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PubMed2002

Whisker maps of neuronal subclasses of the rat ventral posterior medial thalamus, identified by whole-cell voltage recording and morphological reconstruction.

Whole-cell voltage recordings were made in vivo in the ventral posterior medial nucleus (VPM) of the thalamus in urethane-anaesthetised young (postnatal day 16-24) rats. Receptive fields (RFs) on the whisker pad were mapped for 31 neurones, and 10 cells were recovered for morphological reconstruction of their dendritic arbors. Most VPM neurones had antagonistic subthreshold RFs that could be divided into excitatory and inhibitory whiskers. VPM cells comprised different classes, the most frequently occurring being single-whisker excitation (SWE) and multi-whisker excitation (MWE) cells. In SWE cells (36 % of VPM neurones), only principal whisker (PW) deflection evoked an EPSP and was followed by a single action potential (AP) or remained subthreshold. The depolarisation was terminated by a large, delayed IPSP. A stimulus evoked on average 0.74 +/- 0.46 APs (mean +/- S.D.) with short latency (8.1 +/- 1.0 ms) and small temporal scatter (0.31 +/- 0.23 ms dispersion of 50 % of the first APs). In MWE cells (29 % of VPM neurones), deflection of several whiskers evoked EPSPs. PW responses were either subthreshold EPSPs or consisted of an EPSP followed by one or several APs (0.96 +/- 0.99 APs per stimulus). AP responses were often associated with putative low-threshold calcium-dependent regenerative potentials and were followed by a small delayed IPSP. AP responses had a longer latency (12.3 +/- 2.6 ms) and larger temporal scatter (2.5 +/- 1.6 ms) than responses of SWE cells. MWE cells had a lower input resistance than SWE cells. The elongation of dendritic arbors along the representation fields of rows and arcs in VPM barreloids was weakly correlated with the subthreshold RF elongation along whisker rows and arcs, respectively. Evoked EPSP-AP responses exhibited a sharper directional tuning than subthreshold EPSPs, which in turn exhibited a sharper directional tuning than IPSPs. In conclusion, we document two main classes of VPM neurones. SWE cells responded with a precisely timed single AP to the deflection of the PW. In contrast, MWE cell RFs were more broadly tuned and the temporally dispersed multiple AP responses of these cells represented the degree of collective deflection of the PW and several adjacent whiskers.

Action Potentials↗

PubMed2003

Kainate receptor (GluR5)-mediated disinhibition of responses in rat ventrobasal thalamus allows a novel sensory processing mechanism.

Kainate receptors have been studied extensively in vitro, but how they might function physiologically remains unclear. We studied kainate receptor modulation of synaptic responses in the rat ventrobasal thalamus using the novel antagonist LY382884 and the agonist ATPA (selective for GluR5-containing kainate receptors) as tools. No evidence could be found for a direct contribution of kainate receptors to responses of thalamic relay cells to lemniscal (sensory) input in thalamic slices studied with the aid of intracellular and field potential recordings, using selective AMPA and NMDA receptor antagonists and LY382884. However, the GluR5 agonist ATPA reduced the IPSPs originating from the thalamic reticular nucleus. Extracellular single-neurone recordings in anaesthetised rats showed that excitatory responses evoked by physiological vibrissa afferent stimulation were reduced by LY382884 applied iontophoretically at the recording site. This action of the antagonist was occluded when GABA receptors were blocked, indicating that the reduction in excitatory sensory responses by LY382884 is due to an action on GABAergic inhibition arising from the thalamic reticular nucleus. Further experiments showed that these actions depended on whether inhibition was evoked during activation of the excitatory receptive field rather than when inhibition was evoked from a surround vibrissa. We suggest that GluR5 is located presynaptically on inhibitory GABAergic terminals of thalamic reticular nucleus neurones, and that it is normally activated by glutamate spillover from synapses between excitatory afferents and relay neurones during physiological stimulation. We propose that this GluR5-activated disinhibition has an important novel role in extracting sensory information from background noise.

Animals↗

PubMed2006

CaV3.2 is the major molecular substrate for redox regulation of T-type Ca2+ channels in the rat and mouse thalamus.

Although T-type Ca(2+) channels in the thalamus play a crucial role in determining neuronal excitability and are involved in sensory processing and pathophysiology of epilepsy, little is known about the molecular mechanisms involved in their regulation. Here, we report that reducing agents, including endogenous sulfur-containing amino acid l-cysteine, selectively enhance native T-type currents in reticular thalamic (nRT) neurons and recombinant Ca(V)3.2 (alpha1H) currents, but not native and recombinant Ca(V)3.1 (alpha1G)- and Ca(V)3.3 (alpha1I)-based currents. Consistent with this data, T-type currents of nRT neurons from transgenic mice lacking Ca(V)3.2 channel expression were not modulated by reducing agents. In contrast, oxidizing agents inhibited all native and recombinant T-type currents non-selectively. Thus, our findings directly demonstrate that Ca(V)3.2 channels are the main molecular substrate for redox regulation of neuronal T-type channels. In addition, because thalamic T-type channels generate low-threshold Ca(2+) spikes that directly correlate with burst firing in these neurons, differential redox regulation of these channels may have an important function in controlling cellular excitability in physiological and pathological conditions and fine-tuning of the flow of sensory information into the central nervous system.

Animals↗

PubMed1994

Discrimination of speech-like contrasts in the auditory thalamus and cortex.

The neurophysiologic discrimination of acoustic contrasts was investigated as reflected by the mismatch negativity (MMN) response. Evoked responses were recorded from guinea pig thalamus (medial geniculate nucleus) and epidural surface in response to synthesized speech contrasts /ga/-/da/ and /ba/-/wa/. From the caudomedial portion of the medial geniculate nucleus, /ba/-/wa/ elicited a strong mismatch response, whereas /ga/-/da/ did not. Neither stimulus contrast elicited an MMN from the ventral, or primary, portion of medial geniculate. Both stimulus contrasts elicited an MMN from the midline surface. Neither contrast elicited an MMN from the surface over the temporal lobe. Results indicate a hierarchy of processing of the spectrotemporal changes which characterize formant transitions. Also, results indicate that the nonprimary portions of the auditory pathway contribute substantially to the MMN.

Animals↗

PubMed2004

Positive alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor modulators have different impact on synaptic transmission in the thalamus and hippocampus.

Earlier studies showed that positive modulators of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors enhance synaptic responses and facilitate synaptic plasticity. Those studies focused mainly on hippocampal functions. However, AMPA receptors have regionally distinct subunit compositions and thus potencies and efficacies of modulators may vary across the brain. The present study compared the effects of CX546 [1-(1,4-benzodioxan-6-ylcarbonyl) piperidine], a benzamide-type modulator, on synaptic transmission in neurons of the reticular thalamic nucleus (RTN), which regulates the firing mode of relay cells in other thalamic nuclei, and on hippocampal CA1 pyramidal cells. CX546 greatly prolonged synaptic responses in CA1 pyramidal cells, but at the same concentration it had only weak modulatory effects in RTN neurons. Effects on miniature excitatory postsynaptic currents (EPSCs) were similar to those on EPSCs in both regions, suggesting that variations in neuronal morphology and transmitter release kinetics do not account for the differences. Relay cells in the ventrobasal thalamus also exhibited weak modulatory effects that were comparable with those in RTN neurons. Regionally different effects on response duration were also observed with CX516 [BDP-12, 1-(quinoxalin-6-ylcarbonyl)piperidine], a second benzamide drug. In contrast, 100 microM cyclothiazide produced comparable synaptic enhancements in hippocampus and RTN. The regional selectivity of benzamide drugs (ampakines) may be explained, at least in part, by a lower potency at thalamic AMPA receptors, perhaps due to the prevalence of the subunits GluR3 and 4. Although regional preferences of the ampakines were modest in their extent, they may be sufficient to be of relevance when considering future therapeutic applications of such compounds.

Animals↗

PubMed1974

Neural pathways from thalamus associated with regulation of aggressive behavior.

Small electrolytic lesions were made through electrodes in the thalamus of cats at sites where electrical stimulation elicited attack on a rat. Staining by modified Nauta reduced silver methods revealed that significant degeneration passed caudally from the lesions and entered the midbrain dorsal central gray region. Electrical stimulation of this dorsal midbrain region elicited attack on a rat, and destruction of this region suppressed the attack elicited by thalamic stimulation.

Aggression↗

PubMed1999

Reciprocal inhibitory connections and network synchrony in the mammalian thalamus.

Neuronal rhythmic activities within thalamocortical circuits range from partially synchronous oscillations during normal sleep to hypersynchrony associated with absence epilepsy. It has been proposed that recurrent inhibition within the thalamic reticular nucleus serves to reduce synchrony and thus prevents seizures. Inhibition and synchrony in slices from mice devoid of the gamma-aminobutyric acid type-A (GABAA) receptor beta3 subunit were examined, because in rodent thalamus, beta3 is largely restricted to reticular nucleus. In beta3 knockout mice, GABAA-mediated inhibition was nearly abolished in reticular nucleus, but was unaffected in relay cells. In addition, oscillatory synchrony was dramatically intensified. Thus, recurrent inhibitory connections within reticular nucleus act as "desynchronizers."

Animals↗

PubMed1978

Lateralization of norepinephrine in human thalamus.

Norepinephrine has a strongly lateralized distribution in the human thalamus. In the pulvinar region the left hemisphere is rich in norepinephrine, whereas in the somatosensory input area the right hemisphere has a higher concentration of this catecholamine. Such naturally occurring left-right differences in concentration of a neurotransmitter represent a new aspect of hemispheric specialization.

Dopamine↗

PubMed1980

Interaction of laminae of the cingulate cortex with the anteroventral thalamus during behavioral learning.

Neurons in deep laminae of the rabbit cingulate cortex develop discriminative activity at an early stage of behavioral discrimination learning, whereas neurons in the anteroventral nucleus of thalamus and neurons in the superficial cortical laminae develop such activity in a late stage of behavioral learning. It is hypothesized that early-forming discriminative neuronal activity, relayed to anteroventral neurons via the corticothalamic pathway, contributes to the construction of changes underlying the late-forming neuronal discrimination in the anteroventral nucleus. The resultant late discriminative activity in the anteroventral nucleus is then relayed via the thalamocortical pathway back to the superficial cortical laminae, promoting disengagement of cortex from further task-processing.

Animals↗

PubMed1990

Neuronal ceroid-lipofuscinosis: preferential metabolic alterations in thalamus and posterior association cortex demonstrated by PET.

Regional brain glucose utilisation was investigated with positron emission tomography (PET) and fluorodeoxyglucose (FDG) in four siblings with neuronal ceroid-lipofuscinosis. A consistent pattern was found, namely a decrease of glucose utilisation in all grey structures but more marked at the level of the thalamus and posterior association cortex. The severity of metabolic anomalies was correlated with the degree of clinical impairment and with disease duration; they were the most severe in the oldest patient, who was also the most affected clinically, intermediate in two others, and minimal in the subject with the shortest period of development of the disease. These observations suggest that PET is useful for the definition of anatomical targets of metabolic diseases and for the investigation of their pathophysiology.

Age Factors↗

PubMed1993

Evaluation of the effect of treatment on movement disorders in astrocytomas of the basal ganglia and the thalamus.

Twenty patients with movement disorders associated with astrocytomas (grade I-IV according to the WHO tumour classification) of the basal ganglia and the thalamus were evaluated for the effects of treatment. Five patients had more than one movement disorder when the histological diagnosis was verified by stereotactic biopsy. Twelve had tremors, eight hemidystonia, three hemichorea, and one hemichorea/ballismus, and myoclonus respectively. Ten patients died during the follow up period, and for the surviving patients follow up periods ranged from 6-21 years. The movement disorders changed over long periods of time related to therapeutic interventions. CSF shunt operations and percutaneous radiotherapy had no definite effect on the movement disorders. There was a moderate response to medical treatment in a few patients. Stereotactic aspiration of tumour cysts had a marked influence on the movement disorder in two patients, and functional stereotactic surgery abolished tumour induced tremor in one. Interstitial radiotherapy was performed in fifteen patients for treatment of the underlying neoplasm and resulted in different and variable alterations of the movement disorders. These differences may be explained by complex interactions involving structures affected primarily by the tumour, as well as by secondary functional lesions of adjacent structures.

Adolescent↗

PubMed1994

Abnormal movement related potentials in patients with lesions of basal ganglia and anterior thalamus.

Movement-related cortical potentials (MRCPs) were recorded from scalp electrodes during wrist flexion in 15 dystonic patients with bilateral (nine) or unilateral (six) circumscribed lesions in the striatum (eight), pallidum (six), or anterior thalamus (one). The results were compared with those of 10 age-matched healthy volunteers. The early (BP) and late (NS') MRCP components were assessed in terms of their gradients and distribution on the scalp in Cz, C3', and C4'. The gradients of both BP and NS' components were significantly flatter in the patients with bilateral lesions than in the control subjects. Also, the BP gradient was maximum at Cz, and the NS' component was contralaterally predominant in the control subjects but not in the patients. In patients with unilateral lesions, the gradients were flatter (p < 0.05) during movement of the dystonic wrist than during movement of the normal wrist. This difference was significant for BP and NS', regardless of the location of the electrodes. Also, the normal topographic predominance of BP at Cz and of contralateral NS' disappeared. The BP and NS' components of the MRCPs are thought to reflect preparatory activity in the supplementary motor area and the primary motor cortex before movement. Reduced BP and NS' gradients in patients with both bilateral and unilateral lesions of the basal ganglia, which project towards the supplementary motor area, are consistent with this hypothesis. The bilateral nature of these reductions suggests that both the ipsilateral and the contralateral motor cortex are involved in the genesis of the MRCPs and that the dystonia in these patients is associated with impaired motor preparation.

Adult↗

PubMed1994

Unilateral asterixis due to a lesion of the ventrolateral thalamus.

A case of unilateral asterixis in a man with a focal ischaemic lesion of the contralateral ventral thalamus is presented. Atypically, the movements were present at rest and had a pattern of activation that resulted in an initial misdiagnosis of epilepsia partialis continua. This case emphasises the importance of electromyographic analysis in establishing the correct diagnosis of involuntary movements before starting specific treatment.

Aged↗

PubMed1994

Unilateral asterixis due to a lesion of the ventrolateral thalamus.

Aged↗

PubMed2006

Chronic intermittent but not constant hypoxia decreases NAA/Cr ratios in neonatal mouse hippocampus and thalamus.

Chronic constant hypoxia (CCH) and chronic intermittent hypoxia (CIH) are known to have deleterious effects on the central nervous system. Because of the difference in the pattern of hypoxic exposure, it is possible that the pathological outcome would vary. The N-acetyl aspartate/creatine (NAA/Cr) ratio is a reliable marker of neuronal integrity, and this can be noninvasively measured by proton nuclear magnetic resonance spectroscopy. P2 CD1 mouse pups with their dams were exposed to either CCH, where the Fi(O(2)) was maintained at 11% continuously or to CIH, where the Fi(O(2)) was varied between 21 and 11% every 4 min. P30 mice exposed to intermittent hypoxia for 4 wk demonstrated a significant decrease in the NAA/Cr ratio in the hippocampus and thalamus, which was reversed by a subsequent exposure to 4 wk of normoxia. Meanwhile, mice exposed to 4 wk of constant hypoxia did not demonstrate any differences in their NAA/Cr ratios from controls in these brain regions. These results indicate that an intermittent pattern of hypoxic exposure may have a more adverse effect on neuronal function and integrity than a continuous one. The reversal of NAA/Cr levels to baseline during the return to normoxia indicates that therapeutic strategies targeted at alleviating the intermittent hypoxic stress in diseases, such as obstructive sleep apnea, have the potential for inducing significant neurocognitive recovery in these patients.

Animals↗

PubMed1993

Peptides in the parabrachial nucleus modulate visceral input to the thalamus.

The role of neuropeptides in ascending visceral pathways was investigated by recording the changes in the response of thalamic neuronal activity evoked by vagal stimulation before and after peptide injection in the parabrachial nucleus (PB). Male Wistar rats (n = 25) were anesthetized with chloral hydrate and ventilated, and blood pressure and heart rate were continuously monitored. The left cervical vagus nerve was stimulated at submaximal current intensities to elicit changes in single and multiunit activity in the parvocellular visceral relay nuclei in the ventral basal thalamus. Peristimulustime histograms of thalamic activity were made before and after 200-nl injections of peptides or artificial cerebrospinal fluid (CSF) controls in the PB. Injection of calcitonin gene-related peptide (CGRP) at 5 mM or substance P (SP) at 2 mM into the PB significantly attenuated the evoked response of thalamic neuronal activity by 87-100% and 85-100%, respectively. Injections of somatostatin (SOM; 1 mM) did not significantly alter the response evoked by vagal stimulation but significantly inhibited the spontaneous firing of thalamic units, resulting in a 10-fold increase in the response-to-background ratio. This suggests that SOM in the PB inhibits cells in a parallel pathway that terminates on thalamic visceral neurons but that are not part of the ascending visceral sensory pathway. Spontaneous thalamic neuronal activity and vagally evoked responses were significantly enhanced (278-508%) by injection of 1 mM neurotensin (NT) in the PB. Cholecystokinin (CCK) at low doses (0.0002-0.2 mM) attenuated while the highest dose, 2 mM, briefly excited the spontaneous activity of thalamic units before inhibiting their activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Neurotransmitters in the parabrachial nucleus mediating visceral input to the thalamus in rats.

The putative neurotransmitters in ascending visceral pathways were investigated by recording changes in the response of thalamic neuronal activity evoked by vagal stimulation before and after neurotransmitter antagonist injections into the parabrachial nucleus (PB). Male Wistar rats (n = 39) were anesthetized with chloral hydrate and alpha-chloralose, ventilated, and blood pressure and heart rate were continuously monitored. The left cervical vagus nerve was stimulated to elicit changes in single and multiunit activity in the visceral thalamus. Peristimulus-time histograms of thalamic activity were made before and after 200-nl injections of antagonist or control solution into the PB. Synaptic blockade using cobalt (10 mM) injections into the PB inhibited both the thalamic response evoked by vagal stimulation (86-100%) and the spontaneous firing of thalamic neurons (88-92%). Injections of kynurenate (250 mM) or the N-methyl-D-aspartate (NMDA) antagonist, DL-2-amino-5-phosphonopentanoic acid (AP-5; 200 microM), inhibited (87-94% and 92-100%) the thalamic neuronal response evoked by vagal stimulation. The alpha-adrenergic antagonist, phentolamine (0.1 microM), or the specific alpha 2-adrenergic antagonist, yohimbine (0.1 microM), inhibited the spontaneous firing of thalamic units (42-56% and 64-77%) but had no effect on the vagally evoked response. Bicuculline [gamma-aminobutyric acid (GABA) A-subtype antagonist] significantly enhanced spontaneous thalamic neuronal activity (108-125%) without effect on the vagally evoked response. Atropine (0.1 microM) had no significant effect on either the vagally evoked response or the spontaneous firing of thalamic neurons. These results suggest that the relay of visceral afferent sensory information through the PB is mediated by NMDA receptors and that alpha 2 and GABAA receptors contribute to the tonic activity of ventral basal thalamic neurons receiving visceral input.

Amino Acids↗

PubMed1995

Anoxic brain failure in an ectothermic vertebrate: release of amino acids and K+ in rainbow trout thalamus.

The release of excitatory amino acids such as glutamate contributes greatly to anoxic and/or ischemic brain damage in mammals. However, for anoxia-intolerant ectothermic vertebrates, there has been no information on how anoxia affects extracellular amino acid levels, or how such changes relate temporally to major ion movements. We have investigated the effects of environmental anoxia on extracellular amino acid and K+ concentrations in rainbow trout thalamus in vivo at 15 degrees C, using microdialysis and K(+)-selective microelectrodes. Systemic blood pressure was also monitored. In separate experiments, endogenous neurotransmitter release was provoked by perfusing the microdialysis probe with a high-K+ Ringer solution, thereby establishing which amino acids are released by depolarization. Anoxia exposure resulted in the release of several amino acids, including glutamate, aspartate, gamma-aminobutyric acid (GABA), glycine, and taurine. GABA release appeared to be delayed compared with that of glutamate, for example. The loss of ion homeostasis (starting after 23 min) preceded the release of amino acids (starting after > or = 45 min). The amino acid release had no apparent effect on the rate of increase in extracellular K+. Thus, if these events are interrelated, the loss of ion homeostasis is likely to trigger the amino acid release but not vice versa.

Amino Acids↗