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PubMed2001

Corticotropin-releasing hormone messenger RNA distribution and stress-induced activation in the thalamus.

Corticotropin-releasing hormone plays a critical role in mediating the stress response. Brain circuits hypothesized to mediate stress include the thalamus, which plays a pivotal role in distributing sensory information to cortical and subcortical structures. In situ hybridization revealed neurons containing corticotropin-releasing hormone messenger RNA in the posterior thalamic nuclear group and the central medial nucleus of the thalamus, which interfaces with the ventral posteromedial nucleus (parvicellular part). These regions are of interest because they process somatosensory and visceral information. In the first experiment, the effect of acute stress on thalamic corticotropin-releasing hormone messenger RNA levels was assessed. Rats restrained for 1 h and killed 1 h later were found to have increased corticotropin-releasing hormone messenger RNA in the posterior thalamic nuclear group. The time course of these changes was examined in a second experiment in which rats were killed immediately or 3 h after restraint. While no changes occurred in the thalamus immediately after restraint, 3 h after restraint, increases in corticotropin-releasing hormone messenger RNA occurred in both the posterior thalamic nuclear group and the central medial-ventral posteromedial nucleus (parvicellular part) of the thalamus. A different pattern of activation was observed in the paraventricular nucleus of the hypothalamus with increased corticotropin-releasing hormone messenger RNA immediately after restraint, but not 1 or 3 h later. In addition to the stress-induced changes, a prominent decrease in baseline thalamic corticotropin-releasing hormone messenger RNA was observed from 1000 to 1300 h. These results show that the thalamus contains corticotropin-releasing hormone messenger RNA that increases after restraint stress, indicating a role for thalamic corticotropin-releasing hormone systems in the stress response. Stress-induced changes in thalamic corticotropin-releasing hormone messenger RNA expression appears to be regulated differently than that in the paraventricular nucleus of the hypothalamus, and may be influenced by diurnal mechanisms.

Animals↗
PubMed2001

The efferent connections to the thalamus and brainstem of the physiologically defined eye field in the rat medial frontal cortex.

The anterograde tracer Phaseolus vulgaris leucoagglutinin (PHA-L) was injected into sites of the rat frontal eye field (FEF) located in the medial frontal cortex. After a single iontophoretic injection of PHA-L into a FEF site where intracortical microstimulation elicited eye movements, anterogradely labelled fibres and terminal-like elements were found in the thalamus in the anterior nuclei, intralaminar nuclei, lateral portion of the mediodorsal nucleus and posterior nuclear group. In the midbrain and pons, labelled fibres were located in the anterior pretectal area, Darkschewitsch nucleus, superior colliculus and dorsolateral portion of the central gray. When the tracer was injected at the FEF periphery, at a site the stimulation of which evoked both eye and whisker movements, labelling distribution in the thalamus differed from that observed after FEF injections, while a similar distribution was observed in the brainstem. In the thalamus, anterograde labelling was observed in these latter cases in the anterior nuclei, ventral nuclei, medial portion of the laterodorsal nucleus. The present findings point out that the FEF and FEF periphery are connected with numerous subcortical structures of the thalamus and brainstem. In addition, the connections of FEF and FEF periphery with the thalamus differ, whereas the midbrain and pons connections of the two subdivisions share common targets.

Animals↗
PubMed1998

A developmental study of the dopamine D2R receptors in the human basal ganglia and thalamus.

The development of the dopamine D2R receptors (D2R) in the human basal ganglia (BG) and thalamus was investigated in 25 normal brains by means of an immunohistochemical method and Western blotting. Immunoreactivity to D2R was detected in the cytoplasm and dendrites of small and large neurons in the BG and thalamus. D2R-positive neurons were clearly observed at 19 weeks of gestation (GW) in the globus pallidus and thalamus, and at 21 GW in the striatum. The number of D2R-positive neurons gradually increased and reached a peak at 27 GW in the globus pallidus, at 39 GW in the thalamus, and at 1 month of age in the striatum. The number of D2R-positive large neurons in the globus pallidus and small neurons in the striatum decreased after 1 year and about 10 years of age, respectively. Western blotting confirmed the specificity of the immunohistochemistry. Our results suggest that the D2R protein begins to be synthesized at an early fetal stage in the BG and thalamus, and the development of D2R is mostly consistent with neuronal maturation in the BG. D2R may play an important role in regulating the neuronal development of the BG. The decrease in D2R-positive neurons may be related to D2R post-transcriptional regulation.

Adolescent↗
PubMed2004

Functional-anatomical validation and individual variation of diffusion tractography-based segmentation of the human thalamus.

Parcellation of the human thalamus based on cortical connectivity information inferred from non-invasive diffusion-weighted images identifies sub-regions that we have proposed correspond to nuclei. Here we test the functional and anatomical validity of this proposal by comparing data from diffusion tractography, cytoarchitecture and functional imaging. We acquired diffusion imaging data in eleven healthy subjects and performed probabilistic tractography from voxels within the thalamus. Cortical connectivity information was used to divide the thalamus into sub-regions with highest probability of connectivity to distinct cortical areas. The relative volumes of these connectivity-defined sub-regions correlate well with volumetric predictions based on a histological atlas. Previously reported centres of functional activation within the thalamus during motor or executive tasks co-localize within atlas regions showing high probabilities of connection to motor or prefrontal cortices, respectively. This work provides a powerful validation of quantitative grey matter segmentation using diffusion tractography in humans. Co-registering thalamic sub-regions from 11 healthy individuals characterizes inter-individual variation in segmentation and results in a population-based atlas of the human thalamus that can be used to assign likely anatomical labels to thalamic locations in standard brain space. This provides a tool for specific localization of functional activations or lesions to putative thalamic nuclei.

Adult↗
PubMed2005

Effects of human cerebellar thalamus disruption on adaptive control of reaching.

Lesion or degeneration of the cerebellum can profoundly impair adaptive control of reaching in humans. Computational models have proposed that internal models that help control movements form in the cerebellum and influence planned motor output through the cerebello-thalamo-cortical pathway. However, lesion studies of the cerebellar thalamus have not consistently found impairment in reaching or adaptation of reaching. To elucidate the role of the cerebellar thalamus in humans, we studied a group of essential tremor (ET) patients with deep brain stimulation (DBS) electrodes placed in the cerebellar thalamus. The stimulation can be turned on or off remotely and is thought to reduce tremor by blocking the spread of the pathological output from the cerebellum. We studied the effect of thalamic DBS on the ability to adapt arm movements to novel force fields. Although thalamic DBS resulted in a dramatic and significant reduction of tremor in ET, it also impaired motor adaptation: the larger the stimulation voltage, the greater the reduction in rates of adaptation. We next examined ET patients that had undergone unilateral thalamotomy in the cerebellar thalamus and found that adaptation with the contralateral arm was impaired compared with the ipsilateral arm. Therefore, although both lesion and electrical stimulation of the cerebellar thalamus are highly effective in reducing tremor, they significantly impair the ability of the brain to form internal models of action. Adaptive control of reaching appears to depend on the integrity of the cerebello-thalamo-cortical pathway.

Adaptation, Physiological↗
PubMed2003

Protein synthesis in the amygdala, but not the auditory thalamus, is required for consolidation of Pavlovian fear conditioning in rats.

The amygdala is an essential neural substrate for Pavlovian fear conditioning. Nevertheless, long-term synaptic plasticity in amygdaloid afferents, such as the auditory thalamus, may contribute to the formation of fear memories. We therefore compared the influence of protein synthesis inhibition in the amygdala and the auditory thalamus on the consolidation of Pavlovian fear conditioning in Long-Evans rats. Rats received three tone-footshock trials in a novel conditioning chamber. Immediately after fear conditioning, rats were infused intra-cranially with the protein synthesis inhibitor, anisomycin. Conditional fear to the tone and conditioning context was assessed by measuring freezing behaviour in separate retention tests conducted at least 24 h following conditioning. Post-training infusion of anisomycin into the amygdala impaired conditional freezing to both the auditory and contextual stimuli associated with footshock. In contrast, intra-thalamic infusions of anisomycin or a broad-spectrum protein kinase inhibitor [1-(5'-isoquinolinesulphonyl)-2-methylpiperazine, H7] did not affect conditional freezing during the retention tests. Pre-training intra-thalamic infusion of the NMDA receptor antagonist 2-amino-5-phosphonopentanoic acid (APV), which blocks synaptic transmission in the auditory thalamus, produced a selective deficit in the acquisition of auditory fear conditioning. Autoradiographic assays of cerebral [14C]-leucine incorporation revealed similar levels of protein synthesis inhibition in the amygdala and thalamus following intra-cranial anisomycin infusions. These results reveal that the establishment of long-term fear memories requires protein synthesis in the amygdala, but not the thalamus, after auditory fear conditioning. Forms of synaptic plasticity that depend on protein synthesis, such as long-term potentiation, are likely candidates for the encoding and long-term storage of fear memories in the amygdala.

Amygdala↗
PubMed1993

Amino acid levels and gamma-aminobutyric acidA receptors in rat neostriatum, cortex, and thalamus after neonatal 6-hydroxydopamine lesion.

The amino acid gamma-aminobutyric acid (GABA) is the main inhibitory neurotransmitter in brain, and GABAergic neurons have been proposed to play a major role in basal ganglia physiology. In the neostriatum (caudate putamen), medium-sized aspiny interneurons, as well as neostriatal output neurons that project to several brain regions, use GABA as their neurotransmitter. Dopamine fibers arising from the substantia nigra represent a major input to the neostriatum where, besides their classic neurotransmitter role, they are seemingly involved in the regulation of amino acid neurotransmitter release. To further characterize the nature of some of the amino acid/dopamine interactions, selective dopaminergic deafferentations were produced in neonatal rats (3 days postnatal) by intraventricular administration of the neurotoxin 6-hydroxydopamine (6-OHDA); the noradrenergic neurons were protected by prior administration of desmethylimipramine. After a 3-month survival, levels of catecholamines, indoleamines, and amino acids were determined in cingulate cortex, thalamus, and neostriatum. In addition, GABAA receptors were measured in membrane preparations from these three regions, using the specific agonist [3H]muscimol. In the 6-hydroxydopamine-lesioned rats, levels of dopamine and its metabolites homovanillic acid, 3,4-dihydroxyphenylacetic acid, and 3-methoxytyramine were decreased, as expected, in cortex and neostriatum, but remained unmodified in thalamus. In all three regions, serotonin content was increased; its metabolite, 5-hydroxyindole-3-acetic acid, was also elevated, but only in cortex and neostriatum. The levels of GABA were increased in neostriatum and thalamus, but remained unmodified in cortex. Glycine was increased in all three regions examined. There were also increases of phosphatidylethanolamine and serine in thalamus, and of aspartic acid and alanine in neostriatum. The density of GABAA binding sites was increased in neostriatum, but remained unchanged in cortex and thalamus. The changes in amino acid levels and [3H]muscimol binding sites induced by a neonatal 6-hydroxydopamine treatment differ from those found after similar lesions in adult animals, possibly because of the plastic and synaptic rearrangements that can still occur during early postnatal development. The present results also demonstrate that adaptations occur in response to a dopaminergic deafferentation at an early age and that these exhibit a regional specificity.

Amino Acids↗
PubMed1993

Extracellular glutamate is increased in thalamus during thiamine deficiency-induced lesions and is blocked by MK-801.

The current study measured extracellular fluid (ECF) levels of excitatory amino acids before and during the onset of thiamine deficiency-induced pathologic lesions. Male Sprague-Dawley rats were treated with daily pyrithiamine (0.25 mg/kg i.p.) and a thiamine-deficient diet (PTD). Microdialysates were simultaneously collected from probes inserted acutely via guide cannulae into right paracentral and ventrolateral nuclei of thalamus and left hippocampus of PTD and pair-fed controls. Hourly samples were collected from unanesthetized and freely moving animals. Basal levels obtained at a prelesion stage (day 12 of PTD treatment) were unchanged from levels in pair-fed controls. In samples collected 4-5 h after onset of seizures (day 14 of PTD), the levels of glutamate were elevated an average 640% of basal levels in medial thalamus and 200% in hippocampus. Glutamine levels declined, taurine and glycine were elevated, and aspartate, GABA, and alanine were unchanged during this period. Within 7 h after seizure onset glutamine was undetectable in both areas, whereas glutamate had declined to approximately 200% in thalamus and 70% in hippocampus. No significant change in glutamate, aspartate, or other amino acids was observed in dialysates collected from probes located in undamaged dorsal-lateral regions of thalamus. Number of neurons within ventrolateral nucleus of thalamus was significantly greater in PTD animals in which the probe was dialyzed compared with nondialyzed, suggesting that removal of excitatory amino acids was protective. No significant pathologic damage was evident in hippocampus.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗
PubMed2006

Increased thalamus levels of glutamate and glutamine (Glx) in patients with idiopathic generalised epilepsy.

OBJECTIVE: Abnormal thalamo-cortical oscillations underlie idiopathic generalised epilepsy (IGE). Although thalamic involvement has long been indicated by electrophysiological data, it has only recently become feasible to test this with independent methods. In this magnetic resonance (MR) study, we investigated the metabolic and structural integrity of the thalamus. Possible changes in glutamine and glutamate concentrations and signs of neuronal damage were of particular interest. METHOD: Forty three IGE patients and 38 age and sex matched healthy controls were investigated. Quantitative single volume MR spectroscopy (MRS, 1.5 T) was used to measure concentrations of glutamate and glutamine (Glx) and N-acetyl aspartate (NAA) in thalamus and occipital cortex. We also measured thalamic volumes on high resolution gradient-echo images and estimated fractions of thalamic grey and white matter with voxel based morphometry (VBM). RESULTS: IGE patients showed elevated Glx and reduced NAA concentrations in the thalamus compared to controls (12.2+/-2.6 v 8.9+/-4.1 mM, p = 0.0022 for Glx, and 9.9+/-1.0 v 10.7+/-0.9 mM, p = 0.017 for NAA). Thalamic grey matter fraction was reduced in IGE patients, and white matter fraction was increased with the greatest increase in the dorso-medial thalamus. Mean thalamic volume was reduced in patients (6.7+/-0.7 v 7.2+/-0.6 ml in controls, p = 0.0001), as was mean cerebral volume (1163+/-128 v 1250+/-102 ml, p = 0.0003). Patients' thalamus/whole brain ratios were normal. CONCLUSION: Quantitative MRS and VBM provide further evidence for involvement of the thalamus in IGE. The observed elevation of Glx levels together with reductions in NAA levels and grey matter fractions are consistent with epilepsy related excitoxicity as a possible underlying mechanism.

Adult↗
PubMed1992

Responses of neurons in the gracile nucleus of cats to innocuous and noxious stimuli: basic characterization and antidromic activation from the thalamus.

1. Responses to innocuous and noxious mechanical and thermal stimuli were recorded from 90 neurons in the gracile nucleus of anesthetized cats. Cells were tested by antidromic activation for projections to the contralateral ventrobasal thalamus. 2. Cells were characterized broadly by their responses to mechanical stimuli as 1) responding only to tapping (16%), 2) fast-adapting to low-intensity mechanical stimuli (33%), or 3) slowly adapting (51%; most with a fast-adapting component to their responses). All fast-adapting cells and those slowly adapting cells that were tested with noxious heat were further categorized on the basis of their patterns of firing and responses to stimuli. These plus the tap-responsive cells comprised a more restricted sample of 76 categorized cells. 3. Many (22) slowly adapting cells responded to noxious heat (69% of tested slowly adapting cells; 29% of all categorized cells), either on the first application (9 cells) or after sensitization (13 cells), indicating input originating in nociceptors. Nearly all of these (21) responded more to intense pressure than to innocuous pressure. The majority of slowly adapting cells not responsive to noxious heat (5 of 8) or not tested with it (8 of 12) also responded more to intense than to innocuous pressure, suggesting possible input originating in nociceptors. Most cells that responded to noxious heat also had both rapidly and slowly adapting responses with low thresholds. Many were recorded in the range of the cluster region of the gracile nucleus. 4. Cells antidromically activated from the thalamus projected to the rostral part of the ventral posterior lateral nucleus, regardless of their physiological category, and included many with nociceptive input. Latencies of antidromic activation were shorter at more caudal locations in the gracile nucleus, indicating higher conduction velocities to the thalamus. Responses of antidromically activated cells to low-intensity phasic stimuli tended to be greater than those of cells not antidromically activated. 5. Background activity of the neurons was low, most firing at less than one spike/s. Antidromically activated cells had higher background activity than cells not antidromically activated. 6. The results indicate a greater proportion and more widespread distribution of cells with nociceptive input in the cat gracile nucleus than has been previously recognized. Many of these projected to the ventrobasal thalamus, showing that information originating in nociceptors can reach the thalamus through a dorsal column-medial lemniscal pathway in cats.

Adaptation, Physiological↗
PubMed1998

Spike-wave complexes and fast components of cortically generated seizures. I. Role of neocortex and thalamus.

We explored the relative contributions of cortical and thalamic neuronal networks in the generation of electrical seizures that include spike-wave (SW) and polyspike-wave (PSW) complexes. Seizures were induced by systemic or local cortical injections of bicuculline, a gamma-aminobutyric acid-A (GABAA) antagonist, in cats under barbiturate anesthesia. Field potentials and extracellular neuronal discharges were recorded through arrays of eight tungsten electrodes (0.4 or 1 mm apart) placed over the cortical suprasylvian gyrus and within the thalamus. 1) Systemic injections of bicuculline induced SW/PSW seizures in cortex, whereas spindle sequences continued to be present in the thalamus. 2) Cortical suprasylvian injection of bicuculline induced focal paroxysmal single spikes that developed into full-blown seizures throughout the suprasylvian cortex. The seizures were characterized by highly synchronized SW or PSW complexes at 2-4 Hz, interspersed with runs of fast (10-15 Hz) activity. The intracellular aspects of this complex pattern in different types of neocortical neurons are described in the following paper. Complete decortication abolished the seizure, leaving intact thalamic spindles. Injections of bicuculline in the cortex of athalamic cats resulted in similar components as those occurring with an intact thalamus. 3) Injection of bicuculline in the thalamus decreased the frequency of barbiturate spindles and increased the synchrony of spike bursts fired by thalamocortical and thalamic reticular cells but did not induce seizures. Decortication did not modify the effects of bicuculline injection in the thalamus. Our results indicate that the minimal substrate that is necessary for the production of seizures consisting of SW/PSW complexes and runs of fast activity is the neocortex.

Animals↗
PubMed1995

The thalamus of reptiles and mammals: similarities and differences.

Certain aspects of thalamic organization in reptiles and mammals are reviewed. Features shared by the dorsal thalamus of reptiles and that of mammals include projection to the telencephalon, specific and non-specific non-telencephalic afferents, and input from the thalamic reticular nucleus. Differences between the dorsal thalamus of reptiles and that of mammals are the absence of reciprocal telencephalic efferents to the dorsal thalamus and lack of local circuit neurons in reptiles (with the exception of the dorsal geniculate complex in turtles) and their presence in mammals. A thalamic reticular nucleus is present in both reptiles and mammals. In both of these classes of vertebrates, this neuronal aggregate surrounds the dorsal thalamus along its lateral surface, projects to the dorsal thalamus, and is organized into sectors. In one group of reptiles, Caiman crocodilus, the sole reptilian group in which immunocytochemical features have been investigated in detail, the reticular nucleus contains at least three neuronal subpopulations: neurons immunoreactive for glutamic acid decarboxylase (GAD); neurons immunoreactive for parvalbumin; and cells that are not immunoreactive for parvalbumin or, probably, GAD. On the other hand, the reticular nucleus of mammals contains a single population of neurons immunoreactive for GAD, gamma amino butyric acid, and parvalbumin.

Animals↗
PubMed1993

Hypoperfusion and vasoreactivity in the thalamus and cerebellum after stroke.

BACKGROUND AND PURPOSE: Cerebellar hypoperfusion in the contralateral hemisphere after stroke is well studied and termed crossed cerebellar diaschisis. However, studies of hypoperfusion in the ipsilateral thalamus have been few. The purpose of this study was to investigate the prevalence of hypoperfusion and vasoreactivity to acetazolamide in the thalamus and cerebellum after stroke. METHODS: We studied cerebral blood perfusion in the thalamus and cerebellum of 14 patients with unilateral cerebral infarction using [123I]isopropyliodoamphetamine single-photon emission computed tomography (123I-IMP SPECT). We also administered acetazolamide-stressed 123I-IMP SPECT to determine vasodilator capacity in these two areas. Regions of interest were drawn over the bilateral thalami and bilateral cerebellar cortices, and asymmetry indexes were obtained. RESULTS: We found ipsilateral thalamic hypoperfusion in 12 (85.7%) and contralateral cerebellar hypoperfusion in 11 (78.6%) of 14 patients. Hypoperfusion was improved (p < 0.01 by the Wilcoxon signed rank test) in 11 (91.7%) of the 12 patients with ipsilateral thalamic hypoperfusion and in seven (63.6%) of the 11 patients with contralateral cerebellar hypoperfusion. CONCLUSIONS: Hypoperfusion in the ipsilateral thalamus and contralateral cerebellum is common, and vasoreactivity to acetazolamide is preserved in both the thalamus and the cerebellum with hypoperfusion.

Acetazolamide↗
PubMed2003

Effects of alcohol dependence comorbidity and antipsychotic medication on volumes of the thalamus and pons in schizophrenia.

OBJECTIVE: Postmortem and in vivo brain imaging studies have identified abnormalities in the thalamus and the pons in both schizophrenia and alcoholism. The authors sought to determine whether patients with both schizophrenia and alcohol dependence would manifest exaggerated volume deficits in either structure. METHOD: Volumetric measures of the left and right thalamus and the pons were derived from magnetic resonance imaging scans obtained from 27 patients with schizophrenia, 19 patients with schizophrenia and comorbid alcohol dependence, 25 patients with alcohol dependence without comorbid axis I disorders, and 51 healthy comparison subjects. RESULTS: The alcohol-dependent patients had significant volume deficits in both the thalamus and the pons. Among patients with schizophrenia, there were no differences in thalamus volumes between those with and without comorbid alcohol dependence. However, patients with schizophrenia who were taking atypical antipsychotic medications had bilateral thalamic deficits, whereas those taking typical neuroleptics did not. Patients with schizophrenia and comorbid alcohol dependence had deficits in the pons. CONCLUSIONS: Patients with schizophrenia and comorbid alcohol dependence are at risk for alcohol-related reduction of pontine structures that are not necessarily affected by schizophrenia per se. The effect of alcohol dependence on the thalamus in schizophrenic patients may be mitigated by the type of neuroleptic medication they receive.

Adult↗
PubMed2003

Molecular abnormalities of the glutamate synapse in the thalamus in schizophrenia.

Schizophrenia has been associated with dysfunction of glutamatergic neurotransmission. Synaptic glutamate activates pre- and postsynaptic ionotropic NMDA, AMPA, and kainate and metabotropic receptors, is removed from the synapse via five cell surface-expressed transporters, and is packaged for release by three vesicular transporters. In addition, there is a family of intracellular molecules enriched in the postsynaptic density (PSD) that target glutamate receptors to the synaptic membrane, modulate receptor activity, and coordinate glutamate receptor-related signal transduction. Each family of PSD proteins is selective for a given glutamate receptor subtype, the most well characterized being the NMDA receptor binding proteins PSD93, PSD95, NF-L, and SAP102. Besides binding glutamate receptors, many of these proteins also interact with cell surface proteins like cell adhesion molecules, ion channels, cytoskeletal elements, and signal transduction molecules. Given the complexity of the glutamate neurotransmitter system, there are many locations where disruption of normal signaling could occur and give rise to abnormal glutamatergic neurotransmission in schizophrenia. Using multiple cohorts of postmortem tissue, we have examined these synaptic molecules in schizophrenic thalamus. The expression of NR1 and NR2C subunit transcripts is decreased in the thalamus in schizophrenia. Interestingly, three intracellular PSD molecules that link the NMDA receptor to signal transduction pathways are also abnormally expressed. Additionally, several of the cell surface and vesicular transporters are abnormal in the schizophrenic thalamus. While occasional findings of abnormal receptor expression are made, the most dramatic and consistent alterations that we have found in the thalamus in schizophrenia involve the family of intracellular signaling/scaffolding molecules. We propose that schizophrenia has a glutamatergic component that involves alterations in the intracellular machinery that is coupled to glutamate receptors, in addition to abnormalities of the receptors themselves. Our data suggest that schizophrenia is associated with abnormal glutamate receptor-related intracellular signaling in the thalamus, and point to novel targets for innovative drug discovery.

Amino Acid Transport System X-AG↗
PubMed1999

Is the "nonspecific" thalamus still "nonspecific"?

The classical concept of "nonspecific" thalamus, as distinguished from the principal thalamic nuclei (i.e. the primary sensory, motor and limbic relays) is here briefly revisited in the light of anatomical investigations performed in the last decades, and primarily those based on tract tracing techniques. Altogether these data pointed out that the so-called "nonspecific" thalamus is composed by a heterogeneous collection of nuclear masses, which display not only species differences, but also marked internuclear variations in their cytological and neurochemical features, connections, areal and laminar distribution upon the cortex, and functional properties. Thus, the "nonspecific" thalamus exerts a modulatory role on cortical activity, chiefly regulated at the intrathalamic level by the interplay between the thalamic reticular nucleus and the interneurons and projection neurons of the dorsal thalamus. However, each of the components that have been traditionally considered as "nonspecific" also subserves selective roles in the transfer of different kinds of information from the thalamus to the cerebral cortex and basal ganglia.

Animals↗
PubMed2000

Study of projections from the entopeduncular nucleus to the thalamus of the rat.

The entopeduncular nucleus (EP) is a major outflow nucleus of the basal ganglia and innervates the lateral habenula, parafascicular, pedunculopontine, ventrolateral (VL), ventromedial (VM), and mediodorsal thalamic nuclei. This study investigated the morphology of single axons of entopeduncular neurons projecting to the motor thalamus by placing small injections of dextran biotin into the EP and reconstructing drawings of single axons from serial sections. There were two populations of entopeduncular-thalamic projection axons: those that projected only to the motor thalamus (VL and VM) and those that projected to both the motor thalamus and other nuclei (e.g., the habenula). The neurochemistry of EP neurons projecting to the thalamus was investigated by injecting the retrograde tracer FluoroGold into the VL and VM thalamic nuclei to retrogradely fill entopeduncular projection neurons. These were subsequently immunohistochemically labeled for choline acetyl transferase, gamma-aminobutyric acid (GABA), and glutamate. Consistent with previous studies, significant proportions of these neurons were GABA immunoreactive. In addition, approximately half of the entopeduncular-thalamic projecting neurons were found to be cholinergic. This excitatory input is most likely derived from axons that branch as they pass through the motor thalamus to the lateral habenula.

Animals↗
PubMed2004

[Acute onset of somnolence and amnesia due to cerebral infarction of bilateral thalamus accompanied with tuberculous meningitis: a case report].

A 55-year-old man was admitted to our hospital because of somnolence and aspontaneity. He was hospitalized in the psychopathic ward under the initial diagnosis of depression. Chest X-ray showed infiltration in both upper lobe. Twelve days later, Mycobacterium tuberculosis was detected from his sputum and was confirmed by RT-PCR. Cerebrospinal fluid findings showed elevated ADA and mononuclear cells, suggesting the presence of tuberculous meningitis. However, the brain CT revealed no abnormal findings. By applying antituberculous treatment the pulmonary lesion improved but psychological symptoms remained. Three months later follow-up brain MRI was examined. Contrast enhanced granuloma was detected in the ambiens, suprasellar and quadrigeminal cisterns. A strong signal was seen in the left frontal thalamus and a weak enhanced lesion was detected in the right frontal thalamus on a T2 enhanced image. These lesions showed low intensity on a T1 enhanced image, suggesting cerebral infarction affecting the bilateral thalamus. Somnolence and memory disorder was due to cerebral infarction of the bilateral thalamus and tuberculous meningitis contributed to form the intracranial lesion. From the experience of this case, it is needed to consider cerebral infarction (especially the thalamus) due to tuberculous meningitis when we examine the patients with acute onset of psychological symptoms.

Amnesia↗