Thalamic Sensory Relay Nuclei Research Articles

Vaginal allodynia as the presentation of a thalamic tumor

Central pain syndromes associated with damage to the thalamic sensory relay nuclei have been described predominantly in the stroke literature; however, pain syndromes associated with thalamic neoplasms are much less common. We describe a woman with dyspareunia secondary to vaginal allodynia as the presenting sign of a left thalamic juvenile pilocytic astrocytoma. Subsequent to an uneventful stereotactic biopsy, her vaginal allodynia progressed to hemi-body allodynia. We believe that this is the first reported case of isolated vaginal allodynia associated with a thalamic neoplasm or any other structural pathology of the central nervous system.Dyspareunia secondary to vaginal allodynia as the presenting sign of a left thalamic juvenile pilocytic astrocytoma is reported, in a rare case underscoring that thalamic pathology including neoplasms should be considered in evaluating patients with longstanding and unexplained pain syndromes.

Thalamic sensory relay nucleus stimulation and phantom limb pain

Thalamic sensory relay nucleus stimulation and phantom limb pain

Thalamic Sensory Relay Nucleus Stimulation for the Treatment of Peripheral Deafferentation Pain

We applied chronic deep brain stimulation (DBS) of the thalamic nucleus ventralis caudalis (Vc) for the treatment of peripheral deafferentation pain. The subjects included 11 cases of phantom limb pain and 7 of root or nerve injury pain without phantom sensation. In the phantom limb pain patients, the spike density markedly increased in the same area of the Vc where microstimulation induced paresthesia in the part with phantom sensation. Reorganization of the receptive field representation within the Vc was also demonstrated by microrecording and microstimulation. In the root or nerve injury pain patients with severe allodynia and without phantom sensation, oscillating neural hyperactivity appeared when the allodynia was induced during single-cell recording in the Vc. In both groups stimulation of these areas with the DBS electrode was useful for achieving pain reduction. Inhibition of spinothalamic tract neurons, restoration of the original receptive field representation and modulation of thalamocortical rhythmic oscillations are proposed to play important roles in a possible mechanism of Vc-DBS for the treatment of deafferentation pain.

Cyto- and chemoarchitecture of the dorsal thalamus of the monotreme Tachyglossus aculeatus, the short beaked echidna

We have examined the cyto- and chemoarchitecture of the dorsal thalamus of the short beaked echidna ( Tachyglossus aculeatus), using Nissl and myelin staining, immunoreactivity for parvalbumin, calbindin, calretinin and non-phosphorylated neurofilament protein (SMI-32 antibody), and histochemistry for acetylcholinesterase and NADPH diaphorase. Immunohistochemical methods revealed many nuclear boundaries, which were difficult to discern with Nissl staining. Parvalbumin immunoreactive somata were concentrated in the ventral posterior, reticular, posterior, lateral and medial geniculate nuclei, while parvalbumin immunoreactivity of the neuropil was present throughout all but the midline nuclei. Large numbers of calbindin immunoreactive somata were also found within the midline thalamic nuclei, and thalamic sensory relay nuclei. Immunoreactivity for calretinin was found in many small somata within the lateral geniculate “a” nucleus, with other labelled somata found in the lateral geniculate “b” nucleus, ventral posterior medial and ventral posterior lateral nuclei. Immunoreactivity with the SMI-32 antibody was largely confined to somata and neuropil within the thalamocortical relay nuclei (ventral posterior medial and lateral nuclei, lateral and medial geniculate nuclei and the posterior thalamic nucleus). In broad terms there were many similarities between the thalamus of this monotreme and that of eutheria (e.g. disposition of somatosensory thalamus, complementarity of parvalbumin and calbindin immunoreactive structures), but there were some unique features of the thalamus of the echidna. These include the relatively small size of the thalamic reticular nucleus and the preponderance of calbindin immunoreactive neurons over parvalbumin immunoreactive neurons in the ventral posterior nucleus.

Calcium-Binding Proteins in the Turtle Thalamus. Analysis in the Light of Hypothesis of the “Core-Matrix” Thalamic Organization in Relation to the Problem of Homology of Thalamic Nuclei among Amniotes

Distribution of immunoreactivity (IR) to Ca-binding proteins (CaBPr) (calbindin, Calb, parvalbumin, Parv., and calretinin, Calr) was studied in the thalamus of the Central Asian terrestrial turtles (Testudo horsfieldi) and fresh water turtles (Emys orbicularis). There has been established a wide spread of these proteins, which combines overlapping and a relative alternation of distribution of different CaBPr in individual nuclei. A comparison of IR was made in two relay nuclei of the visual system, GLd and Rot. Both nuclei had IR to all CaBPr, but with different degree of intensity. In the terrestrial turtles, the amounts of Calb-, Parv-, and Calr-IR neurons in the cellular plate of the GLd were close. In this plate and in the neuropil part of this nucleus there was observed CaBPr-innervation of various density. Calr-IR neurons in the GLd of the fresh water turtles dominated over Parv- and Calb-IR neurons, whose detection varied significantly. In Rot, a clear predominance of Calb-IR neurons was shown over Parv- and Calr-IR cells by constancy of their detection, the number (1.5–2-fold higher), and intensity of the immune label, as well as the highest density of Calb and Parv innervation. The character of IR in the Rot was similar in the both turtle species. In the auditory and somatic relay thalamic nuclei and in the non-sensory anterior thalamic nuclei (Dma, Dla) there were present neurons and terminals with IR to all CaBPr without any predominance of Parv-IR in the relay nuclei and Calb-IR in the anterior thalamic nuclei. The constant and characteristic feature of Enta in the turtles of both species is a dense population of Parv-IR neurons, whose topography and cellular composition coincide with those of population of GABA-IR neurons in this nucleus. The data obtained have shown that the alternative presence of different CaBPr in the relay sensory and non-sensory thalamic nuclei, which has been established as a characteristic feature of the mammalian thalamus, is not characteristic at all of turtles. It seems that in the course of evolution there occurred a reorganization of distribution of different CaBPr in thalamic nuclei of amniotes due to changes of their functional loading. The reptilian thalamic sensory relay nuclei are likely to be represented mainly by less specific parts comparable with Calb-IR matrix of specific nuclei in the higher amniotes (mammals), while their more specialized (core) Parv-IR regions are formed later in evolution. Therefore, the distribution of Parv- and Calb-IR neurons in the turtle thalamic nuclei cannot be a criterion at evaluation of homology of thalamic nuclei in amniotes, but permits judging about the degree of their specialization.

Striatal input from the ventrobasal complex of the rat thalamus.

We have analyzed whether caudal regions of the caudate putamen receive direct projections from thalamic sensory relay nuclei such as the ventrobasal complex. To this aim, the delivery of the retrograde neuroanatomical tracer Fluoro-Gold into the caudal caudate putamen resulted in the appearance of retrogradely labeled neurons in the ventral posteromedial and ventral posterolateral thalamic nuclei. These projections were further confirmed with injections of the anterograde tracers biotinylated dextran amine or Phaseolus vulgaris leucoagglutinin into these thalamic nuclei, by showing the existence of axonal terminal fields located in the caudal striatum. These results support the existence of direct projections linking the thalamic ventrobasal complex and the caudal striatum in the rat, probably via collateralization of thalamocortical axons when passing through the caudate putamen, and therefore supporting the putative involvement of the caudal striatum in sensory-related functions.

A functional hypothesis for LGN-V1-TRN connectivities suggested by computer simulation.

We employ computer simulation to investigate the function of neural circuitries between thalamic sensory relay nuclei, primary sensory cortices, and the thalamic reticular nucleus (TRN). Computational similarities exist between these circuits and the architecture of a simple artificial neural network. We impose processing parameters on this network architecture in keeping with anatomical and physiological details of the mammalian geniculo-cortical visual pathway, and then run the simulation on a task involving multiple simultaneous inputs from the simulated visual field. After two to three loops through the simulation, activity in cortical and thalamic units whose receptive fields include the stronger stimulus remains constant, while activity in other cortical and thalamic units activated by weaker stimuli declines toward resting values. These results suggest that the modeled neural circuitry functions to "prime" selective attentional mechanisms further up the visual streams toward specific portions of the total visual stimulus. Besides extending existing models and evidence about the function of these neural circuits, our results also provide physiologists with predicted activity profiles of thalamic and cortical elements of the modeled neural system for a task not yet studied experimentally.

Glutamate in thalamic fibers terminating in layer IV of primary sensory cortex

Biochemical and pharmacological experiments support glutamate (Glu) as a thalamocortical transmitter, but do not distinguish direct from indirect effects (via excitation of glutamergic corticocortical fibers); anatomical studies to date have yielded variable results. We identified thalamocortical terminals in layer IV of primary somatic sensory, auditory, and visual cortex by injecting WGA-HRP in the corresponding thalamic sensory relay nuclei of rats. Terminals from each thalamic nucleus were similar, containing abundant mitochondria and loosely packed clear vesicles; they made asymmetric synaptic contacts mainly with dendritic spines. After tracer injections into nearby regions of cortex, most terminals also made asymmetric contacts mainly onto spines, but these corticocortical terminals were smaller, containing sparse mitochondria and densely packed clear vesicles. GABAergic terminals (identified by postembedding immunogold staining) made symmetric synapses mainly onto dendritic shafts; those terminating near thalamocortical terminals were also large and contained abundant mitochondria. To determine whether Glu is enriched in thalamocortical terminals, we performed postembedding double-labeling immunocytochemistry for Glu and GABA, using different gold particle sizes. The density of particles coding for Glu was significantly enriched over identified thalamocortical terminals, in comparison to nearby dendrites, astrocytes, and GABAergic terminals, and this enrichment was similar for all three sensory areas. The degree of enrichment in thalamocortical terminals, but not in GABAergic terminals, was linearly related to vesicle density. We conclude that Glu is likely to be a neurotransmitter for thalamocortical relay neurons.

Distribution of GAP-43 mRNA in the adult rat brain.

Regional distribution of gene expression of the axonal growth-associated protein, GAP-43, was studied in adult rat brains by in situ hybridization autoradiography to determine the features of mature neuronal populations that synthesize GAP-43 protein. Such synthesis appears to correlate with axonal growth during maturation and regrowth after axotomy. In most adult neurons, the sharp decline in GAP-43 gene expression implies a reduced capacity for axonal growth. Neurons capable of extending axonal knobs in the absence of injury may indicate a "plasticity" underlying dynamic processes of interaction between neurons and their synaptic targets. Antisense and sense (control) riboprobes were used on serial sections in the three principal axes, and the magnitude of hybridization signal was examined to determine regional patterns. GAP-43 mRNA levels are pronounced in diverse neuronal groups including the locus coeruleus, raphé nn., dopaminergic nigral and ventral tegmental nn., mitral cells, hippocampal CA3, inferior olivary n., vagal motor n. and other parasympathetic preganglionic neurons, select thalamic midline and intralaminar nn., several specific nn. of the hypothalamus and basal forebrain, the granular layer of cerebellar cortex, the infragranular neocortex, and the granular olfactory paleocortex; there is a substantial range in the magnitude of expression. Regions revealing minimal signal include most thalamic sensory relay nuclei, the granule neurons of the olfactory bulb and dentate gyrus, and the caudate and putamen. Possible concomitants of GAP-43 expression include regulation of ion flux and neurotransmitter release. Those neurons with long, extensively dispersed and numerous synaptic connections display the strongest signals and may possess the greatest propensity for continuous growth and turnover of their axon terminals, in contrast to short-axon and specific projection neurons exhibiting minimal levels. These data may enable inferring which populations display normal or experimentally induced axonal growth.

A comparison of the effects of Propofol with other anaesthetic agents on the centripetal transmission of sensory information

1. 1. A range of anaesthetic agents affect the centripetal transmission of sensory transmission by activating cortico-thalamic inhibitory mechanisms. 2. 2. This transmission of information through thalamic sensory relay nuclei is impeded and the sensory flow to the cerebral cortex is considerably reduced. 3. 3. In addition cortical transfer of information is blocked since cells in layers III and V show an additional sensitivity to anaesthetic agents. 4. 4. Diprivan (2,6-diisopropylphenol, propofol, ICI) appears to exert an action on sensory transmission mainly by acting on cortical cells in layers III and V. 5. 5. Its action on thalamic sensory relay cells is to increase their latency of discharge and disrupt their pattern of firing.

5-HT1c receptor is a prominent serotonin receptor subtype in the central nervous system.

Neurons in rat central nervous system (CNS) that express 5-HT1c receptor mRNA have been localized by in situ hybridization histochemistry. The 5-HT1c receptor is expressed in a wide variety of cortical and subcortical neurons including hippocampal pyramidal neurons, neurons within most of the central monoaminergic cell groups, neurons in thalamic sensory relay nuclei, and neurons involved in the central processing and regulation of nociceptive transmission. Therefore, the 5-HT1c receptor is a prominent but poorly characterized central subclass of serotonin (5-HT) receptor. The distribution of the 5-HT1c receptor within the CNS is considerably more widespread than that of the structurally and functionally related 5-HT2 receptor.

Dissociated mesencephalic responses to medial and ventral thalamic nuclei stimulation in rats. Relationship to analgesic mechanisms.

To investigate the mechanism of analgesia noted with electrical stimulation of the thalamic sensory relay nucleus and medial thalamus, modulations of neuronal activities in the periaqueductal gray matter (PAG) were studied in response to electrical stimulations of the ventroposterolateral nucleus (VPL) and parafascicular nucleus (Pf) and to peripheral noxious stimulations in rats. Extracellular single-unit activities were recorded from 102 neurons in the PAG and the adjacent area in animals under halothane anesthesia. A large population (83%) of the PAG neurons reacted to Pf stimulations with a predominantly excitatory response, whereas smaller numbers (43%) responded to VPL stimulations. There was a significant correlation between the response characteristics of Pf and noxious stimulations, whereas no correlation was found between VPL and noxious stimulations. The PAG neurons that were verified antidromically to project to the nucleus raphe magnus showed a similar pattern of response. The excitatory response to the Pf stimulation was partially attenuated by systemic administration of naloxone, whereas that to the VPL stimulation was not affected. These results suggest that part of the analgesic mechanism of medial thalamus stimulation involves activation of the descending pain suppression system by exciting the PAG neurons through the opioid system, while the analgesia produced by sensory relay nucleus stimulation does not involve the PAG neurons or the opioid system.

Effects of stimulation of the thalamic sensory relay and parafascicular nuclei on periaqueductal gray matter neurons. A study of the analgesic mechanism

Effects of stimulation of the thalamic sensory relay and parafascicular nuclei on periaqueductal gray matter neurons. A study of the analgesic mechanism

Somatosensory evoked potentials from the thalamic sensory relay nucleus (VPL) in humans: correlations with short latency somatosensory evoked potentials recorded at the scalp

Somatosensory evoked potentials (SEPs) were recorded in humans from an electrode array which was implanted so that at least two electrodes were placed within the nucleus ventralis posterolateralis (VPL) of the thalamus and/or the medial lemniscus (ML) of the midbrain for therapeutic purposes. Several brief positive deflections (e.g., P11, P13, P14, P15, P16) followed by a slow negative component were recorded from the VPL. The sources of these components were differentiated on the basis of their latency, spatial gradient, and correlation with the sensory experience induced by the stimulation of each recording site. The results indicated that SEPs recorded from the VPL included activity volume-conducted from below the ML (P11), activity in ML fibers running through and terminating within the VPL (P13 and P14), activity in thalamocortical radiations originating in and running througn the VPL (P15, P16 and following positive components) and postsynaptic local activity (the negative component). The sources of the scalp-recorded SEPs were also analyzed on the basis of the timing and spatial gradients of these components. The results suggested that the scalp P11 was a potential volume-conducted from below the ML, the scalp P13 and P14 were potentials reflecting the activity of ML fibers, the small notches on the ascending slope on N16 may potentially reflect the activity of thalamocortical radiations, and N16 may reflect the sum of local postsynaptic activity occurring in broad areas of the brain-stem and thalamus.

Effects of thalamic sensory relay nucleus stimulation on trigeminal subnucleus caudalis neurons in the cat. Nociceptive activity in response to tooth pulp stimulation.

We investigated the effects of electrical stimulation of the thalamic sensory relay nucleus (TSRN) on the nociceptive neural activity within the trigeminal subnucleus caudalis in the cat. We found that the nociceptive activity of the trigeminal subnucleus caudalis neurons in response to tooth pulp or facial skin stimulation was inhibited by both single-pulse and repetitive TSRN stimulation. However, the period of inhibition induced by single-pulse TSRN stimulation was clearly shorter than that induced by periaqueductal gray (PAG) or nucleus raphe magnus (NRM) stimulation. Furthermore, the nociceptive neurons inhibited by PAG stimulation were not always inhibited by TSRN stimulation. The opioid antagonist naloxone (2.0 mg/kg, i.v.) significantly antagonized the inhibition induced by PAG or NRM stimulation but failed to antagonize that produced by TSRN stimulation. These results are discussed in relation to the differences in clinical effects produced by TSRN and PAG stimulation.

Effects of thalamic sensory relay nucleus stimulation on trigeminal subnucleus caudalis neurons in the cat. Abnormal bursting hyperactivity after trigeminal rhizotomy.

We studied in the cat the effects of thalamic sensory relay nucleus (TSRN) stimulation on abnormal hyperactivity following trigeminal rhizotomy within the contralateral trigeminal subnucleus caudalis, a trigeminal equivalent of the dorsal horn. The animals were subjected to unilateral retrogasserian rhizotomy 2-6 weeks prior to the experiments. Following the rhizotomy, abnormal bursting and continuous nonbursting hyperactivities were recorded from laminae IV-V of the trigeminal subnucleus caudalis on the rhizotomized side. Some of these neurons responded to peripheral stimuli applied to rostral cervical dermatomes in a manner resembling the nociceptive, wide dynamic range (WDR) neurons of the intact side. However, periaqueductal gray (PAG) stimulation inhibited the hyperactive neurons on the rhizotomized side less frequently than the WDR neurons on the intact side. In contrast to PAG stimulation, TSRN stimulation inhibited the hyperactive neurons on the rhizotomized side as frequently as the WDR neurons on the intact side. These results are apparently consistent with our clinical observation that neurogenic pain due to deafferentation can be relieved by TSRN stimulation but not by PAG stimulation. This in turn suggests that the pain relief obtained with TSRN stimulation may result at least in part from inhibition of the nociceptive activity or abnormal hyperactivity of dorsal horn neurons.

Inhibition of hyperactive trigeminal subnucleus caudalis neurons after experimental trigeminal rhizotomy in response to thalamic sensory relay nucleus stimulation.

The effects of thalamic sensory relay nucleus stimulation on the single neuron activity and field potentials within the trigeminal subnucleus caudalis, which is trigeminal equivalent of the dorsal horn were investigated in intact cats as well as in cats subjected to retro-Gasserian rhizotomy 1-6 months before the experiments. Inhibition of nociceptive neural activity and a positive field potential were evoked by thalamic stimulation in the dorsal horn of the intact animals. A positive field potential followed double pulse stimulation with frequencies ranging up to approximately 50 Hz. The inhibitory periods ranged from 60 to 100 ms. Train pulse stimulation with frequencies ranging from 30 to 50 Hz produced long-lasting inhibition of nociceptive neural activity and a positive shift of the field potentials. Essentially identical inhibition of abnormal neural hyperactivity occurring in the rhizotomized dorsal horn was observed. The positive field potential corresponding to this inhibition also displayed characteristics similar to the field potential seen in the intact dorsal horn. These data indicate that the pathways involved in the inhibitory responses induced by thalamic sensory relay nucleus stimulation, unlike some other pain inhibitory systems, can exert their influence even to the dorsal horn which has undergone reorganization of neural circuits after rhizotomy.

Effects of thalamic sensory relay nucleus stimulation on the jaw-opening reflex in response to tooth-pulp stimulation in the cat.

The effects of stimulation of the thalamic sensory relay nucleus (TSRN, nucleus ventralis posteromedialis) on the jaw-opening reflex (JOR) in response to tooth pulp stimulation were compared with the effects of stimulation of the periaqueductal gray (PAG) and nucleus raphe magnus (NRM) in the cat. After stimulation of the TSRN, PAG and NRM, the JOR was inhibited. However, while the inhibitory effects of PAG and NRM stimulation lasted for more than 500 ms and were antagonized by the opiate antagonist, naloxone, the inhibitory effects of TSRN stimulation lasted for approximately 100 ms and were resistant to naloxone. These findings suggest that although TSRN stimulation exerts descending inhibitory effects on segmental nociceptive activity, similarly to PAG or NRM stimulation, the descending inhibitory pathways mediating the effect of TSRN stimulation may be largely distinct physiologically as well as pharmacologically from those mediating the effect of PAG and NRM stimulation.

Deafferentation pain and stimulation of the thalamic sensory relay nucleus: clinical and experimental study.

This report summarizes our clinical experience in which the effects of both thalamic sensory relay nucleus (TSRN) and periaqueductal gray (PAG) stimulation were tested in the same series of patients with various forms of pain. The clinical data indicated that neurogenic pain due to deafferentation at the level of the peripheral nerves or the spinal cord was often controlled by TSRN stimulation but not by PAG stimulation. We also review the results of our experimental investigations in cats which were undertaken in an attempt to clarify the neurophysiologic basis of such differential clinical effects of TSRN and PAG stimulation. It appeared that abnormal hyperactivity within the trigeminal medullary dorsal horn following retrogasserian rhizotomy was far more frequently inhibited by TSRN stimulation than by PAG stimulation.

Thalamic attention circuitry normal and psychotic

Cortex is not preprogrammed to recognise transthalamic sensory patterns or to prioritize them for motor reaction. Network subsets for these abilities are taught into neocortex in early life from the hippocampi where species-significant pattern-recognition and reaction-prioritizing ARE genetically preprogrammed. Thereafter whenever an indoctrinated subset of cortex is activated via thalamic sensory relay nuclei it axonally activates a specific subset of neurons within the thalamic pulvinar. Pulvinar analogically integrates this with concurrent specific inputs from the thalamic dorsomedial nucleus which itself is integrating inputs from the prefrontal cortex (goals) and the amygdaloid nuclei (moods). The pulvinar's specific integral is then axonally projected back to cortex UNDER NON-SPECIFIC BOOST from the thalamic centromedian nucleus. This ensures unitary attention focussing influenced by acquired priorities. Given that neocortex is genetically organized as a classifying mechanism, it also permits virtually limitless part-novel learning and best-match reality-testing of percepts (and concepts in humans). In schizophrenia the non-specific booster system is bilaterally blocked at the centromedian nucleus. In mania the non-specific thalamic system is shunted, at midbrain, into the non-specific direct cortical system. In melancholia both of these brainstem systems are subnormal in non-specific output. Figure 1 schematizes the main axonal circuitry. Analogical integration occurs within predominantly dendro-dendritic networks.