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PubMed1990

Central effect of the non-steroid anti-inflammatory agents, indomethacin, ibuprofen, and diclofenac, determined in C fibre-evoked activity in single neurones of the rat thalamus.

This study aimed to investigate if the non-steroid anti-inflammatory agents, indomethacin, ibuprofen, and diclofenac, are capable of depressing sensory responses of the nociceptive system by a central action. For this purpose, experiments were carried out on rats under urethane anaesthesia in which activity was elicited by electrical stimulation of afferent C fibres in the sural nerve. Recordings were made ipsi- or contralaterally from single neurones in the dorsomedial part of the ventral nucleus (VDM) of the thalamus. The 3 drugs produced a dose-dependent depression of the evoked activity which amounted to about 60% of the controls at the highest doses employed and lasted longer than 60 min. Their potency ranking, according to the ED50 values (in brackets), is: indomethacin (5 mg/kg) greater than diclofenac (10.9 mg/kg) greater than ibuprofen (15.6 mg/kg). The results suggest that a central action might contribute to the analgesia produced by these non-steroid anti-inflammatory agents.

Animals↗
PubMed1983

Do retinal and spinal projections overlap within the turtle thalamus?

The spinal and retinal projections to the turtle thalamus were studied using the autoradiographic tracing technique. Particular attention is given to the regions receiving both spinal and retinal projections: the ovalis complex and a perirotundal stripe. Spinal and retinal projections do not overlap significantly in either of these regions. In the perirotundal stripe there appears to be little likelihood of convergence of these projections on single neurons. In the ovalis complex, the most densely and the most consistently innervated thalamic region, however, the respective spinal and retinal target areas are located immediately adjacent to each other and low order somatosensory and visual projections may converge on single neurons with dendrites extending into both the spinal and retinal terminal arborizations. The ovalis complex in the turtle may be compared with the ventral part of the mammalian lateral geniculate nucleus. Both these nuclei receive spinal and retinal projections and both, reportedly, do not project to the telencephalon. The findings are discussed in relation to the possible evolution of the specific thalamic sensory nuclei in higher mammals as well as to the prosencephalic processing of somatosensory and visual information in turtles and mammals.

Animals↗
PubMed1983

Acetylcholinesterase in the ventrobasal thalamus: transience and patterning during ontogenesis.

In this study, maturational alterations in acetylcholinesterase-dependent staining of the thalamic ventrobasal complex of rat and mouse were examined. The study was undertaken to address the question of whether this nucleus exhibits transient acetylcholinesterase positivity during its development and whether the enzyme is likely to be synthesized by its immature intrinsic neurons. Also, the patterning due to acetylcholinesterase staining of cells and fibers, and the developmental changes in these patterns, have not been described in earlier work. In contrast to surrounding thalamic nuclei, the ventrobasal complex is acetylcholinesterase-positive at birth. In rat, acetylcholinesterase staining of the ventrobasal thalamus is still more intense than in adjacent nuclei at the end of the first week postnatally. Virtually all somata in the nucleus are filled with dense reaction product at this time. Ultrastructurally, reaction product is associated with the granular endoplasmic reticulum. At this stage, there is a marked difference in intensity of staining between the medial and lateral subdivisions of the nucleus, and patterned clustering of somata within each subdivision is readily appreciated in acetylcholinesterase-stained material. In the second postnatal week, intrinsic acetylcholinesterase activity is progressively lost. By the end of the third postnatal week, the nucleus is quite pale except for one area. In the posterior portion of the lateral subdivision, adjacent to the nucleus reticularis, interconnecting bundles of acetylcholinesterase-positive fibers enter the nucleus. They course medially in the lateral subdivision and break up into a plexus of fine fibers. The development of acetylcholinesterase-dependent staining patterns in the mouse is quite similar, except that histochemically detectable levels of enzyme are substantially lower in the neonatal period. It is concluded that the ventrobasal complex can be distinguished from other thalamic nuclei in regard to earlier onset and/or transience of acetylcholinesterase staining. Ultrastructural observations suggest that virtually all immature ventrobasal neurons are synthesizing acetylcholinesterase. It is suggested that the transient staining for enzyme is due primarily to alteration in synthesis and/or turnover in neurons of the ventrobasal complex. In addition, the acetylcholinesterase staining reveals a patterning of fibers and cells that also undergoes developmental alteration. Evidence is discussed suggesting that axons in the barrels of somatosensory cortex (SmI) are derived from these transiently acetylcholinesterase-positive somata. Consequently, the loss of acetylcholinesterase fiber staining in the barrels, during the third postnatal week (noted previously), may be related to a decrease in synthesis of enzyme in the neuronal somata of the ventrobasal complex.

Acetylcholinesterase↗
PubMed1987

Distribution of GABA-immunoreactive neurons in the thalamus of the squirrel monkey (Saimiri sciureus).

A light microscopic study of the cellular localization of GABA in the thalamus of the squirrel monkey (Saimiri sciureus) was undertaken by means of the indirect peroxidase-antiperoxidase method using a highly purified antiserum directed against GABA-glutaraldehyde-lysyl-protein conjugate. GABA-immunoreactive cell bodies and axon terminals were visualized in all thalamic nuclei in the squirrel monkey but their relative density varied from one nucleus to the other. At the level of the anterior nuclear group, GABA-positive cells and terminals abounded in the anterodorsal nucleus but were much less numerous in the anteromedial and anteroventral nuclei. In the nuclei of the ventral group, GABA-immunoreactive cells were found to be smaller and less numerous than nonimmunoreactive neurons. In the ventral anterior nucleus, GABA-positive neuronal profiles formed typical clusters, whereas they were more uniformly distributed in the posterior nuclei of the ventral group. In the intralaminar nuclei, GABA-immunoreactive cells and terminals abounded in the dorsal portion of the paracentral and centrolateral nuclei, whereas more caudally, GABA-positive terminals pervaded the entire parafascicular nucleus. In the mediodorsal nucleus, GABA-positive cell bodies and axon terminals formed typical clusters of various sizes scattered within the lateral parvocellular portion of the nucleus, while GABA-immunoreactive neuronal profiles were less numerous and more uniformly distributed in the medial portion of this structure. In the nuclei of the posterior group, GABA-immunoreactive neuronal profiles were uniformly distributed except in the pulvinar where they abounded in the inferior and oral parts but were scarce in the medial part. In the dorsal lateral geniculate nucleus, the magnocellular layers received the most massive GABA-positive innervation and contained the largest number of GABA-immunoreactive cell bodies. In the ventral lateral geniculate nucleus, GABA-positive cells occurred only ventrolaterally while GABA-immunoreactive terminals pervaded the entire structure. In the medial geniculate nucleus, GABA-immunoreactive cell bodies and terminals abounded particularly within the ventromedial third of the structure. In the habenula, a few GABA-immunoreactive cell bodies and numerous GABA-positive terminals were scattered throughout the lateral habenular nucleus, whereas only a few GABA-immunoreactive terminals surrounded the closely packed unreactive cells in the medial habenular nucleus. In contrast to other thalamic nuclei all neurons in the reticular nucleus displayed GABA immunoreactivity.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

A quantitative study of the projections of the gracile, cuneate and trigeminal nuclei and of the medullary reticular formation to the thalamus in the rat.

Following injection of horseradish peroxidase into the thalamus of one side, the numbers of labelled neurons in the nuclei of the dorsal funiculi and in the trigeminal sensory complex were counted. A comparative study was made of the pattern of labelling after a range of survival times, and animals surviving for 72 h after injection were used to provide detailed quantitative information about the patterns of distribution of labelled cells. The principal sensory nucleus of the trigeminal nerve (8683 labelled neurons) and the nucleus of the spinal trigeminal tract, pars interpolaris (1920) label heavily after thalamic injection. Pars oralis of the spinal nucleus labels more sparsely (524 labelled neurons), while the pars caudalis (260 labelled neurons) shows a laminar labelling pattern which continues across the spinomedullary junction into the upper cervical segments. The gracile (2152 labelled neurons) and cuneate (2339) nuclei also show rostrocaudal variation in labelling density: the middle one-third of each nucleus contains 66% of labelled gracile and cuneate cells. The findings are correlated with known features of the arrangement of the ascending sensory projections from these nuclei in various species, and are compared with previous findings on the distribution of thalamically-projecting cells in the upper cervical segments of the spinal cord.

Animals↗
PubMed1989

Gamma-aminobutyric acid and afferent inhibition in the cat and rat ventrobasal thalamus.

Extracellular single neuron recordings were made in the ventrobasal thalami of anaesthetized rats and cats. Physiological stimulation of vibrissa and hair follicle afferents was performed with an air jet (10-20 ms duration) directed at a single vibrissa or small area of hairy skin. Paired conditioning and test air jets delivered to the excitatory portion of receptive fields revealed inhibition of the response of ventrobasal thalamic neurons to test stimuli following the excitatory response to the conditioning stimulus. Such inhibitions could last up to 500 ms. An increase in neuronal excitability was sometimes observed following this inhibitory period. In addition, it was possible to produce inhibition without an excitatory response using conditioning stimuli delivered adjacent to the excitatory receptive field. Iontophoretic application of bicuculline methochloride, with currents that were adequate to antagonize iontophoretically applied GABA, was found to reduce the inhibition of test responses evoked by conditioning stimuli in almost all of the neurons studied. In most cases, no excitatory responses to conditioning stimuli directed outside the original excitatory receptive field were revealed by application of the GABA antagonist. In rats, bicuculline also led to a decrease in the post-inhibitory excitation, whereas in cats the converse appeared to be the case. These results suggest that GABAergic transmission may underlie inhibitory responses of cat and rat ventrobasal thalamus neurons to physiological stimulation of somatosensory afferents. Furthermore, removal of such inhibition does not appear to reveal excitatory inputs from outside of the original excitatory receptive field.

Acetylcholine↗
PubMed1990

Demonstration of extensive brainstem projections to medial and lateral thalamus and hypothalamus in the rat.

We use the method of retrograde transport of colloidal gold with silver intensification to map locations of brainstem neurons projecting to various nuclei of the medial and lateral thalamus (Menetrey, Histochemistry 83, 391-395, 1985; Seeley and Field, Brain Res. 449, 177-191, 1988). In rats injections of less than 1.0 microliters of a gold-wheatgerm agglutinin-horseradish peroxidase complex were restricted to the centrum medianum, centralis lateralis, medialis dorsalis, zona incerta, ventrobasal thalamic complex, or medial or lateral hypothalamus. Injections in the centralis lateralis, with some involvement of centrum medianum and medial medialis dorsalis, labeled numerous neurons throughout the rostrocaudal extent of the midbrain periaqueductal gray, and adjacent reticular formation, dorsal raphe nucleus and substantia nigra. These labeled neurons were distributed bilaterally, but with a preponderance ipsilaterally. Numerous neurons in the deep layers of the ipsilateral superior colliculus and in the anterior pretectal nucleus were also labeled. Many neurons in the pontomedullary raphe nuclei (including nucleus raphe magnus), locus coeruleus and dorsolateral parabrachial nuclei, and in the pontomedullary reticular formation, were labeled bilaterally. Fewer were seen bilaterally in the lateral reticular nucleus and nucleus of the solitary tract, with relatively few in the dorsal aspect of the trigeminal nucleus caudalis. Injections restricted largely to the centrum medianum labeled fewer cells in the brainstem, but with similar distributions. An injection restricted to the centralis lateralis also resulted in a similar distribution of labeled neurons in midbrain and nucleus raphe magnus but did not label neurons at more caudal medullary levels. An injection restricted to zona incerta labeled numerous neurons in a distribution similar to that following medial thalamic injections, except that many more were observed in the contralateral sensory trigeminal nucleus and in the dorsal column nuclei. Injections of the ventrobasal thalamic nucleus labeled many neurons in the trigeminal and dorsal column nuclei, but many fewer neurons in the midbrain, periaqueductal gray and reticular formation compared with medial thalamic injections. Labeled neurons were also seen in the superior and inferior colliculi, due presumably to involvement by the injection of the lateral posterior and magnocellular medial geniculate nuclei, respectively. Injections in the lateral hypothalamus labeled numerous neurons in a distribution similar to that seen following medial thalamic injections.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1991

A GABA immunocytochemical study of rat motor thalamus: light and electron microscopic observations.

A light and electron microscopic study of GABA-immunoreactive neurons and profiles in the ventroanterior-ventrolateral and ventromedial nuclei of rat dorsal thalamus was conducted using antiserum raised against GABA. Less than 1% of the neurons in these motor-related nuclei exhibited GABA immunoreactivity, confirming previous reports that these nuclei are largely devoid of interneurons. Immunoreactive neurons in the ventral anterior-ventral lateral complex and ventromedial nucleus were bipolar or multipolar in shape, and tended to be smaller than non-immunoreactive neurons. GABA immunoreactivity in the neuropil consisted of labeled axon terminals and myelinated and unmyelinated axons, and was lower in the ventral anterior-ventral lateral complex and ventromedial nucleus than in neighboring thalamic nuclei. The density of neuropil immunolabeling was slightly higher in ventral anterior-ventral lateral complex than in ventromedial nucleus. GABA-immunoreactive axon terminals, collectively termed MP boutons for their medium size and pleomorphic vesicles (and corresponding to "F" profiles of some previous studies of thalamic ultrastructure), formed symmetric synapses and puncta adhaerentia contacts predominantly with large and medium-diameter (i.e. proximal) non-immunoreactive dendrites. Approximately 12 and 18% of boutons in the ventral anterior-ventral lateral complex and ventromedial nucleus, respectively, were GABA-immunopositive. Many of these immunoreactive profiles probably arose from GABAergic neurons in the thalamic reticular nucleus, substantia nigra pars reticulata and entopeduncular nucleus. Two types of non-immunoreactive axon terminals were distinguished based on differences in morphology and synaptic termination sites. Boutons with small ovoid profiles and round vesicles that formed prominent asymmetric synapses onto small-diameter dendrites were observed. Mitochondria were rarely observed within these boutons, which arose from thin unmyelinated axons. These boutons composed approximately 82 and 74% of boutons in the ventral anterior-ventral lateral complex and ventromedial nucleus, respectively, and were considered to arise predominantly from neurons in the cerebral cortex. In contrast, boutons with large terminals that contained round or plemorphic vesicles and formed multiple asymmetric synapses predominantly with large-diameter dendrites were also observed. Puncta adhaerentia contacts were also common. Mitochondria were numerous within large boutons with round vesicles, which arose from myelinated axons. Many of the large boutons were likely to have originated from neurons in the cerebellar nuclei. Approximately 6% of the boutons in the ventral anterior-ventral lateral complex and 8% in ventromedial nucleus were of the large type.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Calretinin distribution in the thalamus of the rat: immunohistochemical and in situ hybridization histochemical analyses.

The distribution of calretinin-containing cells was examined by in situ hybridization histochemistry and compared with the immunohistochemical mapping of calretinin in the thalamus of the rat. Results revealed a close correspondence between the immunohistochemical localization of cell bodies and the messenger RNA label produced by the calretinin oligonucleotide probe. Calretinin cells were most prominent in the midline (paraventricular, reuniens, rhomboid) and intralaminar (central medial, paracentral) nuclei and in a group of cells along the rostral central gray which appeared continuous with the caudal extent of the midline nuclei. A subpopulation of calretinin cell bodies was also identified in the reticular nucleus. The mediorostral lateral posterior nucleus, subparafascicular, lateral geniculate and habenular nuclei also contained calretinin messenger RNA probe label. In contrast, no positive cells were found in the anterior, ventral or posterior thalamic nuclei. The distribution of calretinin cells did not correspond directly with that of other histochemical markers. Thus, the in situ hybridization histochemical and immunohistochemical results revealed calretinin as a unique identifying marker for distinct sets of thalamic neurons.

Animals↗
PubMed1996

Transient expression of acetylcholinesterase messenger RNA and enzyme activity in developing rat thalamus studied by quantitative histochemistry and in situ hybridization.

The molecular basis for transient expression of acetylcholinesterase in noncholinergic regions of the early postnatal rat brain was studied by in situ hybridization histochemistry. A 33P-labelled 63-mer DNA oligonucleotide was used to probe acetylcholinesterase messenger RNA in the brains of rat pups at one, two, six, nine, 12, 16 and 21 days of age (birth = day 0). Cryostat brain-sections were hybridized with probe and exposed to X-ray film or emulsion coatings. Acetylcholinesterase messenger RNA was quantitated by counting silver grains and by measuring X-ray film density with video imaging and computer-based densitometry. Adjacent sections were stained histochemically for acetylcholinesterase activity, also quantitated by video densitometry. Overall there was a significant correlation between apparent levels of acetylcholinesterase activity and acetylcholinesterase messenger RNA. Increases in message tended to accompany the surges of acetylcholinesterase activity that marked the maturation of thalamocortical sensory relay pathways. Acetylcholinesterase expression in the youngest rats was generally sparse but it increased markedly during the first postnatal week, especially in the sensory relay nuclei of the thalamus. Levels of message and enzyme activity in the medial and dorsolateral geniculate and the ventral posteromedial and ventral posterolateral nuclei rose to a peak, typically about day 9. Beyond this time there was a gradual decline. By day 21 the staining and in situ hybridization patterns resembled those in adult brains, whose thalamic relay nuclei are impoverished in acetylcholinesterase activity and messenger RNA. Thus, acetylcholinesterase expression is strongly modulated in certain thalamic systems as they undergo neural morphogenesis.

Acetylcholinesterase↗
PubMed1995

Differential expression of p140trk, p75NGFR and growth-associated phosphoprotein-43 genes in nucleus basalis magnocellularis, thalamus and adjacent cortex following neocortical infarction and nerve growth factor treatment.

A loss of target-derived neurotrophic factors is hypothesized to be one of the major determinants of central nervous system neuronal degeneration. In order to obtain further insight into early neuronal responses to injury, lesion-induced alterations in the expression of high- and low-affinity nerve growth factor receptors, as well as growth-associated phosphoprotein-43 genes in nucleus basalis magnocellularis, thalamic and neocortical neurons were studied. For this purpose, unilateral cortical devascularization operations were conducted on adult rats. Animals received i.c.v. infusions of vehicle or nerve growth factor (12 micrograms/day) and were killed at one, three, seven and 15 days post-lesion. In situ hybridization studies using 35S-labelled oligonucleotide probes for p75NGFR, p140trk and growth-associated phosphoprotein-43 messenger RNAs reveals that these genes were differentially regulated following the lesion. In the nucleus basalis magnocellularis ipsilateral to the lesion, p140trk gene expression significantly decreased on days 3 and 7, while p75NGFR messenger RNA initially increased on day 3 and decreased on days 7 and 15 after lesion. GAP-43 messenger RNA levels were significantly increased in the nucleus basalis magnocellularis on post-lesion days 3 and 7. Moreover, in contrast to p75NGFR or 140trk, growth-associated phosphoprotein-43 messenger RNA levels were significantly increased in pyramidal neurons located in the remaining cortex adjacent to the cortical lesion at all time points. In the lateral and ventroposterior nuclei of the thalamus, growth-associated phosphoprotein-43 messenger RNA level was slightly increased on days 1 and 3 and was dramatically decreased, significantly below the levels in sham-operated controls, on post-lesion days 7 and 15. During nerve growth factor application, the level of p140trk messenger RNA in the lesioned nucleus basalis magnocellularis returned to values observed in the contralateral nucleus basalis magnocellularis while p75NGFR messenger RNA was increased above values noted in all animals not treated with nerve growth factor. Nerve growth factor treatment did not affect the expression of growth-associated phosphoprotein-43 messenger RNA in any of the areas studied. p140trk messenger RNA was not up-regulated during the time that nerve growth factor was applied, as observed for p75NGFR, but only eight days after interrupting nerve growth factor treatment. Three cell types, nucleus basalis magnocellularis, cortical pyramidal and thalamic neurons, were probably affected in different ways by the devascularization with respect to lesion extent. Consequently, the remaining number of synaptic contacts in each of these brain areas is most likely different which may lead to a differential regulation of growth-associated phosphoprotein-43 messenger RNA.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMedDate not supplied

Effects of morphine on cortex, hippocampus and medial thalamus: a comparison between urethane-anaesthetized and paralyzed-awake rats.

Urethane is often used as a central anaesthetic in neurophysiological studies of drug effects. In this experiment, the effect of morphine on cortical EEG and single units of hippocampus and medial thalamus were compared in urethane-anaesthetized and paralyzed-awake rats. In each case, there was evidence of a morphine-urethane interaction, suggesting caution in the interpretation of drug studies using urethane-anaesthetized animals.

Animals↗
PubMedDate not supplied

Attenuation during paradoxical sleep of signals from tooth pulp to thalamus.

Quantitative evaluation of the response of thalamic neurons to tooth pulp stimulation was made in chronically prepared cats. The latency, duration and intensity of the responses were measured from the post-stimulus time histograms to estimate, from various aspects, the alteration in the responsiveness during different phases of sleep and wakefulness. During slow wave sleep, tooth pulp-evoked impulses tended to be transmitted to the thalamus in a similar or slightly higher intensity compared to wakefulness. In contrast, during paradoxical sleep the signals were often attenuated in many aspects. The results seem to be in favor of the idea that the impairment of signal to noise ratio in a variety of neuronal networks is one of the characteristics of paradoxical sleep.

Animals↗
PubMed1986

Cholinergic systems in the rat brain: III. Projections from the pontomesencephalic tegmentum to the thalamus, tectum, basal ganglia, and basal forebrain.

The ascending cholinergic projections of the pedunculopontine and dorsolateral tegmental nuclei, referred to collectively as the pontomesencephalotegmental (PMT) cholinergic complex, were investigated by use of fluorescent tracer histology in combination with choline-O-acetyltransferase (ChAT) immunohistochemistry and acetylcholinesterase (AChE) pharmacohistochemistry. Propidium iodide, true blue, or Evans blue was infused into the anterior, reticular, mediodorsal, central medial, and posterior nuclear areas of the thalamus; the habenula; lateral geniculate; superior colliculus; pretectal/parafascicular area; subthalamic nucleus; caudate-putamen complex; globus pallidus; entopeduncular nucleus; substantia nigra; medial septal nucleus/vertical limb of the diagonal band area; magnocellular preoptic/ventral pallidal area; and lateral hypothalamus. In some animals, separate injections of propidium iodide and true blue were made into two different regions in the same rat brain, usually a dorsal and a ventral target, in order to assess collateralization patterns. Retrogradely transported fluorescent labels and ChAT and/or AChE were analyzed microscopically on the same brain section. All of the above-delimited targets were found to receive cholinergic input from the PMT cholinergic complex, but some regions were preferentially innervated by either the pedunculopontine or dorsolateral tegmental nucleus. The former subdivision of the PMT cholinergic complex projected selectively to extrapyramidal structures and the superior colliculus, whereas the dorsolateral tegmental nucleus was observed to provide cholinergic input preferentially to anterior thalamic regions and rostral portions of the basal forebrain. The PMT cholinergic neurons showed a tendency to collateralize extensively.

Acetylcholine↗
PubMed1988

Afferent projections to the dorsal thalamus of the rat as shown by retrograde lectin transport. II. The midline nuclei.

Afferent projections to midline thalamic cell groups which innervate nucleus accumbens, were identified by the retrograde transport of unconjugated wheat germ agglutinin followed by the identification of labelled cell groups with immunocytochemistry. Large numbers of neurones were labelled in a variety of hypothalamic nuclei; principally in the medial preoptic area, anterior hypothalamic area, ventromedial, periventricular, arcuate and posterior hypothalamic nuclei, and in the supramammillary and lateral hypothalamic areas. Following rostral thalamic injections labelled cells were also found in the lateral septum, bed nucleus of the stria terminalis, and zona incerta. Prominent and localised label was found in the nucleus reticularis of thalamus at its most rostral medial tip. Cortical label was found in the ventral subiculum following rostral injections, and in the perirhinal cortex following mid-thalamic injections. In the brainstem label was found in central grey, laterodorsal tegmental nucleus, raphe, dorsal and ventral parabranchial nuclei and nucleus of the tractus solitarius. The results are discussed in the context of striatal function, particularly the nucleus accumbens, which is a component of the ventral striatum. Thus, the midline thalamic nuclei may provide an interface where a variety of inputs from many limbic regions and hypothalamic nuclei can influence nucleus accumbens function. Comparison of afferents to several thalamic nuclei directly related to striatal function and the prefrontal cortex show, that forebrain thalamic afferents from pallidal and hypothalamic sites, are organised with a clear topography. Some afferents suggest specific routes which may allow the reticular activating system to participate in the regulation of basal ganglia function.

Afferent Pathways↗
PubMed1990

Mapping the effects of motor cortex stimulation on somatosensory relay neurons in the rat thalamus: direct responses and afferent modulation.

Single unit recordings were used to map the spatial distribution of motor (MI) cortical influences on thalamic somatosensory relay nuclei in the rat. A total of 215 microelectrode penetrations were made to record single neurons in tracks through the medial and lateral ventroposterior (VPM and VPL), ventrolateral (VL), reticular (nRt), and posterior (Po) thalamic nuclei. Single units were classified according to their: 1) location within the nuclei, 2) receptive fields, and 3) response to standardized microstimulation in deep layers of the forepaw-forelimb areas of MI cortex. For mapping purposes, only short latency (1-7 msec) excitatory neuronal responses to the MI cortex stimulation were considered. Percentages of recorded thalamic neurons responsive to the MI stimulation varied considerably across nuclei: VL: 42.6%, nRt: 23.0%, VPL: 15.7%, VPM: 9.3%, and Po: 3.9%. Within the VPL, most responsive neurons were found in "border" regions, i.e., areas adjacent to the VL, and (to a lesser extent) the nRt and Po thalamic nuclei. The same parameters of MI cortical stimulation were used in studies of corticofugal modulation of afferent transmission through the VPL thalamus. A condition-test (C-T) paradigm was implemented in which the cortical stimulation (C) was delivered at a range of time intervals before test (T) mechanical vibratory stimulation was applied to digit No. 4 of the contralateral forepaw. The time course of MI cortical effects was analyzed by measuring the averaged evoked unit responses of the thalamic neurons to the T stimuli, and plotting them as a function of C-T intervals from 5-50 msec. Of the 30 VPL neurons tested during MI stimulation, the average response to T stimulation was decreased a mean 43%, with the suppression peaking at about 30 msec after the C stimulus. This suppression was more pronounced in the VPL border areas (-52% in areas adjacent to VL and nRt) than in the VPL center (-25%).

Animals↗
PubMed1995

Calcium deposits in the thalamus following repeated cerebral ischemia and long-term survival in the gerbil.

We investigated the long-term changes in the gerbil brain following three episodes of 2-min forebrain ischemia at 1-h intervals in comparison with a 6-min period of ischemia. The animals were sacrificed after 1 month and 6 months. Following either ischemic insult, the hippocampal CA1 region showed a loss of pyramidal neurons together with a diffuse calcium accumulation as shown by alizarin red S staining. Three 2-min ischemic insults additionally produced neuronal damage in the striatum and thalamus. The thalamic damage was accompanied by an accumulation of small calcium granules after 1 month and large calcium concretions after 6 months. Calcium staining in the striatum was weak. Thus, the thalamic neuronal damage was accompanied by an active process of calcification, which has not been described in experimental cerebral ischemia models. The observations show that repeated ischemic insults produce different long-term effects in different brain regions.

Animals↗
PubMed1996

Nerve growth factor modulates information processing in the auditory thalamus.

The spatio-temporal organization of spike discharges was studied in rat auditory thalamus (i.e., medial geniculate body and auditory sector of thalamic reticular nucleus) following a 2-week continuous intracerebroventricular administration of nerve growth factor (NGF). Recording of extracellular single-unit activity indicated that, in medial geniculate body, NGF induced a significant increase of the mean firing rate. In thalamic reticular nucleus, where units tend to discharge in bursts, NGF increased the average burst size (number of spikes) and the intraburst frequency without affecting the firing rate. Following white noise acoustical stimulation, in medial geniculate body, more onset excitation and a lower signal-to-noise ratio were observed in NGF-treated rats than in controls. Conversely, in thalamic reticular nucleus, NGF-treated animals showed more inhibitory responses than controls. In addition, within the medial geniculate body, functional interactions between pairs of units simultaneously recorded from different electrodes were greatly increased by the nerve growth factor treatment. These data indicate that modifications of temporal pattern of discharges in selected brain regions are among the effects induced by the intracerebroventricular administration of nerve growth factor.

Animals↗