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PubMed2000

Distribution of GABA(B) receptor protein in somatosensory cortex and thalamus of adult rats and during postnatal development.

In the present study we report the immunolocalisation of gamma-aminobutyric acid (GABA)(B) receptors within the cerebral somatosensory cortex (S1) and thalamus of adult and young (1-22 postnatal days) rats. The antibody used recognises a peptide in the carboxy-terminal domain and therefore did not distinguish between the different isoforms GABA(B)1a or GABA(B)1b. The results showed that GABA(B) receptor protein was widely distributed in the brain of both adult and young rats, with different degrees of labelling in separate cerebral nuclei. Antibody labelling was localised both on cells and the neuropil. In the cerebral cortex of adult animals the highest immunolabelling was evident in layers V and VIb, although immunoreactivity was also present in the superficial layers. The strongest signal was evident in the medial habenula.The thalamus showed labelling in the reticular, ventrobasal and geniculate nuclei. In the first postnatal days GABA(B) expression was evident in the cortical cells of layer V, VIb and in the cortical plate. The pattern of labelling in the cerebral cortex of young rats became indistinguishable from that of adult rats by day 12. In the thalamus, the main difference compared to the adult pattern was observed in the mediodorsal nucleus which, in early development, showed a high immunosignal, however, by postnatal day 22 the immunoreactivity decreased with only some scattered cells labelled in the adult brain.

Aging↗
PubMed1999

Do auditory responses recorded from awake animals reflect the anatomical parcellation of the auditory thalamus?

Previous studies performed in anesthetized animals have shown differences between the acoustic responses of neurons recorded from the different divisions of the medial geniculate body (MGB). This study aimed at determining whether or not such differences are also expressed when neurons are recorded from awake animals. The auditory responses of 130 neurons of the auditory thalamus were determined in awake, restrained guinea pigs while the state of vigilance of the animals was continuously monitored. There were significantly more 'on' phasic evoked responses and significantly fewer 'non-responsive' or 'labile' cells in the ventral division of the MGB (MGv) than in the other divisions. The response latencies and the variability of the latencies were smaller in the MGv than in the other divisions. The tuning of the neurons obtained from MGv and from the lateral part of the posterior complex were significantly sharper than those coming from the dorsal division of the MGB and the medial division. The mean threshold and the percentage of monotonic vs. non-monotonic intensity functions were not different in the subdivisions of the auditory thalamus. When compared with previous studies, the quantifications of the acoustic responses obtained in the present study gave values that differed from those reported under deep anesthesia, but were close to those reported under light anesthesia. Lastly, even if none of the physiological characteristic makes it possible, by itself, to determine the locus of recordings in the auditory thalamus, we conclude that the physiological characteristics of the evoked responses obtained in MGv differ from those of other divisions.

Acoustic Stimulation↗
PubMed2001

Reduced NAA in the thalamus and altered membrane and glial metabolism in schizophrenic patients detected by 1H-MRS and tissue segmentation.

Functional and structural abnormalities in the thalamus as well as a generalized phospholipid membrane disorder have been implicated in the pathogenesis of schizophrenic psychosis. To determine whether thalamic neuronal abnormalities and altered membrane-associated metabolites can be detected in schizophrenic patients, we used in vivo proton magnetic resonance spectroscopy (1H-MRS) in 32 acutely-ill, medicated schizophrenic patients and 17 age-matched controls. Thalamic and white matter metabolite concentrations (myo-inositol (mI), choline-containing compounds (Cho), total creatine (Cr) and N-acetylaspartate (NAA)) were estimated and corrected for atrophy (CSF) and gray and white matter contributions (GM, WM) by use of image-based voxel segmentation. Thalamic NAA was significantly reduced in schizophrenic patients, whereas Cho and mI were significantly increased in the parietal white matter. White matter Cr was significantly elevated in patients and correlated positively with the brief psychiatric rating scores (BPRS). Regional metabolite levels were inversely associated with GM and WM content reaching significance for mI and Cr in the thalamus and Cho and NAA in the white matter. Reduced NAA in the left thalamus of schizophrenic patients confirms and extends previous spectroscopic data and agrees well with histologic and imaging findings of reduced neuronal density and volume. Elevated Cho in line with 31P-MRS studies suggests increased myelin degradation thus further supporting a generalized membrane disorder in schizophrenic patients. In addition, we demonstrate the need to correct metabolite concentrations for regional tissue composition in studies employing patients with altered brain morphology.

Adult↗
PubMedDate not supplied

Modelling corticothalamic feedback and the gating of the thalamus by the cerebral cortex.

Morphological studies have shown that excitatory synapses from the cortex constitute the major source of synapses in the thalamus. However, the effect of these corticothalamic synapses on the function of the thalamus is not well understood because thalamic neurones have complex intrinsic firing properties and interact through multiple types of synaptic receptors. Here we investigate these complex interactions using computational models. We show first, using models of reconstructed thalamic relay neurones, that the effect of corticothalamic synapses on relay cells can be similar to that of afferent synapses, in amplitude, kinetics and timing, although these synapses are located in different regions of the dendrites. This suggests that cortical EPSPs may complement (or predict) the afferent information. Second, using models of reconstructed thalamic reticular neurones, we show that high densities of the low-threshold Ca2+ current in dendrites can give these cells an exquisite sensitivity to cortical EPSPs, but only if their dendrites are hyperpolarized. This property has consequences at the level of thalamic circuits, where corticothalamic EPSPs evoke bursts in reticular neurones and recruit relay cells predominantly through feedforward inhibition. On the other hand, with depolarized dendrites, thalamic reticular neurones do not generate bursts and the cortical influence on relay cells is mostly excitatory. Models therefore suggest that the cortical influence can either promote or antagonize the relay of information, depending on the state of the dendrites of reticular neurones. The control of these dendrites may therefore be a determinant of attentional mechanisms. We also review the effect of corticothalamic feedback at the network level, and show how the cortical control over the thalamus is essential in co-ordinating widespread, coherent oscillations. We suggest mechanisms by which different modes of corticothalamic interaction would allow oscillations of very different spatiotemporal coherence to coexist in the thalamocortical system.

Animals↗
PubMedDate not supplied

Astrocytes, spontaneity, and the developing thalamus.

Recent studies in the ventrobasal (VB) thalamus have shown that astrocytes display spontaneous intracellular calcium [Ca(2+)](i) oscillations early postnatally. [Ca(2+)](i) oscillations are correlated in groups of up to five astrocytes, and propagate between cells. NMDA receptor-mediated, long lasting inward currents in thalamocortical (TC) neurons of the VB complex are correlated to [Ca(2+)](i) increases in neighbouring astrocytes, and stimulation of astrocytic [Ca(2+)](i) increases also lead to inward currents in neurons. These findings suggest that astrocytes are spontaneously active and can induce neuronal activity, a reversal of the previously held view of neuron-glia interactions in the central nervous system. This activity occurs at an important period in the development of the thalamus and therefore suggests a potential functional role in a variety of processes. Along with data on the neurotransmitter receptor repertoire of thalamic astrocytes these findings enlarge the body of knowledge on astrocytes in the thalamus, and further contribute to the emerging field of astrocyte-neuron and neuron-astrocyte interactions in the central nervous system.

Animals↗
PubMed1996

A comparison of temporal decay in place memory tasks in rats (Rattus norvegicus) with lesions affecting thalamus, frontal cortex, or the hippocampal system.

Three experiments compared the effects of lesioning areas of thalamus, cortex, and the hippocampal system on delayed matching (DMTS) and nonmatching (DNMTS) to sample. Temporal decay was measured by comparing performances at different retention intervals (RIs) for rats trained to stability. Lesions of the lateral-internal medullary lamina site in thalamus and the medial wall area in frontal cortex produced impairments that were significantly greater than for lesions of the mediodorsal nucleus in thalamus, the fornix, or the dorsal hippocampus. The effects of lesions on temporal decay differed depending on how RIs were manipulated. When RIs were manipulated within training sessions, the DMTS and DNMTS impairments were delay independent (i.e., none of the lesions increased the rate of temporal decay). When RIs were manipulated between sessions, thalamic lesions were associated with an increase in the rate of temporal decay of DNMTS.

Animals↗
PubMed1991

Role of thalamus and white matter in cognitive outcome after head injury.

Local CBF (LCBF) and local partition coefficients (L lambda) were measured by xenon-enhanced computed tomography among 15 patients with remote cerebral trauma resulting from severe head injury. Results were compared with similar measures among age-matched normal volunteers (N = 20). The patients were divided into two groups according to different outcomes based on serial cognitive testing: Group I (N = 10) improved but Group D (N = 5) deteriorated throughout a mean interval of 10 years of follow-up. Initial LCBF measurements were performed at mean intervals of 6.8 years after injury. Cortical LCBF values were decreased in frontal (p less than 0.01) and temporal (p less than 0.05) regions among both groups, but only in Group D were flow values decreased in putamen and thalamus (p less than 0.05). L lambda values were reduced in frontotemporal cortex among both groups but in the thalamus only among Group D (p less than 0.05). Mean white matter flow values were normal in Group I but were reduced in Group D (p less than 0.05). Mean partition coefficients for white matter were reduced in both groups (p less than 0.01) but were lower in Group D (p less than 0.05). Reduced perfusion of frontotemporal gray matter is consonant with neuropathological reports following severe brain trauma of neuronal atrophy, gliosis, and infarction affecting these regions. Group comparisons between patients who cognitively improved versus those that deteriorated demonstrate an association between reductions of CBF in putamen, thalamus and subcortical white matter and impaired cognition after severe head injury.

Adolescent↗
PubMed2005

Auditory thalamus integrates visual inputs into behavioral gains.

By binding multisensory signals, we get robust percepts and respond to our surroundings more correctly and quickly. How and where does the brain link cross-modal sensory information to produce such behavioral advantages? The classical role of sensory thalamus is to relay modality-specific information to the cortex. Here we find that, in the rat thalamus, visual cues influence auditory responses, which have two distinct components: an early phasic one followed by a late gradual buildup that peaks before reward. Although both bimodal presentation and reward value had similar effects on behavioral performance, the cross-modal effect on neural activity showed unique temporal dynamics: it affected the amplitude of the early component and starting level of the late component, whereas reward value affected only the slope of the late component. These results demonstrate that cross-modal cueing modulates gain in the sensory thalamus, potentially providing a priming influence on the choice of an optimal behavior.

Acoustic Stimulation↗
PubMed2005

Inactivation of the central thalamus delays self-timed saccades.

The central thalamus transmits corollary discharge signals for eye movement control, but its role in eye movement generation remains uncertain. Inactivation of the paralaminar part of the ventrolateral thalamus delayed the initiation of contraversive saccades, particularly during a new memory-guided saccade task that required self-triggering of the movement. The results suggest that signals through the thalamus regulate the timing of self-initiated saccades.

Animals↗
PubMed2004

Abnormalities of the NMDA Receptor and Associated Intracellular Molecules in the Thalamus in Schizophrenia and Bipolar Disorder.

Several lines of investigation support a hypothesis of glutamatergic dysfunction in schizophrenia, including our recent reports of altered NMDA receptor subunit and associated intracellular protein transcripts in the thalamus of elderly patients with schizophrenia. In the present study, we used in situ hybridization to measure the expression of NMDA subunits (NR1, NR2A-D), and associated intracellular proteins (NF-L, PSD95, and SAP102) in a second, younger cohort from the Stanley Foundation Neuropathology Consortium, which included patients with both schizophrenia and affective disorders. We wanted to determine whether glutamatergic abnormalities in the thalamus in schizophrenia are present at younger ages, and whether these abnormalities occur in other psychiatric illnesses. In the present work, we observed increased expression of NMDA NR2B subunit transcripts, and decreased expression of all three associated postsynaptic density protein transcripts in schizophrenia. We also found evidence of glutamatergic dysfunction in the thalamus in affective disorders, particularly in bipolar disorder. In particular, we found decreased NF-L, PSD95, and SAP102 transcripts in bipolar disorder, and decreased SAP102 levels in major depression. Interestingly, one of the most consistent findings across diagnostic groups was an abnormality of intracellular signaling molecules that are linked to the NMDA receptor, rather than changes in the receptor subunits themselves. PSD95 and similar scaffolding molecules link the NMDA receptor with intracellular enzymes that mediate signaling, and also provide a physical link between different neurotransmitter systems to coordinate and integrate information from multiple effector systems. Abnormalities of PSD95-like molecules and other intracellular signaling machinery may contribute to dysregulated communication between multiple neurotransmitter systems (such as glutamatergic and dopaminergic systems) that are potentially involved in the neurobiology of schizophrenia and affective disorders.

Adult↗
PubMed2001

Involvement of the cerebellar thalamus in human saccade adaptation.

Saccade adaptation can be experimentally induced by systematically displacing a visual cue during a targeting saccade. Non-human primate studies have highlighted the crucial role of the cerebellum for saccade adaptation, but its neural substrates in humans are poorly understood. Recent physiological experiments suggest that, in addition to cerebellar structures, cortical areas may be involved as well. We have therefore hypothesized that saccade adaptation may rely on a cerebello-cerebral network, in which the cerebellar thalamus may link cerebellar and cerebral structures. To test this hypothesis, we studied saccade adaptation in a group of four patients with a thalamic lesion, with (n = 2) or without (n = 2) involvement of the cerebellar thalamus. Compared to healthy subjects, saccade adaptation was reduced in patients with associated cerebellar syndrome, but normal in patients without cerebellar syndrome. These results are consistent with the hypothesis that cerebello-thalamic pathways contribute to saccade adaptation in humans and suggest that the thalamus relays adaptation-related information from the cerebellum to cerebral cortical oculomotor areas.

Adaptation, Physiological↗
PubMed2001

The midline thalamus: alterations and a potential role in limbic epilepsy.

PURPOSE: In limbic or mesial temporal lobe epilepsy, much attention has been given to specific regions or cell populations (e.g., the hippocampus or dentate granule cells). Epileptic seizures may involve broader changes in neural circuits, and evidence suggests that subcortical regions may play a role. In this study we examined the midline thalamic regions for involvement in limbic seizures, changes in anatomy and physiology, and the potential role for this region in limbic seizures and epilepsy. METHODS: Using two rat models for limbic epilepsy (hippocampal kindled and chronic spontaneous limbic epilepsy) we examined the midline thalamus for evidence of involvement in seizure activity, alterations in structure, changes in the basic in vitro physiology of the thalamic neurons. We also explored how this region may influence limbic seizures. RESULTS: The midline thalamus was consistently involved with seizure activity from the onset, and there was significant neuronal loss in the medial dorsal and reuniens/rhomboid nuclei. In addition, thalamic neurons had changes in synaptically mediated and voltage-gated responses. Infusion of lidocaine into the midline thalamus significantly shortened afterdischarge duration. CONCLUSIONS: These observations suggest that this thalamic region is part of the neural circuitry of limbic epilepsy and may play a significant role in seizure modulation. Local neuronal changes can enhance the excitability of the thalamolimbic circuits.

Anatomy, Cross-Sectional↗
PubMed2002

Chronic anterior thalamus stimulation for intractable epilepsy.

PURPOSE: A significant number of patients with epilepsy remain poorly controlled despite antiepileptic medication (AED) treatment and are not eligible for resective surgery. Novel therapeutic methods are required to decrease seizure burden in this population. Several observations have indicated that the anterior thalamic region plays an important role in the maintenance and propagation of seizures. We investigated neuromodulation of the anterior thalamus by using deep-brain stimulation (DBS) in patients with intractable seizures. METHODS: Five patients with medically refractory epilepsy underwent stereotactic placement of and received stimulation through bilateral DBS electrodes in the anterior thalamus. RESULTS: Treatment showed a statistically significant decrease in seizure frequency, with a mean reduction of 54% (mean follow-up, 15 months). Two of the patients had a seizure reduction of > or =75%. No adverse effects were observed after DBS electrode insertion or stimulation. Unexpectedly, the observed benefits did not differ between stimulation-on and stimulation-off periods. CONCLUSIONS: DBS of the anterior thalamus is a safe procedure and possibly effective in patients with medically resistant seizures.

Adult↗
PubMed2005

The effect of risperidone on metabolite measures in the frontal lobe, temporal lobe, and thalamus in schizophrenic patients. A proton magnetic resonance spectroscopy (1H MRS).

OBJECTIVE: The aim of the study was the evaluation of risperidone effect on metabolite measures in the frontal lobe, temporal lobe and thalamus in schizophrenic patients on the basis of proton magnetic resonance spectroscopy ( (1)H MRS). METHODS: A group of 14 patients with the diagnosis of schizophrenia, according to DSM-IV, were examined in the study. The patients were examined twice, once after a period of at least 7 days without neuroleptics and for the second time at least 4 weeks after stable risperidone doses. RESULTS: The significant differences in the metabolite levels before and after the treatment were observed only in thalamus: an increase in myoinositol (mI) and N-acetylaspartate (NAA) levels. Positive symptoms before the treatment correlated positively with NAA level in the frontal lobes and negatively in the temporal lobes. Negative symptoms before the treatment correlated positively with Glx (a common signal for GABA, glutamine and glutamate) level in the temporal lobes. CONCLUSION: Our results seem to confirm the influence of risperidone on the brain metabolism, specifically in the region of thalamus.

Adult↗
PubMed1994

Neuropathological findings in the brain of Karen Ann Quinlan. The role of the thalamus in the persistent vegetative state.

BACKGROUND: Karen Ann Quinlan had a cardiopulmonary arrest in 1975 and died 10 years later, having never regained consciousness. Her story prompted a national debate about the appropriateness of life-sustaining treatment in patients who are in a persistent vegetative state and led to the development of medicolegal guidelines for the care of such patients. This report describes the neuropathologic features of Quinlan's brain. METHODS: The entire brain and spinal cord were systematically sampled for histologic examination. The brain stem and central cerebrum were embedded en bloc and serially sectioned. Three-dimensional computer reconstructions helped visualize the topographic features of the lesions. RESULTS: Contrary to expectation, the most severe damage was not in the cerebral cortex but in the thalamus, and the brain stem was relatively intact. The neuropathological findings included extensive bilateral thalamic scarring, bilateral cortical scars primarily in the occipital pole and parasagittal parieto-occipital region, and bilateral damage to cerebellar and focal-basal-ganglia regions. The brain stem and basal forebrain and the hypothalamic components of the ascending arousal systems and brainstem regions critical to cardiac and respiratory control were undamaged. The lesions were consistent with hypoxia-ischemia after the cardiopulmonary arrest. CONCLUSIONS: Although the neuropathological findings in the case of Karen Ann Quinlan were complex, the disproportionately severe damage in the thalamus as compared with the cerebral cortex supports the hypothesis that the thalamus is critical for cognition and awareness and may be less essential for arousal.

Adult↗
PubMed2003

Change of conduction velocity by regional myelination yields constant latency irrespective of distance between thalamus and cortex.

The widely spanning sensory cortex receives inputs from the disproportionately smaller nucleus of the thalamus, which results in a wide variety of travelling distance among thalamic afferents. Yet, latency from the thalamus to a cortical cell is remarkably constant across the cortex (typically, approximately 2 ms). Here, we found a mechanism that produces invariability of latency among thalamocortical afferents, irrespective of the variability of travelling distances. The conduction velocity (CV) was calculated from excitatory postsynaptic currents recorded from layer IV cells in mouse thalamocortical slices by stimulating the ventrobasal nucleus of the thalamus (VB) and white matter (WM). In adults, the obtained CV for VB to WM (CV(VB-WM); 3.28 +/- 0.11 ms) was approximately 10 times faster than that of WM to layer IV cells (CV(WM-IV); 0.33 +/- 0.05 ms). The CV(VB-WM) was confirmed by recording antidromic single-unit responses from VB cells by stimulating WM. Exclusion of synaptic delay from CV(WM-IV) did not account for the 10-fold difference of CV. By histochemical staining, it was revealed that VB to WM was heavily myelinated, whereas in the cortex staining became substantially weaker. We also found that such morphological and physiological characteristics developed in parallel and were accomplished around postnatal week 4. Considering that VB to WM is longer and more variable in length among afferents than is the intracortical region, such an enormous difference of CV makes conduction time heavily dependent on the length of intracortical region, which is relatively constant. Our finding may well provide a general strategy of connecting multiple sites irrespective of distances in the brain.

Aging↗
PubMed1987

Origin of short latency somatosensory evoked potential in cats: especially potentials derived from thalamus and cortex.

Short latency somatosensory evoked potential (SSEP) was recorded in cats to identify the potentials originating from the cortex and the thalamus, and the following results were obtained. When SSEP was elicited on the bregma by stimulation of the contralateral superficial radial nerve, P2, P4, P4.5, P5.5, P7, P8, N8.5, P11, P9.5, N11.5, N12.5 and N14 were recognized. Of these components N11.5, N12.5 and N14 consisted of large negative potential (LNP). When KCl was applied to the sensorimotor cortex to induce spreading depression, the positive component of the primary evoked potential was markedly decreased and the negative component disappeared. In SSEP, components preceding N8.5 were unchanged. N8.5-P11 and P11-N12.5, however, markedly diminished or disappeared. The latency of the first component of the field potential recorded in the VPL nucleus of the thalamus was about 5 ms. When a small amount of Nembutal was injected into VPL nucleus, components between P2 and P4.5 remained unchanged, but P5.5 disappeared. P7, P8 and N8.5 were preserved. The amplitude of N8.5-P11 was markedly decreased and LNP disappeared. From these results, among various components of SSEP, P5.5 should originate from the thalamus, and P7, P8 and N8.5 from the extralemniscal system. N8.5-P11 should mainly represent post-synaptic potential (PSP) in the deep somatic layer, and P11-N12.5 represent PSP in the apical dentrites of the sensorimotor cortex. N14 probably represents PSP via the diffuse projection system. Thus, LNP should consist of complex potentials of specific and non-specific sensory systems.

Animals↗
PubMed2005

The role of the human thalamus in processing corollary discharge.

Corollary discharge signals play an important role in monitoring self-generated movements to guarantee spatial constancy. Recent work in macaques suggests that the thalamus conveys corollary discharge information of upcoming saccades passing from the superior colliculus to the frontal eye field. The present study aimed to investigate the involvement of the thalamus in humans by assessing the effect of thalamic lesions on the processing of corollary discharge information. Thirteen patients with selective thalamic lesions and 13 healthy age-matched control subjects performed a saccadic double-step task in which retino-spatial dissonance was induced, i.e. the retinal vector of the second target and the movement vector of the second saccade were different. Thus, the subjects could not rely on retinal information alone, but had to use corollary discharge information to correctly perform the second saccade. The amplitudes of first and second saccades were significantly smaller in patients than in controls. Five thalamic lesion patients showed unilateral deficits in using corollary discharge information, as revealed by asymmetries compared with the other patients and controls. Three patients with lateral thalamic lesions including the ventrolateral nucleus (VL) were impaired contralaterally to the side of damage and one patient with a lesion in the mediodorsal thalamus (MD) was impaired ipsilaterally to the lesion. The largest asymmetry was found in a patient with a bilateral thalamic lesion. The results provide evidence for a thalamic involvement in the processing of corollary discharge information in humans, with a potential role of both the VL and MD nuclei.

Adult↗