamocortical pathways of the rat

Abstract: Each region of neocortex receives synaptic input from several thalamic nuclei, but the response properties of thalamocortical pathways may differ. We have studied the frontoparietal (motor and somatosensory) neocortex of the rat and have examined the responses induced by stimulating two convergent thalamocortical projections originating in the ventrolateral (VL) nucleus and ventroposterior lateral (VPL) nucleus. Depth recordings and current-source density (CSD) analysis revealed two primary responses with different laminar and temporal patterns when VL and VPL were stimulated. Single shocks to VL produced a characteristic small current sink in layer V, which strongly enhanced in response to a second pulse delivered within a 50–200 msec interval (i.e., the augmenting response). In contrast, a shock to VPL evoked a large current sink that originated in layer IV, spread strongly into the supragranular layers, and was almost abolished in response to a second pulse at intervals of <200 msec (i.e., the decremental response). Control experiments determined that these responses could not be attributed to the antidromic firing of corticothalamic cells, intrathalamic mechanisms, or anesthesia. Topographic response maps were obtained from a grid of 30 sites across frontoparietal cortex. One shock to VL excited a very limited cortical region, but an augmenting response evoked 50–200 msec later spread at approximately 1 m/sec to synchronize the activity across an area up to 25 times larger. In contrast, a single shock to VPL activated a relatively large area, but the area activated by a second shock delivered within 200 msec was much smaller. We conclude that overlapping thalamocortical projections, originating in different thalamic nuclei, have distinct spatiotemporal response characteristics that may serve the functional specializations of these pathways.

Interhemispheric Modulation of Somatosensory Receptive Fields: Evidence for Plasticity in Primary Somatosensory Cortex

Abstract: Extracellular recordings were made from single and multiple neurons in primary somatosensory cortex (area 3b) of macaque monkeys and flying foxes. When a smell region of area 3b (or adjacent area 1) in the opposite hemisphere was cooled, thereby blocking activity that is normally transferred via the corpus callosum, larger receptive fields (RFs) were immediately unmasked for most neurons. RF expansion presumably reflects the expression of afferent inputs that are normally inhibited, suggesting that callosal inputs provide a source of tonic inhibition that contributes to the shaping of neuronal RFs. Quantitative analyses of single neuron responses revealed other effects that were consistent with a release from inhibition, such as increases in response magnitude to stimulation of points within the original RF and decreases in response latency. An unexpected finding was the reversal of these unmasking effects with extended periods of cooling: RFs returned to their original dimensions and within-field response magnitude decreased. In contrast to the initial effects, this reversal of disinhibition cannot be readily explained by an unmasking of previously unexpressed inputs. Any explanation for the reversal requires an increase in the efficacy of interneuron-mediated inhibition, and presumably occurs in response to ongoing, altered patterns of activity.

Thalamic stimulation-evoked sensations in chronic pain patients and in nonpain (movement disorder) patients.

Abstract: 1. Little is known about the effect of central and peripheral nervous system injury on the processing of somatosensory information at the thalamic level in humans. The role of the human thalamic ventrocaudal nucleus (Vc) in nociception is not well understood because reports of nociceptive neuronal responses and stimulation-evoked pain are rare. In this study, we have characterized effects of microstimulation in the tactile region of Vc. Specifically, we investigated the incidence of painful sensations evoked by thalamic microstimulation in patients with and without chronic pain. 2. Data were obtained during stereotactic thalamic procedures for relief of pain or motor disorders. Patients were divided into three groups, those with 1) central poststroke pain (PSP, n = 13); 2) nonstroke pain (NSP, n = 23); and 3) movement disorders (controls, n = 24). Most (15 of 23) of the NSP patients had peripheral nerve damage. Tungsten microelectrodes were used to record neuronal responses in the thalamus and to deliver stimuli. Localization of tactile Vc was determined according to stereotactic coordinates and neuronal responses to innocuous somatic stimuli. At selected sites, microstimulation (1-s trains, 300 Hz, 0.1-0.2 ms pulses, 98% of Vc sites evoked paresthesia. By contrast, in the PSP patients, 28% of Vc sites stimulated evoked painful sensations at threshold. Suprathreshold stimuli evoked painful sensations at 46% of Vc sites in the PSP patients but at only 8% of Vc sites in NSP patients and 12% of Vc sites in the movement disorder patients. 4. The thresholds to evoke paresthesia in the NSP and movement disorder patients were significantly lower than the thresholds in the PSP patients. However, stimulation thresholds to elicit pain were similar in all patient groups. 5. All patients were capable of differentiating stimulation-evoked paresthesia from pain. Stimulation-evoked painful sensations in the PSP patients were often described as burning and sometimes as "sharp," "shocking," or "unpleasant." By contrast, the quality of pain evoked in the other patient groups was typically described as unpleasant or shocking. Pain could be evoked at sites throughout tactile Vc, although most sites were located in the ventral 2/3 of the nucleus. 6. In the movement disorder patients, the location of the projected sensation usually corresponded to the location of the receptive fields of the tactile neurons recorded at the same site. By contrast, in both groups of pain patients there was a high incidence of mismatches between the projected and receptive fields. 7. These results suggest that the effective thalamic output from Vc to the cortex is affected by somatosensory deafferentation in pain patients. In addition, in the PSP patients there are also changes in the thalamocortical processing of noxious information. The increased incidence of thalamic-evoked pain in PSP patients may be due to 1) loss of low-threshold mechanoreceptive thalamic neurons such that nociceptive neuronal output is now prominent, 2) reduced tonic inhibition of thalamic or cortical nociceptive neurons, and/or 3) unmasking or strengthening of nociceptive pathways.

Central nervous system modifications in patients with lesion of the anterior cruciate ligament of the knee

Abstract: Patients with traumatic lesion of the anterior cruciate ligament often experience knee instability, which, recent studies suggest, is probably due to reduced knee proprioception. We studied knee proprioception and somatosensory evoked potentials (SEPs) after stimulation of the common peroneal nerve at the knee above the articular branches subserving the sensory innervation of the anterior cruciate ligament, in 19 patients with traumatic anterior cruciate ligament lesion. Ten patients showed decreased position sense of the knee, and of these, seven presented loss of cortical P27 potential while preserving lemniscal P20 and spinal N14 responses to common peroneal nerve stimulation on the side of the anterior cruciate ligament lesion. All our patients had normal SEPs to stimulation of the posterior tibial nerve at both the ankle and the knee. We suggest that in patients showing SEP abnormalities, the dysfunction of the central somatosensory conduction is located above the medial lemniscus and is limited to common peroneal nerve somatosensory pathways. Therefore, it is likely that in the seven patients showing SEP abnormalities, the loss of the knee mechanoreceptors was followed by remodelling of the CNS above the medial lemniscus. In five patients with P27 absence after common peroneal nerve stimulation, we also recorded SEPs after stimulation of the peroneal nerve at the ankle and obtained a normal cortical positive response; moreover, in our healthy subjects, cortical responses were significantly higher in amplitude after peroneal nerve than after common peroneal nerve stimulation. These findings strongly suggest that proprioceptive afferent inputs from the knee are more effective than distal afferent inputs in generating the greater part of the common peroneal nerve cortical SEPs. Since common peroneal nerve stimulation probably allows selective recording of the responses produced by the activation of the cortical representation of the knee, minor lesions with a reduction in the number of knee mechanoceptors could result in SEP changes after common peroneal nerve stimulation.

Somatosensory findings in patients with spinal cord injury and central dysaesthesia pain.

Abstract: OBJECTIVE: To determine whether central pain in patients with spinal cord injury is only dependent on the lesioning of spinothalamic pathways. METHODS: In sixteen patients with spinal cord injury and central dysaesthesia pain, somatosensory abnormalities in painful denervated skin areas were compared with somatosensory findings in normal skin areas as well as in non-painful denervated skin areas. RESULTS: The threshold values for detection of thermal (heat, cold, heat pain, or cold pain) and tactile stimulation were significantly changed in denervated skin areas although there were no significant differences in the threshold values between painful and non-painful denervated skin areas. The reductions of sensations of touch, vibration, joint position, and two point discrimination in painful and non-painful denervated skin areas were not significantly different. Allodynia (pain caused by non-noxious stimulation) and wind up-like pain (pain caused by repeatedly pricking the skin) were significantly more common in painful than non-painful denervated skin areas. CONCLUSIONS: Because pain and thermal sensory perception are primarily mediated to the brain via spinothalamic pathways, whereas the sensations of touch, vibration and joint position are primarily mediated by dorsal column-medial lemniscal pathways, the results indicate that central pain is not only dependent on the lesioning of either dorsal column-medial lemniscal pathways or spinothalamic pathways. The findings of abnormal evoked pain (allodynia and wind up-like pain) may be consistent with the experimental findings of hyperexcitability in nociceptive spinothalamic tract neurons, that may be involved in the pathogenesis of central pain.

Contribution of somatosensory cortex to responses in the rat cerebellar granule cell layer following peripheral tactile stimulation

Abstract: The spatial coincidence of somatosensory cerebral cortex (SI) and trigeminal projections to the cerebellar hemisphere has been previously demonstrated. In this paper we describe the temporal relationship between tactilely-evoked responses in SI and in the granule cell layer of the cerebellar hemisphere, in anesthetized rats. We simultaneously recorded field potentials in areas of common receptive fields of SI and of the cerebellar folium crus IIa after peripheral tactile stimulation of the corresponding facial area. Response of the cerebellar granule cell layer to a brief tactile stimulation consisted of two components at different latencies. We found a strong correlation between the latency of the SI response and that of the second (long-latency) cerebellar component following facial stimulation. No such relationship was found between the latency of the SI response and that of the first (short-latency) cerebellar component, originating from a direct trigeminocerebellar pathway. In addition, lidocaine pressure injection in SI, cortical ablation, and decerebration all significantly affected the second cerebellar peak but not the first. Further, when tactile stimuli were presented 75 ms apart, the response in SI failed, as did the second cerebellar peak, while the short-latency cerebellar response still occurred. We found a wide spatial distribution of the upper lip response beyond the upper lip area in crus IIa for the long-latency component of the cerebellar response. Our results demonstrate that SI is the primary contributor to the cerebellar long-latency response to peripheral tactile stimulation. These results are discussed in the context of Purkinje cell responses to tactile input.

Variation of functional MRI signal in response to frequency of somatosensory stimulation in α‐chloralose anesthetized rats

Abstract: The dependence of functional MRI contrast on the repetition rate (1.5-9 Hz) of a sensory stimulus was investigated with a T2*-weighted gradient echo method during forepaw stimulation of alpha-chloralose anesthetized rats (n = 5). An activation area was observed in the left or right somatosensory cortex dependent on the stimulation of the right or left forepaw, respectively. The activation intensity decreased for stimulation frequencies above 3 Hz, and was negligible at 9 Hz. The interpretation is that at low stimulation rates the neurons can respond to each stimulus, but at higher rates there is insufficient recovery time so that the response is progressively occluded.

Saccades to somatosensory targets. III. eye-position-dependent somatosensory activity in primate superior colliculus

Abstract: 1. We recorded from cells with sensory responses to somatosensory stimuli in the superior colliculus (SC) of awake monkeys. Our goal was to determine the frame of reference of collicular somatosens...

Effect of methamphetamine on glutamate-positive neurons in the adult and developing rat somatosensory cortex

Abstract: The neurotoxic effects of methamphetamine (MA) on dopaminergic and serotonergic terminals have been well-documented. Another neurotoxic effect of MA is neuronal degeneration in the somatosensory cortex, as seen by silver staining. The neurochemical characteristics of these degenerating neurons are unknown. Using glutamate and glial fibrillary acid protein (GFAP) immunohistochemistry, it was found that MA exposure in adult rats (10 mg/kg given 4 times intraperotoneally (i.p.) at 2-h intervals) causes localized depletion of glutamate-positive neurons and astrogliosis in the somatosensory cortex 3 days following treatment. The affected region covered the middle one-third portion from the longitudinal fissure to the rhinal sulcus and was predominately seen in layers II-III of the cortex. This pattern of depletion is consistent with that demonstrated previously with silver staining following MA, d-amphetamine, and 3,4-methylenedioxymethamphetmine (MDMA) exposures. Comparable efforts were not found in developing animals at ages previously shown to also be resistant to MA-induced effects on dopaminergic terminals (age 20 and 40 days). Results suggest that MA exposure induces degeneration of glutamatergic neurons in the somatosensory cortex of adult rats.

Functional anatomy of human hippocampal formation and related structures.

Abstract: Data on the internal organization, and neuronal connections of the human hippocampal formation and related structures of the limbic system are briefly reviewed. In the healthy brain, somatosensory, visual, and auditory input proceeds through neocortical core and belt fields to a variety of association areas, and from here the data is transported via long cortico-cortical pathways to the extended prefrontal association cortex. Tracts generated from this highest organizational level of the brain guide the data via the frontal belt (premotor cortex) to the frontal core (primary motor area). The striatal and cerebellar loops provide the major routes for this data transfer. The main components of the limbic system (the hippocampal formation, the entorhinal region, and the amygdala) maintain a strategic position between the sensory and the motor association areas. Part of the stream of data from the sensory association areas to the prefrontal cortex branches off and eventually converges on the entorhinal region...

Central reorganization of sensory pathways following peripheral nerve regeneration in fetal monkeys.

Abstract: Transection of a sensory nerve in adults results in profound abnormalities in sensory perception, even if the severed nerve is surgically repaired to facilitate accurate nerve regeneration. In marked contrast, fewer perceptual errors follow nerve transection and surgical repair in children. The basis for this superior recovery in children was unknown. Here we show that there is little or no topographic order in the median nerve to the hand after median nerve section and surgical repair in immature macaque monkeys. Remarkably, however, in the same animals the representation of the reinnervated hand in primary somatosensory cortex area (area 3b) is quite orderly. This indicates that there are mechanisms in the developing brain that can create cortical topography, despite disordered sensory inputs. Presumably the superior recovery of perceptual abilities after peripheral nerve transection in children depends on this restoration of somatotopy in the central sensory maps.

Somesthesis and the neurobiology of the somatosensory cortex

Abstract: Structural basis of information processing and neocortical neurotransmitters.- Divergence of thalamocortical projections and limits on somatosensory cortical plasticity.- Inhibitory circuitry in relation to the functional organization of somatosensory cortex.- Pain, temperature, and the sense of the body.- The functional role of a noninactivating sodium current in neocortical neurons.- Psychophysics of somatosensation.- Information processing channels in the sense of touch.- A novel approach for studying direction discrimination.- Tactile directional sensibility theoretical and functional aspects.- Experimental assessment of the temporal hypothesis of velocity scaling.- Vibrotactile adaptation of the RA system: A psychophysical analysis.- Tactile neural codes for the shapes and orientations of objects.- Tactual discrimination of softness: Abilities and mechanisms.- Representation of the shape and contact force of handled objects in populations of cutaneous afferents.- Haptic object processing I: Early perceptual features.- Haptic object identification II: Purposive exploration.- Cortical representation of somatosensation.- The somatosensory cortex.- The organization of lateral somatosensory cortex in primates and other mammals.- Serial processing in the somatosensory system of macaques.- Parallel processing in somatosensory areas I and II of the cerebral cortex.- Linearity as the basic law of psychophysics: Evidence from studies of the neural mechanisms of roughness magnitude estimation.- Form processing and attention effects in the somatosensory system.- Functional plasticity of cortical representations of the hand.- Sensory-motor interface.- Somatosensory signals and sensorimotor transformations in reactive control of grasp.- Strain-sensitive mechanoreceptors in the human skin provide kinaesthetic information.- A second tactile system in the human skin with unmyelinated primary afferents.- Factors influencing the perception of tactile stimuli during movement.- Changing the intended direction of movement.- Disturbances of motor behavior after parietal lobe lesions in the human.- Neuronal population behavior: Imaging techniques.- PET and fMRI scans of the cerebral cortex in humans and single neuron responses from SI in monkeys to rubbing embossed dot and grating patterns across a fingerpad.- Magnetic resonance functional mapping of cortical activation associated with differing sensorimotor hand paradigms.- Whole-head neuromagnetic recordings of human somatosensory cortical functions.- Optical imaging of intrinsic signals in somatosensory cortex.- Somatosensory and frontal cortical processing during pain experience.- Cortical Neurocomputation and modelling.- Local receptive field diversity within cortical neuronal populations.- Functional segregation and integration in the nervous system: Theory and models.