Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “THALAMUS”

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

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

At least 901 records · Page 50Linked to original sources

Distribution and density of GABA cells in intralaminar and adjacent nuclei of monkey thalamus.

The density of GABA-immunoreactive neurons was examined in the intralaminar and certain principal relay nuclei of the macaque monkey thalamus. Counts were made in 10-microns-thick frozen sections and in 1-micron-thick plastic sections and stereological formulae applied to obtain an accurate assessment of the volumetric density of GABA cells in the nuclei. It was found that GABA-immunoreactive cells account for at least 27% of the cells per unit area of all the thalamic nuclei investigated and up to as much as 50% by unit volume. The intralaminar nuclei show only slightly fewer GABA cells than the principal relay nuclei. Previous reports of their absence or relatively low numbers in the intralaminar nuclei probably stem from their smaller size, relatively weaker immunoreactive staining and from failure to apply stereometric formulae that reveal the density of neurons per volume of tissue. These results suggest that the cellular elements of the intralaminar nuclei are not fundamentally different from those of the principal relay nuclei of the thalamus.

Animals↗

Effect of electrical stimulation of the reticular nucleus of the rat thalamus upon c-fos immunoreactivity in the retrosplenial cortex.

Electrical stimulation of the reticular nucleus of the rat thalamus results in activation of c-fos immunoreactivity in nerve cells of the ipsilateral retrosplenial cortex. The c-fos immunoreactive neurons are mainly concentrated in lamina IV of the retrosplenial cortex. Conversely, electrical stimulation of the retrosplenial cortex induced c-fos immunoreactivity in the ipsilateral reticular nucleus of the thalamus. The results of the electrical stimulation suggest a direct synaptic connection between the cerebral cortex and the ipsilateral reticular thalamic nucleus. Simultaneous immunohistochemical staining proves that the majority of nerve cells and dendro-dendritic terminals in the reticular thalamic nucleus contain parvalbumine and, at the same time, also GABA. The role of GABA-ergic parvalbumine immunoreactive terminals in the reticular thalamic nucleus seems to be related to integration and processing of impulses and attentional gating, distinguishing between noxious and innocuous inputs.

Animals↗

Hypothermia-induced changes of afferent sensory transmission to the VPM thalamus of rats and hamsters.

Effects of hypothermia on the afferent somatosensory transmission to the ventroposteromedial (VPM) thalamus were determined in anesthetized rats and hamsters. Hamsters showed a gradual suppression of afferent sensory transmission during cooling (to 18 degrees C) and disinhibition during subsequent warming of body temperature (Tb). However, rats exhibited steep inhibition from Tb 26 degrees C to complete absence of sensory transmission at Tb 20 degrees C and abrupt disinhibition during subsequent warming. Species difference at thalamic level was quite similar to our previous results in the primary somatosensory (SI) cortex, suggesting that changes of sensory transmission observed in the SI cortex may have already occurred at thalamic level. Differences between the cortex and the thalamus were observed only during deep hypothermia in rat and during the final period of warming in hamster. Conduction latencies of thalamocortical system of both species were not influenced during Tb lowering until 24 degrees C (equivalent to brain temperature 25-26 degrees C). These results suggest inherently different adaptability to hypothermia in processing somatosensory information between hibernator and non-hibernator, but similar sustainability of sensory functions of the thalamocortical system during hypothermia in both species.

Animals↗

A theory of blindsight--the anatomy of the unconscious: a proposal for the koniocellular projections and intralaminar thalamus.

This paper extends the concepts introduced by the theory of premotor relations to unconscious cognitive mechanisms. According to the theory conscious mechanisms are associated with behavioural diversity, whereas unconscious output is proposed to have an obligatory association with stereotypical behaviour. The respective processes are by definition a function of the type of reafferent motor input. Concepts of simple and complex premotor networks are introduced as a means of describing unconscious and conscious processes, respectively. Evidence shows that unconscious cognitive performance differs qualitatively from conscious mechanisms suggesting parallel processes. Although the postulated anatomical substrates for conscious and unconscious processes will function in this model as parallel segregated networks, it is proposed they are distributed throughout the same cortical areas of the brain. Motor reafference is postulated to be mediated via pallidal projections to the thalamic reticular nucleus, which is known to modulate thalamocortical pathways. The role of the koniocellular pathway of the lateral geniculate nucleus remains an enigma and has some properties in common with the well-described magnocellular and parvocellular projections. There is also much speculation about the intralaminar and midline nuclei, the so-called non-specific thalamus. The paper will examine the distinctive features of thalamocortical networks and the role of the koniocellular pathway and intralaminar nuclei (ILN) of the thalamus and suggest that they form a neuroanatomical substrate for the categorizing of unconscious cognitive processes. The ILN has unique projections back to the basal ganglia, which could serve in constraining associated neocortical networks with stereotypical behaviour and thus putative unconscious processing. Only after establishing such a theoretical framework can one hope to successfully analyze the empirical literature on the syndrome of blindsight, of which a detailed account is presented. Blindsight refers to the apparent visual abilities of patients with damage to the striate visual cortex (VI). Patients will 'guess' the shape of an object or reach towards it when presented in the blind field, in spite of denying actually seeing it, i.e., they are unconsciously aware of it. Unlike the magnocellular and parvocellular geniculate pathways the koniocellular extrastriate projections partially conserve retinal information in these patients. Could the proposed network represent an anatomical model of the Freudian subconscious?

Blindness, Cortical↗

Serotonin receptors modulate trigeminovascular responses in ventroposteromedial nucleus of thalamus: a migraine target?

Triptans, serotonin 5-HT(1B/1D), receptor agonists, which are so effective in acute migraine, are considered to act directly on the trigeminovascular system. Using an in vivo model of trigeminovascular nociception, we report a potentially novel action for the triptans within the somatosensory thalamus. Both microiontophoretically applied and intravenous naratriptans potently and reversibly modulate nociceptive neurotransmission by trigeminovascular thalamic neurons in the ventroposteromedial nucleus (VPM) driven by stimulation of the superior sagittal sinus. Naratriptan also suppresses l-glutamate activated trigeminovascular VPM neurons. Co-ejection of naratriptan with the 5-HT(1B/1D) receptor antagonist GR127935 antagonized this effect. (S)-WAY 100135 the 5-HT(1A) receptor antagonist also partially inhibited the effect of naratriptan in the VPM when co-ejected with it. Taken together, the new data suggest a potential effect of triptans in the VPM nucleus of the thalamus acting through 5-HT(1A/1B/1D) mechanisms, and offer an entirely new direction for the development of and understanding of the effects of anti-migraine medicines.

Afferent Pathways↗

Burst firing induces a slow after hyperpolarization in rat auditory thalamus.

The Ca2+-activated slow after hyperpolarization (sAHP) is found in many CNS regions where it may induce post-spike suppression of neuronal firing over many seconds. Nevertheless, the presence of sAHP in sensory thalamus remains uncertain. Here we show that a robust sAHP could be evoked in the rat medial geniculate body of auditory thalamus in vitro following a low-threshold Ca2+ spike and burst firing. The evoked sAHP exhibited kinetic and pharmacological features similar to that found elsewhere in the CNS. The sAHP was resistant to TTX or apamin but eliminated by muscarine. Furthermore, activation of low-threshold Ca2+ conductance alone is sufficient to induce the sAHP. Therefore, the membrane conductance underlying sAHP is functionally expressed in lemniscal thalamic relay neurons which may be preferably activated during burst firing.

Action Potentials↗

The formation of auditory fear memory requires the synthesis of protein and mRNA in the auditory thalamus.

The medial geniculate nucleus of the thalamus responds to auditory information and is a critical part of the neural circuitry underlying aversive conditioning with auditory signals for shock. Prior work has shown that lesions of this brain area selectively disrupt conditioning with auditory stimuli and that neurons in the medial geniculate demonstrate plastic changes during fear conditioning. However, recent evidence is less clear as to whether or not this area plays a role in the storage of auditory fear memories. In the current set of experiments rats were given infusions of protein or messenger RNA (mRNA) synthesis inhibitors into the medial geniculate nucleus of the thalamus 30 min prior to auditory fear conditioning. The next day animals were tested to the auditory cue and conditioning context. Results showed that rats infused with either inhibitor demonstrated less freezing to the auditory cue 24 h after training, while freezing to the context was normal. Autoradiography confirmed that the doses used were effective in disrupting synthesis. Taken together with prior work, these data suggest that the formation of fear memory requires the synthesis of new protein and mRNA at multiple brain sites across the neural circuit that supports fear conditioning.

Acoustic Stimulation↗

Cortical feedback to the thalamus is selectively enhanced by nitric oxide.

The brain somehow merges visual information with the behavioral context in which it is being processed, a task that is often attributed to the cerebral cortex. We have identified a new role of the gaseous neurotransmitter, nitric oxide (NO), in the early selective enhancement of corticogeniculate communication that may participate in this process at the level of the thalamus. Visual information is dynamically gated through the thalamus by brainstem neurons that release acetylcholine and NO. Using in vitro electrophysiology, we characterized NO effects on excitatory postsynaptic potentials and currents (EPSCs) elicited from retinal and cortical pathways in the lateral geniculate nucleus of the ferret. NO selectively and reversibly increased cortically-evoked postsynaptic responses, and this effect was mimicked by cyclic guanosine 3',5'-monophosphate (cGMP). Conversely, NO inhibited retinally-evoked responses independently of cGMP. We demonstrated that these differential effects were specific to postsynaptic N-methyl-d-aspartate (NMDA) receptors by studying treatment effects on pharmacologically isolated EPSCs from each pathway. We propose that when brainstem activity is increased during behavioral arousal or rapid eye movement sleep, NO may increase the relative sensitivity of relay neurons to corticogeniculate feedback. The net effect of these changes in synaptic processing may be to selectively suppress peripheral information while unifying data carried by reentrant corticogeniculate loops with the behavioral context in which the visual information is processed.

Animals↗

Somatotopic reorganization in the brainstem and thalamus following peripheral nerve injury in adult primates.

Injury-induced reorganization of central somatotopic maps is a phenomenon that has proven to be useful for elucidating the mechanisms and time course of neural plasticity. To date, the overwhelming majority of this line of research has focused on such plastic events in cortical areas, at the expense of subcortical structures. In this study, we used multi-unit electrophysiological recording techniques to assess the somatotopic organization of brainstem and thalamic areas following chronic survival from paired median and ulnar nerve section in adult squirrel monkeys. We report that the extent of cutaneously-driven reorganization in both the cuneate nucleus of the brainstem and the ventroposterior lateral nucleus of the thalamus is comparable to that previously documented for area 3b of cortex. These observations are consistent with those previously reported in thalamus, and are unique for brainstem.

Action Potentials↗

Quantitative analysis of glutamic acid decarboxylase-immunoreactive neurons in the anterior thalamus of the human brain.

Local circuit neurons in the human anterior thalamus (AT) were identified on the basis of glutamic acid decarboxylase immunoreactivity (GAD-IR). GAD-IR neurons of the AT displayed small diameter somas with thin, sparsely-branching dendrites, consistent with the morphological characteristics of local circuit neurons found in the thalami of other mammals. Sampling techniques revealed an average of 42% of all neurons within the AT were GAD-IR, one of the highest reported percentages of local circuit neurons in the mammalian thalamus. The presence of high proportion of local circuit neurons in the AT may indicate the extent to which the Papez circuit has evolved within the human brain in comparison to other mammals.

Adult↗

Quantitative comparisons of corticothalamic topography within the ventrobasal complex and the posterior nucleus of the rodent thalamus.

To compare the topographic precision of corticothalamic projections to the ventrobasal (VB) complex and the medial part of the posterior (POm) complex, different anterograde tracers were placed in neighboring parts of the primary (SI) and secondary (SII) somatosensory cortical areas. The location of labeled corticothalamic terminals and their beaded varicosities were plotted, and the digital reconstructions were analyzed quantitatively to determine the extent of overlapping projections from the cortical injection sites. Among animals that received all tracer injections in SI cortex, tracer overlap in the thalamus varied according to the proximity of the cortical injection sites. Regardless of which combination of somatic representations were injected in SI, within each animal the amount of tracer overlap in POm was similar to that observed in VB, and a matched-sample statistical analysis failed to reveal significant differences in the proportion of the labeled regions that contained overlapping projections from the injected cortical sites. Among those animals in which the tracers were injected into the whisker representations of SI and SII, the amount of tracer overlap in the thalamus was not affected by the proximity of the cortical injection sites. Instead, tracer overlap appeared to be related to the degree of somatotopic correspondence. Furthermore, within each of these animals, the amount of tracer overlap in POm was similar to that found in the VB complex. These results indicate that POm has a well-defined topographic organization that is comparable to the degree of topography observed in the VB complex.

Animals↗

Actions of 8-bromo-cyclic-GMP on neurones in the rat thalamus in vivo and in vitro.

The diffusible intercellular messenger nitric oxide may have a modulatory role in the thalamus and this action may be mediated via activation of soluble guanylate cyclase. In order to investigate this possibility, we applied the cyclic-GMP analogue 8-Bromo-cyclic-GMP (8-Br-cGMP) onto neurones in the ventrobasal and lateral geniculate nuclei of the thalamus in anaesthetised rats, and compared its effects with those of a nitric oxide donor. 8-Br-cGMP enhanced the responses of neurones to iontophoretically applied NMDA and AMPA. Furthermore, somatosensory and visual responses of ventrobasal and lateral geniculate neurones were enhanced to 274+/-76% and 217+/-69% of control values, respectively. These effects were similar to those seen with nitric oxide donors in this study and previous work from this laboratory. When applied to thalamic neurones in an in vitro slice preparation, 8-Br-cGMP caused a membrane depolarisation associated with a decrease in input resistance. These findings indicate that activation of guanylate cyclase can cause a membrane depolarisation of thalamic neurones in vitro, and that this effect is sufficient to enhance action responses to ionotropic glutamate receptor stimulation via either exogenous agonists or sensory stimulation.

Action Potentials↗

Infusion of beta-FNA into the thalamus attenuates morphine-induced c-Fos induction in the rat caudate putamen.

The medial thalamus contains mu opioid receptors and sends a glutamatergic projection to the caudate putamen (CPu) in rat. Morphine-induced c-Fos expression in the CPu has been shown to be blocked by pretreatment with antagonists to N-methyl-D-aspartate receptors, indicating the involvement of glutamate in this morphine-induced response. The importance of the glutamatergic projections from the thalamus was assessed by infusing the mu opioid receptor antagonist, beta-funaltrexamine (beta-FNA), prior to systemic morphine injection. Infusion of beta-FNA near specific medial thalamic nuclei attenuated morphine-induced c-Fos expression in the CPu.

Analgesics, Opioid↗

The paraventricular nucleus of the thalamus alters rhythms in core temperature and energy balance in a state-dependent manner.

Exposure to chronic stress facilitates activity within the hypothalamic-pituitary-adrenal (HPA) axis and is associated with enhanced neuronal activity in a discreet set of brain regions, including the posterior division of the paraventricular nucleus of the thalamus (pPVTh). Because HPA function is intimately associated with systems that regulate metabolism, including core temperature and energy balance, we examined the effects of chronic stress on circadian rhythms in temperature, locomotor activity, body weight gain and food intake and adipose depot weights in rats. We also examined the potential role of the pPVTh in mediating these functions using ibotenate lesions of this nucleus. Chronic stress lowered the amplitude of core temperature rhythms, and lesions of the pPVTh blocked this effect in chronically stressed animals, but did not affect the amplitude of temperature rhythms in unstressed controls. In addition, lesions of the pPVTh increased cumulative food intake and overall body weight gain in controls but they increased subcutaneous white adipose depot weight in chronically stressed animals. Thus, the functional paraventricular nucleus of the thalamus appears to inhibit both temperature rhythms and specific white adipose depots only in chronically stressed animals. Together with our previous results, we show that the PVTh affects rhythms in food intake and body weight and is a nexus that differentially regulates core temperature rhythms/HPA activity/specific white adipose depots depending on the stress state of the animal.

Adipose Tissue↗

Autoradiographic study of [3H]flunitrazepam binding sites in the subnuclei of the thalamus of rats rendered tolerant to and dependent on pentobarbital.

We examined changes in benzodiazepine binding sites labeled by [3H]flunitrazepam in five nuclei of the thalamus, the central medial, central lateral, intermediodorsal, ventroposterior, and laterodorsal nuclei, in rats made tolerant to and dependent on pentobarbital. Animals were made tolerant by intracerebroventricular infusion with pentobarbital (300 microg (10 microl)(-1) h(-1) for six days) through pre-implanted cannulae. Pentobarbital dependence was assessed 24 h after abrupt withdrawal from pentobarbital. Pentobarbital-tolerant rats showed no significant change in [3H]flunitrazepam binding sites (Bmax and Kd) in any nucleus examined in the thalamus. In the rats made dependent on pentobarbital, significant increases in the Bmax of [3H]flunitrazepam binding without changes in Kd were noted in central medial and central lateral nuclei. GABAergic (gamma-aminobutyric acid) neurons in the ventrobasal nucleus and in nuclei in the midline group are important in seizure regulation and arousal. These findings suggest that alterations of benzodiazepine receptors in certain nuclei of thalami are involved in the physiological changes induced by pentobarbital dependence. There were no changes in the binding parameters for [3H]flunitrazepam in pentobarbital-tolerant rats.

Animals↗

Direct identification of ventrointermediate nucleus of the thalamus on magnetic resonance and computed tomography images.

OBJECTIVE: The ventro-intermediate (Vim) nucleus of the thalamus is a commonly used target for the treatment of tremor. The thalamic fasciculus contains myelinated fibers, believed to play a role in the generation of tremor, that converge into a dense bundle at the inferior aspect of the Vim nucleus, making it visible on magnetic resonance (MR) and computed tomography (CT) images. This structure, therefore, can be visualized directly and targeted for thalamotomy. METHODS: Thalamotomies were performed on nine patients (who have a follow-up of 13-23 months) with parkinsonian and essential tremors using MR and CT images. The tremor target was hypointense on MR images obtained in inversion recovery sequence and hypointense on CT images. It was therefore visualized, directly targeted, and probed. Stimulation studies were done to physiologically confirm accuracy of the probe placement and then a radiofrequency lesion was made. RESULTS: Stimulation of the target identified as the Vim nucleus on MR and CT images produced responses similar to those expected from the Vim nucleus. After this site was lesioned tremor disappeared in all nine patients. CONCLUSION: The Vim nucleus of the thalamus is visible on MR and CT images. Destruction of this target abolishes parkinsonian and essential tremors.

Aged↗

Training-stage related neuronal plasticity in limbic thalamus and cingulate cortex during learning: a possible key to mnemonic retrieval.

This study is part of an ongoing project concerned with the analysis of the neural substrates of discriminative avoidance learning in rabbits. Multi-unit activity was recorded in 5 anterior and lateral thalamic nuclei and in 4 layers of 2 posterior cingulate cortical areas (29c/d and 29b) during learning. The rabbits learned to step in response to a warning tone to avoid a foot-shock, and to ignore a different tone not followed by shock. Excitatory training-induced unit activity (TIA, increased tone-elicited activity during training relative to a pretraining session with unpaired tone-shock presentations) and/or discriminative TIA (greater discharges to the warning than to the safe tone) developed during training in 11 of the 13 areas. Discriminative TIA in the thalamic nuclei increased monotonically as learning occurred. Anterodorsal (AD) thalamic excitatory TIA peaked in an early stage (the first session of training), laterodorsal thalamic and parvocellular anteroventral (AVp) excitatory TIA peaked in an intermediate stage (the session of the first behavioral discrimination), and magnocellular anteroventral (AVm) and anteromedial (AM) thalamic excitatory TIA peaked in a late stage (the session in which asymptotic behavioral discrimination first occurred). The excitatory TIA in these nuclei declined as training continued beyond the stage in which the peak occurred. Peaks of excitatory TIA developed in area 29c/d of posterior cingulate cortex in the early (layer IV), intermediate (layers I-III and V) and late (layer IV) training stages, as just defined. Only layer IV in area 29b of posterior cingulate cortex exhibited a peak of excitatory TIA, which occurred in the early and intermediate training stages. As in limbic thalamus, discriminative TIA increased monotonically over training stages in layers V and VI of areas 29c/d and in layer VI of area 29b. However, layers I-III and IV in area 29c exhibited peak discriminative TIA in the intermediate and late training stages, respectively. Lesion studies indicate that limbic thalamus and cingulate cortex are essential for learning. The peaks represent a unique topographic pattern of thalamic and cortical excitation elicited by the CS+. It is proposed that the peaks constitute a retrieval pattern, i.e. a unique topographic array of excitation. This pattern encodes the spatio-temporal context which defines the learning situation and is necessary for recall and output of the learned response.

Animals↗

Hypermetabolism in the ventrolateral thalamus in unilateral Parkinsonian resting tremor: a positron emission tomography study.

Tremorogenesis in Parkinson's disease (PD) is assumed to involve a cerebral network including the thalamus. An imaging study was performed on eight PD patients with strictly unilateral resting tremor using fluorodeoxyglucose positron emission tomography coregistered to 3-dimensional magnetic resonance imaging. Increased metabolic activity of high statistical significance (P<0.001) was found in the anterior ventrolateral nuclear group of the thalamus located contralateral to the tremor side. The metabolic changes significantly covaried with tremor amplitudes. For the first time, it could be demonstrated that thalamic metabolic changes associated with tremor in PD are localized in the ventral lateral anterior nucleus (VLa). The results are discussed with respect to previous studies on tremor generation.

Aged↗