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At least 1,225 records · Page 68Linked to original sources
PubMed2006

GABAA receptor alpha 4 subunits mediate extrasynaptic inhibition in thalamus and dentate gyrus and the action of gaboxadol.

The neurotransmitter GABA mediates the majority of rapid inhibition in the CNS. Inhibition can occur via the conventional mechanism, the transient activation of subsynaptic GABAA receptors (GABAA-Rs), or via continuous activation of high-affinity receptors by low concentrations of ambient GABA, leading to "tonic" inhibition that can control levels of excitability and network activity. The GABAA-R alpha4 subunit is expressed at high levels in the dentate gyrus and thalamus and is suspected to contribute to extrasynaptic GABAA-R-mediated tonic inhibition. Mice were engineered to lack the alpha4 subunit by targeted disruption of the Gabra4 gene. alpha4 Subunit knockout mice are viable, breed normally, and are superficially indistinguishable from WT mice. In electrophysiological recordings, these mice show a lack of tonic inhibition in dentate granule cells and thalamic relay neurons. Behaviorally, knockout mice are insensitive to the ataxic, sedative, and analgesic effects of the novel hypnotic drug, gaboxadol. These data demonstrate that tonic inhibition in dentate granule cells and thalamic relay neurons is mediated by extrasynaptic GABAA-Rs containing the alpha4 subunit and that gaboxadol achieves its effects via the activation of this GABAA-R subtype.

Animals↗
PubMed1993

Dynamic and distributed properties of many-neuron ensembles in the ventral posterior medial thalamus of awake rats.

The traditional view that the map of the face in the ventral posterior medial thalamus (VPM) is static and highly discrete was derived largely from qualitative studies that reported only small, robust, and nonoverlapping receptive fields (RFs). Here, by using more quantitative techniques, we have provided evidence for an alternative hypothesis: the RFs in the VPM are large and overlapping and tend to shift as a function of post-stimulus time. These results were obtained through simultaneous recordings of up to 23 single neurons across the whisker representation in the VPM of rats. Under both awake and anesthetized conditions, these neurons responded robustly at short (4-6 ms) and/or long (15-25 ms) latencies to discrete vibromechanical stimulation of single facial whiskers. Computer graphics were used to construct three-dimensional plots depicting the magnitudes of neuronal responses to stimulation of each of several whiskers as a function of post-stimulus time. These "spatiotemporal RFs" demonstrated that (i) the RFs of VPM neurons are quite large, covering up to 20 whiskers and (ii) the spatial locations of these RFs may shift dramatically over the first 35 ms of post-stimulus time, especially from the caudal-most to the rostral-most whiskers on the face. These results suggest that the VPM contains a dynamic and distributed representation of the face, in which stimulus information is coded in both spatial and temporal domains.

Animals↗
PubMed1996

Localization of alpha type II calcium calmodulin-dependent protein kinase at glutamatergic but not gamma-aminobutyric acid (GABAergic) synapses in thalamus and cerebral cortex.

The alpha subunit of type II calcium/calmodulin-dependent protein kinase (CAM II kinase-alpha) plays an important role in longterm synaptic plasticity. We applied preembedding immunocytochemistry (for CAM II kinase-alpha) and postembedding immunogold labeling [for glutamate or gamma-aminobutyric acid (GABA)] to explore the subcellular relationships between transmitter-defined axon terminals and the kinase at excitatory and inhibitory synapses in thalamus and cerebral cortex. Many (but not all) axon terminals ending in asymmetric synapses contained presynaptic CAM II kinase-alpha immunoreactivity; GABAergic terminals ending in symmetric synapses did not. Postsynaptically, CAM II kinase-alpha immunoreactivity was associated with postsynaptic densities of many (but not all) glutamatergic axon terminals ending on excitatory neurons. CAM II kinase-alpha immunoreactivity was absent at postsynaptic densities of all GABAergic synapses. The findings show that CAM II kinase-alpha is selectively expressed in subpopulations of excitatory neurons and, to our knowledge, demonstrate for the first time that it is only associated with glutamatergic terminals pre- and postsynaptically. CAM II kinase-alpha is unlikely to play a role in plasticity at GABAergic synapses.

Animals↗
PubMed1997

Representation of sound localization cues in the auditory thalamus of the barn owl.

Barn owls can localize a sound source using either the map of auditory space contained in the optic tectum or the auditory forebrain. The auditory thalamus, nucleus ovoidalis (N.Ov), is situated between these two auditory areas, and its inactivation precludes the use of the auditory forebrain for sound localization. We examined the sources of inputs to the N.Ov as well as their patterns of termination within the nucleus. We also examined the response of single neurons within the N.Ov to tonal stimuli and sound localization cues. Afferents to the N.Ov originated with a diffuse population of neurons located bilaterally within the lateral shell, core, and medial shell subdivisions of the central nucleus of the inferior colliculus. Additional afferent input originated from the ipsilateral ventral nucleus of the lateral lemniscus. No afferent input was provided to the N.Ov from the external nucleus of the inferior colliculus or the optic tectum. The N.Ov was tonotopically organized with high frequencies represented dorsally and low frequencies ventrally. Although neurons in the N.Ov responded to localization cues, there was no apparent topographic mapping of these cues within the nucleus, in contrast to the tectal pathway. However, nearly all possible types of binaural response to sound localization cues were represented. These findings suggest that in the thalamo-telencephalic auditory pathway, sound localization is subserved by a nontopographic representation of auditory space.

Acoustic Stimulation↗
PubMed1999

Molecular characterization of a slowly gating human hyperpolarization-activated channel predominantly expressed in thalamus, heart, and testis.

Rhythmic activity of neurons and heart cells is endowed by pacemaker channels that are activated by hyperpolarization and directly regulated by cyclic nucleotides (termed HCN channels). These channels constitute a multigene family, and it is assumed that the properties of each member are adjusted to fit its particular function in the cell in which it resides. Here we report the molecular and functional characterization of a human subtype hHCN4. hHCN4 transcripts are expressed in heart, brain, and testis. Within the brain, the thalamus is the predominant area of hHCN4 expression. Heterologous expression of hHCN4 produces channels of unusually slow kinetics of activation and inactivation. The mean potential of half-maximal activation (V(1/2)) was -75.2 mV. cAMP shifted V(1/2) by 11 mV to more positive values. The hHCN4 gene was mapped to chromosome band 15q24-q25. The characteristic expression pattern and the sluggish gating suggest that hHCN4 controls the rhythmic activity in both thalamocortical neurons and pacemaker cells of the heart.

Amino Acid Sequence↗
PubMed2003

A role for the thalamus in memory for unique entities.

Recent case studies of amnesic patients have yielded patterns of impairment that challenge Tulving's (1972) division of retrograde memory into two categories (namely, episodic and semantic memory). Here we describe a patient (JG) who developed partially blocked access to previously stored knowledge following the onset of a medial thalamic infarction. Having previously demonstrated that JG has a dense, pervasive amnesia for autobiographical material, famous people and famous events (Miller et al. , 2001), in this study, we show that he is unable to access information about unique entities across a range of domains. In contrast, his memory for more general semantic knowledge (such as word meanings) is intact. JG's memory impairment is discussed in the context of a model of neural functioning put forward by Damasio (1990), in which it was proposed that recall of unique entities depends on many cortical regions being activated in synchrony. This activity, thought to be triggered and coordinated by anterior temporal and frontal lobe regions is, in turn, modulated by projections from the thalamus. We propose that JG's thalamic lesion has disrupted the coordination of the diffuse cortical networks necessary to generate highly specific memories from the past, be they episodic or semantic.

Acoustic Stimulation↗
PubMed1999

Differential expression of acetylcholinesterase in the brainstem, ventrobasal thalamus and primary somatosensory cortex of perinatal rats, mice, and hamsters.

Acetylcholinesterase (AChE) is transiently expressed by thalamocortical axons in the rat, and staining for this enzyme has been used extensively to study the development of thalamocortical projections. In the present study, patterns of AChE staining were compared in the trigeminal brainstem, thalami and primary somatosensory cortices of perinatal rats, mice, and hamsters. As previously reported, the ventral posteromedial nucleus (VPM) of rats showed dense AChE staining from P-0 at least through P-8. The ventral posterolateral nucleus (VPL) contained heavy AChE staining at least through P-60. In the cortex, there was also dense AChE staining which was organized somatotopically in patches similar to those observed with other methods such as cytochrome oxidase (CO) staining. However, by adulthood, AChE staining revealed a negative image of the CO staining pattern in lamina IV. In the mouse and hamster, there was dense AChE staining inVPL from P-0 through adulthood, but VPM was much less heavily stained for this enzyme. Moreover, the staining in VPL of mice was markedly reduced after transection of axons that travel to the thalamus in the medial lemniscus, suggesting that much of it was contained in these afferent fibers. In the cortices of both perinatal and adult mice and hamsters, AChE staining yielded a negative image of the somatotopically organized patches demonstrable with CO staining. This negative image was apparent by P-2 in the mouse and P-4 in the hamster. These results document a dramatic species difference with respect to the expression of AChE in the thalami and cortices of developing rodents. The differences between the patterns observed in rats vs mice and hamsters probably reflect the fact that cortical AChE in the latter species is not contained in thalamocortical afferents arising from either VPM or VPL.

Acetylcholinesterase↗
PubMed1981

Brain-stem auditory-evoked potentials recorded directly from human brain-stem and thalamus.

Brain-stem auditory-evoked potentials were recorded in neurosurgical patients from surface electrodes applied to the VIIIth nerve, medulla, pons, midbrain and cortex; from depth electrodes in the thalamus; and from a movable electrode in the IVth, IIIrd, and lateral ventricles. The potentials recordable over the scalp within 10 ms after click stimulation are characterized by a slow positive wave (peaking at 5 to 6 ms) and a negative wave (8 to 10 ms) with 7 small positive wavelets superimposed upon them. The sources of these components have been identified by observing their increased amplitude in depth recordings, and by tracing the potentials from their intracranial maxima to the scalp. Wave I is generated within the most distal portion of the VIII nerve; Wave V in the midbrain (inferior colliculus); and Wave VI the medial geniculate body. Both low positive and negative components have their origins in the inferior colliculus. Intracranially-recorded brain-stem auditory-evoked potential showed very rapid changes in amplitude within the brain-stem but only slight changes in the more rostral regions, although their amplitude gradients varied in the different components. They also demonstrated minor but systematic shifts in latency with distance from the potential sources, reflecting a significant overlap of separate potentials. This effect must be taken into account in the interpretation of a 'concurrent' intracranial potential as the source of a far-field surface-recorded potential.

Auditory Pathways↗
PubMed1997

Synchronized activities of coupled oscillators in the cerebral cortex and thalamus at different levels of vigilance.

The cerebral cortex and thalamus constitute a unified oscillatory machine displaying different spontaneous rhythms that are dependent on the behavioral state of vigilance. In vivo multi-site recordings from a variety of neocortical areas and related thalamic nuclei in cat, including dual simultaneous intracellular recordings, demonstrate that corticofugal volleys are effective in synchronizing fast (20-50 Hz) and low-frequency (< 15 Hz) oscillations in thalamocortical networks, characterizing activated and de-afferented states. (i) Fast spontaneous oscillations depend on the depolarization of thalamic and cortical cells and appear in a sustained manner during waking and REM sleep. Corticothalamic neurons, discharging high-frequency (400 Hz) spike-bursts at 30-40 Hz, are good candidates to synchronize fast oscillations in reentrant thalamocortical loops. Weakly synchronized, fast spontaneous oscillations may be reset and become robustly coherent after relevant sensory stimuli in waking or internal signals during the dreaming state. (ii) During quiescent sleep, the long-range synchronization of brain electrical activity results from synchronous hyperpolarizations in forebrain neurons. The corticothalamic inputs during the depolarizing component of the slow oscillation (< 1 Hz) are effective in grouping the thalamic-generated sleep rhythms (spindles at 7-14 Hz and delta at 1-4 Hz) into complex wave-sequences. These inputs also control the shape of spindles, and favor the long-range synchronization and nearly simultaneous appearance of spindles. (iii) The cortical control of thalamic activity is also demonstrated in spike-wave-seizures developing from sleep patterns. More than half of thalamocortical neurons are silent during spike-wave seizures, being tonically hyperpolarized, and display IPSPs (closely related to the paroxysmal depolarizing shifts of cortical cells) that are determined by the pattern of activities in thalamic reticular cells. All these data congruently show the power of cortical control upon thalamic oscillators.

Animals↗
PubMed2005

Distribution of activity across the monkey cerebral cortical surface, thalamus and midbrain during rapid, visually guided saccades.

To examine the distribution of visual and oculomotor activity across the macaque brain, we performed functional magnetic resonance imaging (fMRI) on awake, behaving monkeys trained to perform visually guided saccades. Two subjects alternated between periods of making saccades and central fixations while blood oxygen level dependent (BOLD) images were collected [3 T, (1.5 mm)3 spatial resolution]. BOLD activations from each of four cerebral hemispheres were projected onto the subjects' cortical surfaces and aligned to a surface-based atlas for comparison across hemispheres and subjects. This surface-based analysis revealed patterns of visuo-oculomotor activity across much of the cerebral cortex, including activations in the posterior parietal cortex, superior temporal cortex and frontal lobe. For each cortical domain, we show the anatomical position and extent of visuo-oculomotor activity, including evidence that the dorsolateral frontal activation, which includes the frontal eye field (on the anterior bank of the arcuate sulcus), extends anteriorly into posterior principal sulcus (area 46) and posteriorly into part of dorsal premotor cortex (area 6). Our results also suggest that subcortical BOLD activity in the pulvinar thalamus may be lateralized during voluntary eye movements. These findings provide new neuroanatomical information as to the complex neural substrates that underlie even simple goal-directed behaviors.

Animals↗
PubMed2006

Hemispheric asymmetry for auditory processing in the human auditory brain stem, thalamus, and cortex.

We report evidence for a context- and not stimulus-dependent functional asymmetry in the left and right human auditory midbrain, thalamus, and cortex in response to monaural sounds. Neural activity elicited by left- and right-ear stimulation was measured simultaneously in the cochlear nuclei, inferior colliculi (ICs), medial geniculate bodies (MGBs), and auditory cortices (ACs) in 2 functional magnetic resonance imaging experiments. In experiment 1, pulsed noise was presented monaurally to either ear, or binaurally, simulating a moving sound source. In experiment 2, only monaural sounds were presented. The results show a modulation of the neural responses to monaural sounds by the presence of binaural sounds at a time scale of tens of seconds: In the absence of binaural stimulation, the left and right ICs, MGBs, and ACs responded stronger to stimulation of the contralateral ear. When blocks of binaural stimuli were interspersed in the sound sequence, the contralateral preference vanished in those structures in the right hemisphere. The resulting hemispheric asymmetry was similar to the asymmetry demonstrated for spatial sound processing. Taken together, the data demonstrate that functional asymmetries in auditory processing are modulated by context. The observed long time constant suggests that this effect results from a "top-down" mechanism.

Acoustic Stimulation↗
PubMed1977

Synaptic vesicle fraction devoid of adenosine triphosphatase activity from bovine caudatolenticular nuclei and thalamus.

1. As a part of studies on the mechanism by which catecholamines are released from the nerve terminals, the synaptic vesicle fraction was isolated from bovine caudatolenticular nuclei and thalamus by differential centrifugation essentially according to the method of Kadota and Kadota (17). 2. Further centrifugation on a sucrose density gradient of the synaptic vesicle fraction by the method of Whittaker et al. (1) yielded white materials on the upper portion of 0.4 M sucrose, which consisted of vesicles averaging 600-800 A in diameter, and did not show Mg2+-dependent ATpase activity. On the other hand, the denser materials centering on 0.6 M sucrose, consisting of a mixture of microsomes and synaptic vesicles of 400-500 A diameter, showed an ATpase activity activated by either Mg2+ or Ca2+ but not inhibited by ouabain. 3. The white materials on 0.4 M sucrose were almost free of mitochondria, but they contained a large amount of non-heme iron, as reported elsewhere (2). Furthermore, the protein components analyzed on SDS-polyacrylamide gels were similar to those already reported for purified synaptic vesicles (3). 4. Based on these results, the white materials were assumed to be synaptic vesicles devoid of Mg2+-dependent ATPase activity.

Adenosine Triphosphatases↗
PubMed2002

Proton magnetic resonance spectroscopy (1H MRS) in schizophrenia: investigation of the right and left hippocampus, thalamus, and prefrontal cortex.

Single voxel proton magnetic resonance spectroscopy (1H MRS) was used to study the metabolites N-acetylaspartate (NAA), choline (CHO), and myo-inositol (ml) in order to test a neurodegenerative hypothesis in schizophrenia (decrease of NAA, increase of CHO, and increase of ml) and a cerebral asymmetry of these metabolites. 1H MRS was performed in 17 schizophrenia patients and 14 healthy subjects in three cerebral areas highly involved in the pathophysiology of schizophrenia (the prefrontal cortex, the thalamus, and the hippocampus). The ratio amplitudes between metabolites and creatine plus phosphocreatine (Cr) were determined. No difference in the metabolites existed between patients and healthy subjects. However, relationships were noted between NAA/Cr and age in the thalami of the schizophrenia patients (r = -0.37; p = 0.14) and healthy subjects (r = -0.52; p = 0.05). A significant correlation was observed between NAA/Cr and age of onset of illness in the hippocampi of schizophrenia patients (r = -0.59; p < 0.05). Moreover, NAA/Cr was lower in the right than in the left prefrontal cortex in both schizophrenia patients and healthy subjects. There was no relationship between the metabolites and duration of illness or dose of antipsychotics. These findings might suggest a neurodegenerative process in the hippocampi of schizophrenia patients with late onset of illness, and the NAA/Cr ratio could be a marker of aging in the thalami.

Adult↗
PubMed1999

d-Fenfluramine produces neuronal degeneration in localized regions of the cortex, thalamus, and cerebellum of the rat.

d-Fenfluramine is a potent serotonin (5-HT) reuptake inhibitor/releaser and, until its recent recall, was prescribed as an anoretic agent. This study demonstrates that 10 mg/kg d-fenfluramine i.p., when administered to rats in a warm (27 degrees C) environment, produces neuronal degeneration within select brain regions. Degeneration was detected and localized using a recently developed fluorescent marker of neuronal degeneration, Fluoro-Jade. The most extensive cortical damage was in the anterior cingulate region. In the medial thalamus, degeneration was frequently seen within the intralaminar nuclei, and somewhat less frequently observed within the paraventricular nucleus, the mediodorsal nucleus, and the gelatinosis nucleus. Cerebellar damage occurred primarily in medial Purkinje cells and occasionally in granule cells or basket cells. Degeneration was not observed in either saline-injected control animals or in rats given even higher doses of 25 mg/kg d-fenfluramine but kept in a cooler environment (23 degrees C). The degeneration was clearly most prominent in animals with body temperatures of 41 degrees to 42 degrees C, but this degeneration was not seen in animals given saline that became extremely hyperthermic in a 37 degrees C environment. Behavioral signs such as tremors, myoclonus, rigidity, and splayed legs were seen in all animals with extensive neurodegeneration. The areas damaged by d-fenfluramine, when hyperthermia occurs, could play a role in the expression of the serotonin syndrome. Elevated extracellular 5-HT levels alone are probably not sufficient for neurotoxicity, and additional factors such as hyperthermia, regional specificity of 5-HT receptor subtypes, blood flow, and/or neuronal networks may be involved.

Animals↗
PubMed2004

A maternal blood-borne factor promotes survival of the developing thalamus.

In this report, we describe the identification of a polypeptide survival-promoting factor that is produced by maternal and early postnatal peripheral blood mononuclear cells (PBMCs) of the immune system in Long-Evans rats and humans. The factor, termed Y-P30, most likely arises from proteolytic processing of a larger precursor protein and accumulates mainly in pyramidal neurons of the developing cortex and hippocampus but not in astrocytes. It was released from neurons grown in culture and substantially promotes survival of cells in explant monocultures of perinatal thalamus from the offspring. Y-P30 mRNA was not detectable in infant or adult brain and was present only in blood cells of pregnant rats and humans but not in nonpregnant controls. However, Y-P30 transcription could be induced in PBMCs of adult animals by a central nervous system lesion (i.e., optic nerve crush), which points to a potential role of the factor not only in neuronal development but also in neuroinflammation after white matter injury.

Animals↗
PubMed1997

Electrophysiological study of the connection between medial thalamus and anterior cingulate cortex in the rat.

We characterized the neuronal properties of the anterior cingulate cortex (ACC) evoked by electrical stimulation of the medial thalamus (MT). MT stimulation sites were found by their neuronal responses to noxious stimuli. Of 487 units identified histologically in the rat ACC, 94% were activated trans-synaptically at different areas of the ACC. Six percent of MT-evoked ACC units were activated antidromically and all of these units projected to a specific nucleus of MT. We suggest that MT nuclei mediate different aspects of nociceptive information to specific ACC areas, and that nociceptive information in the MT is modulated reciprocally by activities from the ACC.

Animals↗
PubMed2000

Nicotinic receptor subunit mRNA in the thalamus of the rat: relevance to schizophrenia?

Recent evidence suggests that aberrant nicotinic receptor (nAChR) expression plays an important role in schizophrenia. The present study sought to examine the distribution of nAChRs within the thalamus and associated cholinergic structures by examining nAChR subunit mRNA expression using in situ hybridization histochemistry. Transcripts for alpha4 and beta2 subunits were found in high levels in all thalamic nuclei and at lower levels in cholinergic nuclei (PPTg and MS/VDB). Distribution of mRNA encoding for additional subunits was restricted; lower alpha3 subunit transcript levels were detected in the anterior thalamic nuclei and portions of the lateral and posterior thalamic nuclei, with alpha7 transcripts being detected in cholinergic nuclei, the IMD and very low levels in the RTN. Low levels of alpha6 and beta3 transcript were found only within the RTN.

Animals↗
PubMed2004

Dopaminergic effects of caffeine in the human striatum and thalamus.

Epidemiological studies have provided evidence that caffeine, an adenosine receptor antagonist, reduces the risk for Parkinson's disease. There are indications of specific interactions between striatal adenosine A(2A) and dopamine D(2) receptors, but the in vivo effects of caffeine on human dopamine system have not been investigated. In the present study, the dopaminergic effects of caffeine were examined with [(11)C]raclopride positron emission tomography (PET) in eight healthy habitual coffee drinkers after 24 h caffeine abstinence. Compared to oral placebo, 200 mg oral caffeine induced a 12% decrease in midline thalamic binding potential (p < 0.001). A trend-level increase in ventral striatal [(11)C]raclopride binding potential was seen with a correlation between caffeine-related arousal and putaminal dopamine D(2) receptor binding (r = -0.81, p = 0.03). The findings indicate that caffeine has effects on dopaminergic neurotransmission in the human brain, which may be differential in the striatum and the thalamus.

Adult↗