Primary somatosensory cortex activation is not altered in patients with ventroposterior thalamic lesions: a PET study.
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BACKGROUND AND PURPOSE: We know remarkably little about the mechanisms underlying cortical activation. Such mechanisms might be better understood by studying the effect of well-localized lesions on the cortical activations in simple paradigms. METHODS: We used H(2)(15)O and positron emission tomography to measure regional cerebral blood flow (rCBF) at rest and during hand vibration in 7 patients with unilateral thalamic lesion involving the ventroposterior (VP) somatosensory thalamic relay nuclei. We compared the results with those obtained in 6 patients with thalamic lesions sparing the VP nuclei and 6 healthy controls. RESULTS: The patients with VP lesions had a selective hypoperfusion at rest in the ipsilesional primary sensorimotor cortex (SM1). This hypoperfusion was significantly correlated with the degree of contralateral somatosensory deficit. This abnormality may reflect the deafferentation of SM1 from its somatosensory thalamic input. Despite this deafferentation, the ipsilesional SM1 was normally activated by the vibration of the hypoesthetic hand. CONCLUSIONS: The fact that a lesion of the somatosensory thalamic relay nuclei alters the rCBF at rest in SM1 but not its activation by hand vibration indicates that the mechanism of cortical activation is complex, even in the case of simple sensory stimulation. In addition, a dissociation may occur between obvious neurological deficits and apparently normal activation patterns, which suggests that activation studies should be interpreted cautiously in patients with focal brain lesions. (+info)
Effects of superior colliculus inhibition on visual motion processing in the lateral suprasylvian visual area of the cat.
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PURPOSE: To clarify whether visual inputs of the tectothalamocortical pathway influence motion processing within the lateral suprasylvian (LS) area of the cat. METHODS: This study was conducted in five cats. Tungsten microelectrodes were used for recording visual evoked potentials. The electrodes were introduced into the LS area. An array of 120 randomly located dots was projected onto the stimulus field (40 degrees x 40 degrees) in front of the animal by a slide projector. The dots were moved rightward and leftward alternatively with interstimulus intervals by a mirror attached to a galvanometer, the movements of which were controlled by a microcomputer. Each motion sequence consisted of an abrupt onset of motion that continued for 100 msec followed by an abrupt offset and a stationary phase of 900 msec; the total duration of each sequence was thus 1000 msec. The velocity of the motion was varied in 12 steps. The onset of motion was used as the trigger for recording evoked potentials. Single or multiple injections (two to three) of muscimol were made, mainly into the rostral superior colliculus (SC). The amplitudes of evoked potentials before and after the muscimol injection were compared. RESULTS: A large negative wave (N1) with the peak latency of 89.80+/-16.39 msec (mean +/- SD, n = 191) was recorded consistently. The amplitude of N1 was not altered by the muscimol injection into the SC when the velocity of motion was 50 deg/sec or less. When the velocity of motion was 75 deg/sec or more, however, the amplitude of N1 was reduced to 62% to 72% of that noted before the muscimol injection. CONCLUSIONS: These findings suggest that the LS area processes the visual motion inputs reaching through the two parallel pathways, the geniculostriate pathway and the tectothalamocortical pathway, when the velocity of visual motion is 75 deg/sec or more. (+info)
Circuit dynamics and coding strategies in rodent somatosensory cortex.
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Previous experimental studies of both cortical barrel and thalamic barreloid neuron responses in rodent somatosensory cortex have indicated an active role for barrel circuitry in processing thalamic signals. Previous modeling studies of the same system have suggested that a major function of the barrel circuit is to render the response magnitude of barrel neurons particularly sensitive to the temporal distribution of thalamic input. Specifically, thalamic inputs that are initially synchronous strongly engage recurrent excitatory connections in the barrel and generate a response that briefly withstands the strong damping effects of inhibitory circuitry. To test this experimentally, we recorded responses from 40 cortical barrel neurons and 63 thalamic barreloid neurons evoked by whisker deflections varying in velocity and amplitude. This stimulus evoked thalamic response profiles that varied in terms of both their magnitude and timing. The magnitude of the thalamic population response, measured as the average number of evoked spikes per stimulus, increased with both deflection velocity and amplitude. On the other hand, the degree of initial synchrony, measured from population peristimulus time histograms, was highly correlated with the velocity of whisker deflection, deflection amplitude having little or no effect on thalamic synchrony. Consistent with the predictions of the model, the cortical population response was determined largely by whisker velocity and was highly correlated with the degree of initial synchrony among thalamic neurons (R(2) = 0.91), as compared with the average number of evoked thalamic spikes (R(2) = 0.38). Individually, the response of nearly all cortical cells displayed a positive correlation with deflection velocity; this homogeneity is consistent with the dependence of the cortical response on local circuit interactions as proposed by the model. By contrast, the response of individual thalamic neurons varied widely. These findings validate the predictions of the modeling studies and, more importantly, demonstrate that the mechanism by which the cortex processes an afferent signal is inextricably linked with, and in fact determines, the saliency of neural codes embedded in the thalamic response. (+info)
Component perimetry: a fast method to detect visual field defects caused by brain lesions.
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PURPOSE: Noise field campimetry, performed according to Aulhorn and Kost, confronts patients with a large field of irregularly flickering dots, and many patients immediately perceive their visual field defects. The original method had a somewhat low specificity and sensitivity, especially for patients with visual field defects caused by cortical lesions. METHODS: The method was improved in two ways. First, the grain of the visual noise was increased toward the periphery of the visual field to accommodate the peripheral decrease in visual acuity. Second, the type of stimulus pattern was varied to include separate investigations of different visual components or functions (color, motion, temporal resolution, line orientation, stereoscopic depth, acuity, and figure-ground segmentation). To evaluate the reliability of the method, the visual fields were compared, as assessed by the new method, with those of conventional perimetry in 41 patients with neurologic disorders and 22 normal control subjects. RESULTS: The results were encouraging. All patients with suprageniculate lesions subjectively experienced visual field defects in component perimetry. Sizes of visual field defects obtained with both methods corresponded qualitatively with each other, with a highly significant correlation. The specificity of component perimetry was higher than that of the original noise field campimetry. CONCLUSIONS: This pilot study indicates that component perimetry is a subjective but relatively reliable method for detecting disorders of visual perception caused by lesions at different stages along the visual pathway, permitting fast screening of the visual field. In addition, this method seems to allow examination of the visual field, not only for defects in contrast sensitivity, as does conventional light perimetry, but also for the status of other components of vision such as color or motion perception. Further evaluation with larger patient cohorts is needed to allow exact assessment of the clinical usefulness of the method. (+info)
Activation of thalamic ventroposteriolateral neurons by phrenic nerve afferents in cats and rats.
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It has been demonstrated that phrenic nerve afferents project to somatosensory cortex, yet the sensory pathways are still poorly understood. This study investigated the neural responses in the thalamic ventroposteriolateral (VPL) nucleus after phrenic afferent stimulation in cats and rats. Activation of VPL neurons was observed after electrical stimulation of the contralateral phrenic nerve. Direct mechanical stimulation of the diaphragm also elicited increased activity in the same VPL neurons that were activated by electrical stimulation of the phrenic nerve. Some VPL neurons responded to both phrenic afferent stimulation and shoulder probing. In rats, VPL neurons activated by inspiratory occlusion also responded to stimulation on phrenic afferents. These results demonstrate that phrenic afferents can reach the VPL thalamus under physiological conditions and support the hypothesis that the thalamic VPL nucleus functions as a relay for the conduction of proprioceptive information from the diaphragm to the contralateral somatosensory cortex. (+info)
Distinct firing properties of higher order thalamic relay neurons.
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It has been proposed that the thalamus is composed of at least two types of nuclei. First-order relay nuclei transmit signals from the periphery to the cortex while higher order nuclei may route information from one cortical area to another. Although much is known about the functional properties of relay neurons in first-order nuclei, little is known about relay neurons belonging to higher-order nuclei. We investigated the electrophysiological properties of relay cells in a higher-order thalamic nucleus using in vitro intracellular recordings from thalamic slices of the rat's lateral posterior nucleus (LPN). We found neurons of the LPN possess many of the same membrane properties as first-order relay neurons. These included low-threshold calcium spikes (IT) and burst firing, a mixed cation conductance (IH) that prevented membrane hyperpolarization, and a transient K+ conductance that delayed spike firing (IA). The repetitive firing characteristics of LPN neurons were more distinct. One group of cells, located in the more caudal regions of the LPN responded to depolarizing current pulses with a train of action potentials or in a regular spiking (RS) mode. This form of firing showed a steep but highly linear increase in firing frequency with increasing levels of membrane depolarization. Another group of cells, located in the more rostral regions of the LPN, responded to depolarizing current pulses with clusters of high-frequency bursts or in a clustered spiking (CS) mode. The overall firing frequency rose nonlinearly with membrane depolarization, but the frequency of a given burst remained relatively constant. The caudal LPN receives input from the superior colliculus, whereas the rostral LPN receives input from layers V and VI of the visual cortex. Thus the RS and CS cells may be driven by subcortical and cortical inputs respectively, and the distinct temporal properties of their response modes may be a necessary component of the LPN circuitry. (+info)
Processing of periodic whisker deflections by neurons in the ventroposterior medial and thalamic reticular nuclei.
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Rats employ rhythmic whisker movements to sample information in their sensory environment. To study frequency tuning and filtering characteristics of thalamic circuitry, we recorded single-unit responses of ventroposterior medial (VPm) and thalamic reticular (Rt) neurons to 1- to 40-Hz sinusoidal and pulsatile whisker deflection in lightly narcotized rats. Neuronal entrainment was assessed by a measure of the relative modulation (RM) of firing at the stimulus frequency given by the first harmonic (F1) of the cycle time histogram divided by the mean firing rate (F0). VPm signaling of both sinusoidal and periodic pulsatile whisker movements improved gradually over 1-16 and was maximal at 20-40 Hz. By contrast, the RM of Rt responses increased over 1-8 Hz, but deteriorated progressively over the 12- to 40-Hz range. In Rt, response adaptation occurred at lower stimulus frequencies and to a greater extent than in VPm. Within a train of high-frequency stimuli, Rt responses progressively decremented, possibly due to the accumulation of inhibition, whereas those of VPm neurons augmented. Mean firing rates in Rt increased 42 spikes/s over 1-40 Hz, providing tonic (low RM) inhibition during high-frequency stimulation that may enhance VPm signal-to-noise ratios. Consistent with this view, VPm mean firing rates increased only 13 spikes/s over 1-40 Hz, and inter-deflection activity was suppressed to a greater extent than stimulus-evoked responses. Rt inhibition is likely to act in concert with actions of neuromodulators in optimizing thalamic temporal signaling of high-frequency whisker movements. (+info)
Widespread thalamic terminations of fibers arising in the superficial medullary dorsal horn of monkeys and their relation to calbindin immunoreactivity.
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The relay of pain fibers from the spinal and medullary dorsal horn in the thalamus has become a controversial issue. This study analyzed the relationship of fibers arising in lamina I to nuclei in and around the caudal pole of the ventral posterior nuclear complex and especially to a zone of calbindin-dense immunoreactivity (VMpo) identified by some authors as the sole thalamic relay for these fibers. We show that the densest zone of calbindin immunoreactivity is part of a more extensive, calbindin-immunoreactive region that lies well within the medial tip of the ventral posterior medial nucleus (VPM), as delineated by other staining methods, and prove that the use of different anti-calbindin antibodies cannot account for differences in interpretations of the organization of the posterior thalamic region. By combining immunocytochemical staining with anterograde tracing from injections involving lamina I, we demonstrate widespread fiber terminations that are not restricted to the calbindin-rich medial tip of VPM and show that the lamina I arising fibers are not themselves calbindin immunoreactive. This study disproves the existence of VMpo as an independent thalamic pain nucleus or as a specific relay in the ascending pain system. (+info)