Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “THALAMUS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources
PubMed1977

Vestibular-related neuronal activity in the thalamus of the alert monkey during sinusoidal rotation in the dark.

1. In the alert monkey neuronal activity was recorded in the ventro-posterior nucleus (VP) of the thalamus in the dark during sinusoidal rotation over a frequency range from 0.01-1 Hz. 2. From 57 neurons 38 (67%) were activated with rotation to the ipsilateral side (type I) and 19 (33%) to the contralateral side (type II). The spontaneous activity was low (average 10.1 imp/sec) and irregular. No activity changes were found with eye movements. 3. At 0.2-0.1 Hz neuronal activity showed a phase lead of 10-20 degrees relative to chair velocity. At the lowest frequency (0.01 Hz) the phase lead was only slightly higher (about 30 degrees). Accordingly the decrease in gain was only moderate. 4. At lower frequencies the simultaneously recorded eye movements (nystagmus) showed an increase in phase lead comparable to the values for the neuronal activity in the thalamus. For both neuronal activity in the thalamus and nystagmus a time constant between 25-35 sec was calculated. 5. The data are compared with vestibular nerve and nuclei recordings. It is argued that the time constants of vestibular neurons in the thalamus are very similar to the time constants of neurons in the vestibular nuclei in alert animals.

Animals↗
PubMedDate not supplied

The effects of the mediodorsal nucleus of the thalamus on respiratory neurons of the medulla oblongata and respiration in rats in conditions of hypoxia.

The effects of the associated mediodorsal nucleus of the thalamus on spike activity of respiratory neurons in the medulla oblongata and on respiration were studied in normal conditions and in oxygen insufficiency. At normal atmospheric pressure, before animals were elevated to low pressures, electrical stimulation of the mediodorsal nucleus of the thalamus had predominantly inhibitory effects. At the initial phase of hypoxia, at a "height" of 4,000-5,000 m, hypoxic activation of neuron discharge frequency occurred. with an increase in the frequency of respiration. In these conditions, the inhibitory effect of stimulation of the mediodorsal nucleus of the thalamus was less marked than in normoxic conditions. The opposite effect occurred at the second phase of hypoxia (7,500-8,000 m)-inhibition of activity in the medulla oblongata and thalamic center. In severe hypoxia, there was inhibition of neuron spike activity and a decrease in the frequency of respiration, which became superficial; in these conditions, the inhibitory effect of the thalamus was insignificant.

Action Potentials↗
PubMed2003

Cells in midline thalamus, central amygdala, and nucleus accumbens responding specifically to antipsychotic drugs.

RATIONALE: Determining brain regions in which neuroleptic drugs of different types produce similar effects, especially where these effects are not shared with drugs lacking antipsychotic efficacy, provides evidence as to how and where the clinical effects of neuroleptic drugs are mediated. OBJECTIVE: For this study, the pattern of expression of the protein Fos, a marker of cellular activation, was compared after administration of the typical neuroleptic haloperidol, the antipsychotic drug clozapine, and the atypical neuroleptic olanzapine, as well as the sedative drug diphenhydramine and the anxiolytic lorazepam. METHODS: Animals (Sprague-Dawley rats, three per cohort) received intraperitoneal injections of haloperidol (1 mg/kg), clozapine (20 mg/kg), olanzapine (5 mg/kg), diphenhydramine hydrochloride (1 mg/kg), lorazepam (5 mg/kg) or vehicle (2% lactic acid, 1 ml/kg). Two hours after drug administration, animals were killed. Patterns of activated cells were observed by immunohistochemistry for Fos-like antibodies in regions previously suggested as responding to all antipsychotic drugs, including nucleus accumbens, central amygdala, and central medial thalamus. Cells staining for Fos were counted by semi-automated methods. RESULTS. A very similar pattern and number of Fos positive cells in nucleus accumbens, central amygdala, and central medial thalamus followed administration of each antipsychotic drug. The numbers of apparently activated cells were much greater following antipsychotic drug administration than after vehicle, with differences between each drug and vehicle being highly statistically significant in each region. Lorazepam produced apparent activation of cells of the central amygdala similar in degree and location but not identical in distribution to that of antipsychotic drugs. Diphenhydramine produced no apparent activation of cells in any of the sites tested. CONCLUSION: Typical and atypical antipsychotic drugs shared a distinctive pattern of robust activation of cells in nucleus accumbens, central medial thalamus, and central amygdala. Antipsychotic drug-induced activation of amygdala was shared by lorazepam, but activation of thalamus and nucleus accumbens was much greater following antipsychotic drugs than following lorazepam. The pattern of activated cells may be relevant to the therapeutic actions of antipsychotic drugs.

Amygdala↗
PubMed2000

Reduction of the synaptic protein rab3a in the thalamus and connecting brain regions in post-mortem schizophrenic brains.

Although the psychotic symptoms in schizophrenia can be alleviated by treatment with dopaminergic receptor antagonists, the etiology and underlying neurochemical pathology remains obscure. Both neuropathological and magnetic resonance imaging studies have found evidence for neuronal loss and atrophy in the thalamus in schizophrenia, implicating this key structure for gating information to cortical areas in the pathophysiology. Recent studies have also found evidence of synaptic loss in the thalamus in schizophrenia. To further examine possible synaptic disturbances, we studied the synaptic related protein rab3a as a marker for synaptic density, using both quantitative Western blotting and immunohistochemistry. The material consisted of brains from 22 schizophrenic patients (mean age 79.3 years), and 24 control subjects (74.8 years). Reduced rab3a protein levels were found in the left thalamus in schizophrenia (0.47 +/- 0.17 vs. 1.00 +/- 0.18; p < 0.0001), while a less marked decrease was found also in the right thalamus (0.75 +/- 0.13 vs. 1.00 +/- 0.09; p < 0.0001). Immunohistochemistry, performed on two schizophrenic and two control brains, revealed that rab3a immunoreactivity was most reduced in the left anterior and mediodorsal thalamic nuclei. Therefore, we extended the study to brain regions connected these thalamic nuclei. Reduced rab3a protein levels were found schizophrenia also in the frontal cortex, hippocampus, gyrus cinguli, and parietal cortex, while no significant differences were found in the temporal cortex, or in cerebellum. The reduction in rab3a was not found to be secondary to confounding factors such as age-differences, post-mortem delay time, generalized brain atrophy, or antipsychotic medication. Therefore, the reduction of rab3a probably reflects synaptic disturbances, possibly synaptic loss, in the limbic system and neocortical areas, in schizophrenia. This part of the brain is known to be involved in behavioral and emotional control, and thus to be crucial for higher mental functions, suggesting that synaptic disturbances in the limbic system may be of importance in the development of psychotic symptoms in schizophrenia.

Adult↗
PubMed1984

Immunocytochemical localization of corticotropin releasing factor (CRF)-like immunoreactivity in the thalamus of the rat.

The distribution of corticotropin releasing factor (CRF)-immunoreactive structures in the rat thalamus was studied after treatment with high doses of colchicine (100 micrograms/100 g b.wt.) with peroxidase-antiperoxidase (PAP) immunocytochemistry in vibratome sections. CRF-immunopositive perikarya were found in the 'posteromedial complex' of the thalamus, including the ventromedial, paracentral, mediodorsal, rhomboid, parafascicular nuclei, centrum medianum and ventromedial portion of the posterolateral nucleus. In addition, CRF-containing perikarya were observed in the pretectal and subthalamic nuclei. CRF-immunoreactive processes were seen in most of the medial nuclei of the thalamus. The presence of CRF-immunopositive structures in the thalamus suggests that CRF not only functions as a hypophysiotropic hormone regulating the release of ACTH and beta-endorphin from the pituitary, but also as a neurotransmitter or neuromodulator, playing an important role in nociception and analgesia.

Afferent Pathways↗
PubMed1986

Immunocytochemical study of enkephalin-like cell bodies in the thalamus of the cat.

Using an indirect immunoperoxidase technique, the localization of enkephalin-like cell bodies in the thalamus of the cat was carried out. Enkephalin-like cell bodies are widely distributed in the cat thalamus. However, immunoreactive cells may be regrouped in 4 clusters which do not exactly correlate with the anatomical subdivisions of the thalamus. One is located in the dorsocaudal aspect of the thalamus, another in the midline area, and the others are formed by the nuclei geniculatum mediale and laterale.

Animals↗
PubMed1989

Modulatory effects of serotonin on excitatory amino acid responses and sensory synaptic transmission in the ventrobasal thalamus.

Excitatory amino acid receptors are thought to mediate sensory input to the ventrobasal thalamus. There is evidence for a brainstem serotonergic projection to the ventrobasal thalamus which may have a modulatory role. The possibility that serotonin may selectively modulate responses to excitatory amino acid receptor agonists, and its effects on sensory synaptic transmission has been examined in the rat ventrobasal thalamus in vivo. Iontophoretic ejection of serotonin at low currents produced a marked facilitation of responses to excitatory amino acids. In contrast, excitatory responses to cholinomimetic agonists were attenuated. Synaptic transmission was concomitantly enhanced or unchanged in these circumstances. Higher serotonin ejection currents reversed the facilitation, or inhibited excitatory amino acid responses and synaptic transmission. It is concluded that serotonin can modulate responses to excitatory amino acids relatively selectively and that synaptic transmission of somatosensory information through the ventrobasal thalamus may be susceptible to brainstem serotonergic modulation.

Action Potentials↗
PubMed1984

Cytoarchitecture of the dorsal thalamus of the rat.

Although several neuroanatomical studies have previously described various subdivisions of the rat thalamus, no comprehensive description of the entire thalamus accompanied by photomicrographs has been available. To provide such a description, the cytoarchitecture of the normal rat thalamus was studied in the coronal plane using a series of celloidin embedded, Nissl-stained 33 micrometers sections spaced 400 micrometers apart. Using the criteria of cell packing density, relative cell size, and the presence or absence of fibers, the thalamus can be subdivided into a ventral nuclear complex which includes the ventrolateral, ventromedial, and ventrobasal nuclei; the intralaminar nuclei which include central medial, central lateral, paracentral and parafascicular nuclei; the midline nuclei which include the medioventral, paratenial, rhomboid, paraventricular, and submedial nuclei; the anterior nuclear group which include the anterodorsal, anteroventral, and anteromedial nuclei; the mediodorsal nucleus; the lateral nuclear complex including both lateral posterior and lateral dorsal; the posterior nuclear complex; the reticular nucleus; and the diencephalic-mesencephalic junction. The terminology used is based on previous studies.

Animals↗
PubMed1996

Calretinin immunoreactivity in the thalamus of the squirrel monkey.

The distribution of the calcium-binding protein, calretinin, in the thalamus of the squirrel monkey (Saimiri sciureus) was studied with immunohistochemical methods. Calretinin was found to be heterogeneously distributed in the primate thalamus and to occur only in specific neuronal populations of certain thalamic nuclei. Neuronal cells and fibers in midline nuclei and their dorsolateral extension, which includes the parataenial and central superior lateral nuclei, displayed the most intense calretinin immunoreactivity. The immunoreactivity for cells and fibers in the intralaminar nuclei was moderate rostrally but very weak caudally. The centre mèdian nucleus, together with the medial habenular nucleus, were virtually devoid of calretinine immunostaining. The mediodorsal nucleus displayed a markedly heterogeneous staining, with numerous clusters of labeled cells and fibers in its central parvicellular part. Cell and fiber immunoreactivity ranged from moderate to high in the nuclei of the anterior and lateral groups, but was very weak in the nuclei of the ventral and posterior groups. There was a small to moderate number of heterogeneously distributed calretinin-immunoreactive cells and fibers in the lateral and medial geniculate bodies, as well as in the reticular nucleus. The present study provides the first evidence for the existence of calretinin in primate thalamus, where this protein is distributed according to a highly heterogeneous pattern. This specific pattern of distribution suggests that calretlnin may play a role that is complementary to those of the other calcium-binding proteins parvalbumin and calbindin D-28k in the thalamus of primates.

Animals↗
PubMed2000

Nucleus-specific expression of ionotropic glutamate receptor subunit mRNAs and binding sites in primate thalamus.

Thalamic afferents and efferents utilize glutamate as their primary neurotransmitter. There are four families of glutamate receptors that can transduce this activity, as well as regulate glutamate release from thalamic relay neurons. The three ionotropic subtypes are of particular importance, because subunit composition confers variability in functional properties of each subtype. We have quantified the expression of NMDA, AMPA and kainate receptors in the thalamus of the macaque using receptor autoradiography and in situ hybridization. NMDA receptors are multimeric associations of NR1 and NR2A-NR2D subunits that form ligand-gated ion channels. Particular subunits are associated with modulatory binding sites that affect receptor activity. NR1 was the most abundant subunit mRNA; NR2A, NR2B, and NR2D subunit mRNAs were also present, but were expressed in nucleus-specific patterns. Very high levels of [3H]ifenprodil binding to the polyamine site of the NMDA complex were detected in a fairly homogeneous distribution. Binding of the ion channel ligand [3H]MK-801 was also abundant, and limbic nuclei expressed higher levels than motor nuclei or the reticular nucleus. [3H]CGP39653 binding to the glutamate site of the NMDA receptor was the least abundant of the NMDA receptor binding sites. There was variability in the stoichiometric relationships of binding sites across nuclei, suggesting that there is heterogeneity in the pharmacological properties of NMDA receptors expressed in the thalamus. AMPA and kainate are also multimeric associations of specific subunits that form ligand-gated ion channels. These subunits are encoded by specific genes: gluR1-gluR4 for AMPA receptors, and gluR5-gluR7 and KA1-KA2 for kainate receptors. GluR4 and gluR6 mRNAs were, respectively the most abundant of the AMPA and kainate receptor subunit transcripts. Both AMPA and kainate receptor subunit transcripts were expressed in a nucleus-specific pattern. The binding of [3H]kainate was higher than that of [3H]AMPA throughout the thalamus, but AMPA subunit mRNA levels were three to five orders of magnitude higher than those encoding the kainate receptor subunits. The mismatch between the levels of expression of kainate receptor subunit transcripts and binding sites is suggestive of a presynaptic localization of kainate receptors on thalamic afferents. These results suggest that ionotropic glutamate receptors are heterogeneously expressed in the thalamus of the primate, and that their differential expression is both subunit- and nucleus-specific.

2-Amino-5-phosphonovalerate↗
PubMed2001

Induction of Fos-like immunoreactivity in the ventral thalamus after electrical or chemical stimulation of various subcortical centres of rats.

We have examined the patterns of Fos-like immunoreactivity in the ventral thalamus (thalamic reticular nucleus (Rt), zona incerta (ZI) and ventral lateral geniculate nucleus (LGv)) after electrical or chemical stimulation of nuclei in either the brainstem (midbrain reticular nucleus), basal forebrain (substantia innominata) or dorsal thalamus (parafascicular nucleus). Sprague-Dawley rats were anaesthetised with Halothane or Ketamil/Rompun and the above mentioned centres were stimulated either electrically or chemically (using kainic acid). Brains were then processed for Fos-like immunocytochemistry using standard methods. We detected no major differences in the labelling patterns after either electrical or chemical stimulation or after using Halothane or Ketamil/Rompun anaesthesia. After brainstem or dorsal thalamic stimulations, many Fos-like immunoreactive cells were seen within the rostral pole of the Rt, the dorsal sector of the ZI and the parvocellular lamina of the LGv. After basal forebrain stimulations, many Fos-like immunoreactive cells were seen in the rostral pole of the Rt and rostral sector of the ZI, but very few were apparent in the LGv. Overall, our results show that distinct groups of cells in the ventral thalamus show increased levels of Fos-like immunoreactivity after stimulation of different subcortical centres. These activated cells of the ventral thalamus, are in turn, in a position to influence particular thalamocortical pathways through their dorsal thalamic projections.

Animals↗
PubMed2000

Somatostatin inhibits GABAergic transmission in the sensory thalamus via presynaptic receptors.

The action of somatostatin on GABA-mediated transmission was investigated in cat and rat thalamocortical neurons of the dorsal lateral geniculate nucleus and ventrobasal thalamus in vitro. In the cat thalamus, somatostatin (10 microM) had no effect on the passive membrane properties of thalamocortical neurons and on the postsynaptic response elicited in these cells by bath or iontophoretic application of (+/-)baclofen (5-10 microM) or GABA, respectively. However, somatostatin (1-10 microM) decreased by a similar amount (45-55%) the amplitude of electrically evoked GABA(A) and GABA(B) inhibitory postsynaptic potentials in 71 and 50% of neurons in the lateral geniculate and ventrobasal nucleus, respectively. In addition, the neuropeptide abolished spontaneous bursts of GABA(A) inhibitory postsynaptic potentials in 85% of kitten lateral geniculate neurons, and decreased (40%) the amplitude of single spontaneous GABA(A) inhibitory postsynaptic potentials in 87% of neurons in the cat lateral geniculate nucleus. Similar results were obtained in the rat thalamus. Somatostatin (10 microM) had no effect on the passive membrane properties of thalamocortical neurons in this species, or on the outward current elicited by puff-application of (+/-)baclofen (5-10 microM). However, in 57 and 22% of neurons in the rat lateral geniculate and ventrobasal nuclei, respectively, somatostatin (1 microM) reduced the frequency, but not the amplitude, of miniature GABA(A) inhibitory postsynaptic currents by 31 and 37%, respectively. In addition, the neuropeptide (1 microM) decreased the amplitude of evoked GABA(A) inhibitory postsynaptic currents in 20 and 55% of rat ventrobasal neurons recorded in normal conditions and during enhanced excitability, respectively: this effect was stronger on bursts of inhibitory postsynaptic currents(100% decrease) than on single inhibitory postsynaptic currents (41% decrease). These results demonstrate that in the sensory thalamus somatostatin inhibits GABA(A)- and GABA(B)-mediated transmission via a presynaptic mechanism, and its action is more prominent on bursts of GABAergic synaptic currents/potentials.

2-Amino-5-phosphonovalerate↗
PubMed2003

Investigations of the cholinergic modulation of GABA release in rat thalamus slices.

The thalamus receives a dense cholinergic projection from the pedunculopontine tegmentum. A number of physiological studies have demonstrated that this projection causes a dramatic change in thalamic activity during the transition from sleep to wakefulness. Previous anatomical investigations have found that muscarinic type 2 receptors are densely distributed on the dendritic terminals of GABAergic interneurons, as well as the somata and proximal dendrites of GABAergic cells in the thalamic reticular nucleus. Since these structures are the synaptic targets of cholinergic terminals in the thalamus, it appears likely that thalamic pedunculopontine tegmentum terminals can activate muscarinic type 2 receptors on GABAergic cells. To test whether activation of muscarinic type 2 receptors affects the release of GABA in the thalamus, we have begun pharmacological studies using slices prepared from the rat thalamus. We have found that the application of the nonspecific muscarinic agonist, methacholine, and the muscarinic type 2-selective agonist, oxotremorine.sesquifumarate, diminished both the baseline, and K(+) triggered release of [(3)H]GABA from thalamic slices. This effect was calcium dependent, and blocked by the nonselective muscarinic antagonist atropine, the muscarinic type 2-selective antagonist, methoctramine, but not the muscarinic type 1 antagonist, pirenzepine. Thus, it appears that one function of the pedunculopontine tegmentum projection is to decrease the release of GABA through activation of muscarinic type 2 receptors. This decrease in inhibition may play an important role in regulating thalamic activity during changes in states of arousal.

Acetylcholine↗
PubMed1999

Distribution and properties of GABA(B) antagonist [3H]CGP 62349 binding in the rhesus monkey thalamus and basal ganglia and the influence of lesions in the reticular thalamic nucleus.

GABA(B) receptors are believed to be associated with the efferents of the nucleus reticularis thalami, which is implicated in the regulation of activity in the thalamocortical-corticothalamic circuit and plays a role in absence seizures. Yet, the distribution of GABA(B) receptors in the thalamus has only been studied in the rat, and there is no comparable information in primates. The potent GABA(B) receptor antagonist [3H]CGP 62349 was used to study the distribution and binding properties of the receptor in control monkeys and those with small ibotenic acid lesions in the anterodorsal segment of the nucleus reticularis thalami. Eight-micrometer-thick cryostat sections of the fresh frozen brains were incubated in the presence of varying concentrations of the ligand. Autoradiographs were analysed using a quantitative image analysis technique, and binding parameters were calculated for select thalamic nuclei as well as basal ganglia structures present in the same sections. The overall number of GABA(B) binding sites in the monkey thalamus and basal ganglia was several-fold higher than previously reported values for the rat. In the thalamus, the receptors were distributed rather uniformly and the binding densities and affinities were high (Bmax range of 245.5-437.9 fmol/ mg of tissue, Kd range of 0.136-0.604 nM). In the basal ganglia, the number of binding sites and the affinities were lower (Bmax range of 51.1-244.2 fmol/mg of tissue; K(d) range of 0.416-1.394 nM), and the differences between nuclei were more pronounced, with striatum and substantia nigra pars compacta displaying the highest binding densities. Seven days post-lesion, a 20-30% decrease in Bmax values (P < 0.05) was found in the nuclei receiving input from the lesioned nucleus reticularis thalami sector (the mediodorsal nucleus and densicellular and magnocellular parts of the ventral anterior nucleus) without changes in affinity. No significant changes were detected in any other structures. The results of the lesioning experiments suggest that a portion of thalamic GABA(B) receptors is in a presynaptic location on the nucleus reticularis thalami efferents. The overall distribution pattern in the thalamus also suggests a partial association of GABA(B) receptors with corticothalamic terminals presynaptically.

Animals↗
PubMed2002

Distinct localization of GABA(B) receptors relative to synaptic sites in the rat cerebellum and ventrobasal thalamus.

Metabotropic gamma-aminobutyric acid receptors (GABA(B)Rs) are involved in modulation of synaptic transmission and activity of cerebellar and thalamic neurons. We used subtype-specific antibodies in pre- and postembedding immunohistochemistry combined with three-dimensional reconstruction of labelled profiles and quantification of immunoparticles to reveal the subcellular distribution of pre- and postsynaptic GABA(B)R1a/b and GABA(B)R2 in the rat cerebellum and ventrobasal thalamus. GABA(B)R1a/b and R2 were extensively colocalized in most brain regions including the cerebellum and thalamus. In the cerebellum, immunoreactivity for both subtypes was prevalent in the molecular layer. The most intense immunoreactivity was found in Purkinje cell spines with a high density of immunoparticles at extrasynaptic sites peaking at around 240 nm from glutamatergic synapses between spines and parallel fibre varicosities. This is in contrast to dendrites at sites around GABAergic synapses where sparse and random distribution was found for both subtypes. In addition, more than one-tenth of the synaptic membrane specialization of spine-parallel fibre synapses were labelled at pre- or postsynaptic sites. Weak immunolabelling for both subtypes was also seen in parallel fibres but only rarely in GABAergic axons. In the ventrobasal thalamus, immunolabelling for both receptor subtypes was intense over the dendritic field of thalamocortical cells. Electron microscopy demonstrated an extrasynaptic localization of GABA(B)R1a/b and R2 exclusively in postsynaptic elements. Quantitative analysis further revealed the density of GABA(B)R1a/b around GABAergic synapses was higher than glutamatergic synapses on thalamocortical cell dendrites. The distinct localization of GABA(B)Rs relative to synaptic sites in the cerebellum and ventrobasal thalamus suggests that GABA(B)Rs differentially regulate activity of different neuronal populations.

Amino Acid Sequence↗
PubMed2000

Tone-evoked oscillations in the rat auditory cortex result from interactions between the thalamus and reticular nucleus.

This study investigates the origins of tone-evoked oscillations (5-13 Hz) in the thalamo-cortical auditory system of anaesthetized rats. In three separate experiments, the auditory sector of the reticular nucleus (RE), the auditory cortex and the auditory thalamus were inactivated by local applications of muscimol (1 mg/mL). To assess the efficacy of this procedure, recordings were performed in the inactivated structure in each experiment; and to determine the extent of the drug diffusion autoradiographic experiments were carried out. The evolution of the strength of the oscillations was followed using power spectra during the whole recording session. In the first experiment, muscimol injection in the auditory RE totally suppressed the tone-evoked oscillations in the auditory thalamus and cortex. In the second experiment, inactivation of the auditory cortex did not interfere with the presence of tone-evoked oscillations in the auditory RE. In the third experiment, inactivation of the auditory thalamus impaired the oscillations produced by cortical stimulation in the auditory RE. From these results, it appears that both the auditory thalamus and the auditory sector of the RE, but not the auditory cortex, are involved in the generation of stimulus-evoked oscillations in the thalamo-cortical auditory system.

Acoustic Stimulation↗
PubMed1999

Distribution of angiotensin II binding sites in the mouse thalamus: receptor-binding study with fluorescent coupled peptides and their conversion to a light stable product.

Fluorescence-coupled peptides allow a non-radioactive receptor binding study whereby single cells can be examined under a fluorescence microscope. By the combination of such a method with immunohistochemistry, using an HRP-coupled anti-fluorescein antibody, a permanent labeling can be achieved. By using this method the distribution of angiotensin II binding sites has been examined in the mouse thalamus. The results show that a moderate staining was obvious within the thalamus and that the distribution of binding sites in the thalamus is very homogeneous in the mouse brain. In detail, angiotensin II binding sites were found in the anterodorsal nucleus, in the laterodorsal and posterior nucleus of the thalamus, as well as in the lateral geniculate nucleus, the reticular thalamic nucleus and in the zona incerta.

Angiotensin II↗
PubMed2000

Cytoarchitectonic and immunohistochemical characterization of a specific pain and temperature relay, the posterior portion of the ventral medial nucleus, in the human thalamus.

Previous studies in the macaque monkey have identified a thalamic nucleus, the posterior portion of the ventral medial nucleus (VMpo), as a dedicated lamina I spinothalamocortical relay for pain and temperature sensation. The dense plexus of calbindin-immunoreactive fibres that characterizes VMpo in primates enables its homologue to be identified in the human thalamus by immunohistochemical labelling for calbindin. We have now analysed in detail the cytoarchitectonic characteristics of VMpo and its relationship with immunoreactivity for calbindin, substance P and calcitonin gene-related peptide (CGRP) in the human thalamus. The area in the posterolateral thalamus in which dense calbindin-immunoreactive fibre terminations are present coincides nearly completely with a distinct region that contains small to medium-sized cells with round or oval shapes that are aggregated in clusters separated by cell sparse areas. This region, which we identify as VMpo, is located posteromedial to the ventral posterior lateral (VPL) and ventral posterior medial (VPM) nuclei, ventral to the anterior pulvinar and centre médian nuclei, lateral to the limitans and parafascicular nuclei and dorsal to the medial geniculate nucleus. Calbindin-immunoreactive fibres enter VMpo from the spinal lemniscus and form large patches of dense terminal-like staining over clusters of VMpo neurons. A few of these clusters also display terminal-like substance P labelling. Small bursts of CGRP staining are intercalated between the calbindin-labelled clusters, but there is little or no overlap between these two markers. CGRP immunoreactivity is also present over small, non-clustered neurons in the calbindin-negative area that separates VMpo from the VPL and VPM nuclei, which we denote as the posterior nucleus (Po). These observations provide a concise description of VMpo in the human thalamus. Further, they suggest that the lamina I spinothalamic tract fibres (represented by calbindin and probably also substance P immunoreactivity) and vagal-solitary-parabrachial afferents (represented by CGRP immunoreactivity) form closely related, but separate, termination fields that can be considered to represent different aspects of enteroceptive information regarding the physiological status of the tissues and organs of the body. The location of VMpo and the adjacent Po fits with clinical descriptions of the thalamic area from which pain, temperature and visceral sensations can be evoked by microstimulation, and where nociceptive and thermoreceptive neurons have been recorded in humans. It also corresponds to the area in which infarcts cause analgesia and thermoanaesthesia and can lead to the paradoxical development of central pain.

Afferent Pathways↗