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PubMed2006

[The functional cooperation of the hippocampus and anterior thalamus via the fimbria-fornix in spatial memory in rats].

This study examined whether the cooperation of the hippocampus, and anterior thalamus via the fimbria-fornix is involved in the spatial memory. We compared the effect of contralateral lesions (Contra) with ipsilateral lesions (Ipsi) of the fimbria-fornix and anterior thalamus on the performance of an object exploration task and the Morris water maze task. If the hippocampus and anterior thalamus take part in a same functional system via fornix, the performance of Contra group will be more disruptive than that of Ipsi group. In the object exploration task, Contra and Ipsi groups did not differ from Control group in the performance of object recognition test. However, the performance of Contra group was significantly impaired in the spatial recognition test, compared with two other groups. In the Morris water maze task, only Contra group showed deficits in spatial learning but not the Ipsi group. These results indicate that contralateral, but not ipsilateral lesion caused deficits in spatial memory, supporting the notion that the functional cooperation of hippocampus and anterior thalamus via fornix is vital for spatial memory.

Animals↗
PubMed1999

Location of muscarinic type 2 receptors within the synaptic circuitry of the cat visual thalamus.

A cholinergic projection from the parabrachial region (PBR) of the brainstem to the visual thalamus has been studied in great detail during the past 20 years. A number of physiological studies have demonstrated that this projection causes a dramatic change in thalamic activity during the transition from sleep to wakefulness. Additionally, the PBR may mediate more subtle changes in thalamic activity as attentional levels fluctuate during the waking state. The synaptic circuitry underlying these events has been identified in the cat thalamus. However, there is currently no anatomical information regarding the distribution of cholinergic receptors in relation to this circuitry. To begin to understand how the PBR projection modulates thalamic activity, we used immunocytochemical techniques to examine the distribution of muscarinic type 2 (M2) receptors in the visual thalamus of the cat. The distribution of M2 receptors correlates well with previous reports of the distribution of cholinergic terminals in the visual thalamus. At the light microscopic level, dense M2 staining was seen in the neuropil of the dorsal lateral geniculate nucleus (dLGN) and pulvinar nucleus and in somata and proximal dendrites of cells in the thalamic reticular nucleus (TRN). In the dLGN and pulvinar nucleus, we quantitatively analyzed the distribution of M2 receptors using electron microscopy. Postembedding immunocytochemistry for gamma aminobutyric acid (GABA) was used to determine whether M2 receptors are present on interneurons or thalamocortical cells. In particular, we examined the distribution of M2 receptors with respect to the known sites of PBR terminations. The dendrites of both thalamocortical cells and interneurons were stained for the M2 receptors in both the glomerular and extraglomerular neuropil. However, the densest staining was found in glomerular GABAergic profiles that displayed the morphology associated with interneuron dendritic terminals (F2 profiles). Our data suggest that M2 receptors play an important role both in blocking thalamic spindle oscillations and in increasing the efficacy of signal transmission during increased attentional states.

Animals↗
PubMedDate not supplied

Oxidative stress in the thalamus of Wistar rats treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.

Experimental parkinsonism was induced in adult Wistar rats by selective nigrostriatal neurotoxine, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in a single dose of 0.09 g/kg, by unilateral intrastriatal application using stereotaxic instrument. Control group included rats treated with 0.9% saline solution in the same manner. Animals were sacrificed by decapitation seven days after the treatment. Total glutathione was measured in the crude mitochondrial fraction of thalamus and striatum. Total glutathione content, as a measure of reduced cell atmosphere, was mutually decreased in the thalamus and striatum of MPTP-treated animals, compared to controls: thalamus ipsi- = 24.8 +/- 3.11, contralateral = 26.81 +/- 5.31; striatum ipsi- = 19.96 +/- 4.13, contralateral = 17.3 +/- 4.09 nmol/mg prot. Mutually depleted glutathione content in the thalamus and contralateral striatum, the structures distant from ipsilateral treated striatum, could indicate on spatial propagation of oxidative stress, not only in the selective vulnerable dopaminergic nigrostriatal neurons, but in the structures included in the motor and cognitive loops of basal ganglia.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1999

Organization of projections to the lateral amygdala from auditory and visual areas of the thalamus in the rat.

Projections to the amygdala from the auditory thalamus have been implicated in the associative conditioning of fear responses to acoustic stimuli. Thalamo-amygdala auditory projections enter the amygdala via the lateral nucleus (LA). It is well documented that these projections originate in the medial division (MGm) of the medial geniculate nucleus (MGN), the posterior intralaminar nucleus (PIN), and the suprageniculate nucleus (Sg). It is not known, however, whether these thalamic projections terminate in a topographic fashion within the LA. We therefore used several retrograde tract tracing techniques to determine whether the terminations of thalamo-amygdala fibers have a topographic organization within the LA. These tracers were injected into various locations within the LA, and the distribution of the retrogradely labeled cells throughout the thalamus was analyzed. In general, rostral to caudal distinctions in the thalamus are maintained in the LA, such that projections from throughout the MGN terminate in the anterior part of the LA, whereas the caudal part of the MGN projects to the caudal part of the LA. Furthermore, the density of cells that give rise to thalamo-amygdala projections varies within each thalamic nucleus along the rostro-caudal axis. The patterns of thalamo-amygdala connectivity observed support previous parcellation schemes that segregate the LA into dorsal, medial, and lateral areas, and suggest that the LA should be further divided into anterior and posterior parts. In addition to the well-known projections to the LA originating from PIN, MGN, and Sg, we also found substantial projections from the dorsal portion of the MGN (MGd) and the lateral posterior thalamic nucleus (LP). These findings suggest that some of the functional segregation in the thalamus may be preserved in the LA, and that the role of the MGd and LP in thalamo-amygdala transmission should be reconsidered.

Amygdala↗
PubMed1999

Projections from subnucleus oralis of the spinal trigeminal nucleus to contralateral thalamus via the relay of juxtatrigeminal nucleus and dorsomedial part of the principal sensory trigeminal nucleus in the rat.

Following injection of HRP into contralateral thalamus, retrogradely labeled cells were observed in principal sensory trigeminal nucleus (Vp) and an area of juxtatrigeminal nucleus (JX) formerly described by John and Tracey (1987). When PHA-L was delivered to dorsomedial part of the subnucleus oralis (Vodm), PHA-L labeled terminals were seen in dorsomedial part of the Vp (Vpdm) and in the JX region. Comparing the distribution of PHA-L labeled terminal field with that of HRP labeled JX neurons showed that the labeled terminals and neurons were overlapped closely in the JX. The distribution patterns of the labeled terminals and JX neurons were also the same: viewed on the coronal planes caudal-rostrally, both of the labelings began to appear at the levels where the facial nerve root was just broken. Rostrally, at middle levels of the motor trigeminal nucleus (Vmo), the labelings showed their typical view covering dorsal and ventral JX (dJX, vJX). The labelings disappeared at rostral poles of the Vmo and Vp. When injections of PHA-L into the Vodm and HRP into the contralateral thalamus was made in one rat, the contacts between Vodm projecting terminals labeled with PHA-L and HRP labeled trigemino-thalamic neurons were seen in the JX and also in the Vpdm. Then, electron microscopic (EM) study was done, injections of kainic acid into the Vodm and HRP into the contralateral thalamus was performed simultaneously. After EM embedding, the JX and Vpdm regions were selected, ultrathin sections were cut and observed with EM. In both areas, axo-somatic and axo-dendritic synapses were seen between degenerated boutons and HRP labeled somata or dendrites. Namely, the Vodm projecting terminals synapsed on trigemino-thalamic neurons in the JX and Vpdm. Anyway, axo-dendritic synapses was the main type of observed synapses. Thus, the present work demonstrated 1. the JX containing a group of trigemno-thalamic neurons was a target of special projections froin the Vodm; 2. The Vodm neurons projected to the contralateral thalamus through the relay of JX and Vpdm neurons.

Animals↗
PubMed2001

Delayed neurodegeneration in neonatal rat thalamus after hypoxia-ischemia is apoptosis.

Brain injury in newborns can cause deficits in motor and sensory function. In most models of neonatal brain injury, thalamic damage often occurs. Using the Rice-Vannucci model of neonatal hypoxic-ischemic brain injury, we have shown that neuronal degeneration in somatosensory thalamus is delayed in onset ( approximately 24 hr) compared with cortical and striatal injury and exhibits prominent structural features of apoptosis. In the present study, we examined whether cell death in the thalamus has molecular features of apoptosis. Fas death receptor protein expression increased rapidly after neonatal hypoxia-ischemia, in concert with cleavage of procaspase 8 to its active form. Concurrently, the levels of Bax in mitochondrial-enriched cell fractions increase, and cytochrome c accumulates in the soluble fraction. Mitochondria accumulate in a perinuclear distribution by 6 hr after hypoxia-ischemia. Cytochrome oxidase subunit 1 protein levels also increase at 6 hr after hypoxia-ischemia. Increased levels of Fas death receptor, Bax, and cytochrome c, activation of caspase 8, and abnormalities in mitochondria in the thalamus significantly precede the activation of caspase 3 and the appearance of neuronal apoptosis at 24 hr. We conclude that the delayed neurodegeneration in neonatal rat ventral basal thalamus after hypoxic-ischemic injury is apoptosis mediated by death receptor activation.

Animals↗
PubMed2001

Zona incerta: Substrate for contralateral interconnectivity in the thalamus of rats.

We have shown previously that the zona incerta (ZI), a small nucleus deriving from the ventral thalamus, has extensive ipsilateral connections with the higher order and intralaminar nuclei of the dorsal thalamus and that there are many ipsilateral interconnections between the different cytoarchitectonic sectors of the ZI. In this study, we explore the contralateral connections that the ZI has with its opposing nucleus as well as with the other nuclei of the thalamus. Injections of biotinylated dextran or cholera toxin subunit B were made into each of the different ZI sectors (rostral, dorsal, ventral, and caudal) and into intralaminar and higher order dorsal thalamic nuclei of Sprague-Dawley rats by using stereotaxic coordinates. Brains were fixed in aldehyde and processed using standard methods. Our results show that, after injections limited to a given ZI sector, labelled terminal-like elements and cells were seen across the other sectors of the ZI of the contralateral side. Furthermore, after each of these ZI injections, labelling was seen in the intralaminar (e.g., parafascicular, central lateral, and central medial) and higher order (e.g., posterior thalamic, lateral posterior, and lateral dorsal) nuclei of the contralateral side. These patterns of labelling were confirmed after tracer injections into intralaminar and higher order nuclei; after such injections, labelling was seen in the contralateral ZI. In all cases, there was labelling on the ipsilateral side as well, and this was generally heavier than on the contralateral side. Overall, our results indicate that there is a network of interconnections between the ZI of both sides of the thalamus and that the ZI has contralateral connections with the intralaminar and higher order nuclei. Hence, the ZI furnishes a substrate that spreads activity to both sides of the brain.

Animals↗
PubMed2003

Adaptive plasticity in the auditory thalamus of juvenile barn owls.

Little is known about the capacity of the thalamus for experience-dependent plasticity. Here, we demonstrate adaptive changes in the tuning of auditory thalamic neurons to a major category of sound localization cue, interaural time differences (ITDs), in juvenile barn owls that experience chronic abnormal hearing. Abnormal hearing was caused by a passive acoustic filtering device implanted in one ear that altered the timing and level of sound differently at different frequencies. Experience with this device resulted in adaptive, frequency-dependent shifts in the tuning of thalamic neurons to ITD that mimicked the acoustic effects of the device. Abnormal hearing did not alter ITD tuning in the central nucleus of the inferior colliculus, the primary source of input to the auditory thalamus. Therefore, the thalamus is the earliest stage in the forebrain pathway in which this plasticity is expressed. A visual manipulation, chronic prismatic displacement of the visual field, which causes adaptive changes in ITD tuning at higher levels in the forebrain, had no effect on thalamic ITD tuning. The results demonstrate that, during the juvenile period, auditory experience shapes neuronal response properties in the thalamus in a frequency-specific manner and suggest that this thalamic plasticity is driven by self-organizational forces and not by visual instruction.

Acoustic Stimulation↗
PubMedDate not supplied

Effects of beta-adrenergic agents on the regional cerebral blood flow in cortex and thalamus of the cat.

The effects of the beta-adrenergic agents isoprenaline, terbutaline, l,d-propranolol, acebutolol, as well as d-propranolol, on the regional cerebral blood flow (rCBF) in cortex and thalamus and arterial blood pressure (ABP) were investigated following i.v. administration. The experiments were performed in 64 cats anaesthetized with ether and chloralose. The rCBF was measured using the thermistor thermoclearance technique. Isoprenaline, as well as terbutaline (1, 3, 5 micrograms/kg) decreased the cortical rCBF and the ABP (p less than .05). Both adrenergic agonists increased the thalamic rCBF despite the decrease in ABP (p less than .05). L,d-propranolol (1 mg/kg) abolished the effects of isoprenaline and terbutaline on thalamic rCBF. Acebutolol (0.6 mg/kg) or d-propranolol (0.5 mg/kg) did not alter isoprenaline- and terbutaline-induced effects on rCBF in thalamus. L,d-propranolol decreased the thalamic rCBF, whereas d-propranolol increased the rCBF in thalamus (p less than .05). Acebutolol did not change the thalamic rCBF significantly. The results obtained indicate that beta-adrenergic agents have heterogeneous effects on rCBF in cortex and thalamus. Their effects on thalamic rCBF seem to be accomplished by beta 2-adrenoceptor stimulation.

Adrenergic beta-Agonists↗
PubMed1986

[Role of the thalamus in the physiopathology of epilepsy].

Early hypotheses on the origin of primary generalized epilepsy suggested a determinant role for the "centrencephalon" in the triggering of discharges of generalized spike-waves (GSW) and tonic-clonic crises (TCC). It was demonstrated in this respect that bilateral cortical spike-wave discharges at 3 c/sec were obtained by electrical stimulation of intralaminar nuclei in the rat. The role of the thalamus in the genesis of GSW and TCC was subsequently demonstrated in several experimental models. However, the thalamus is apparently not involved in the genesis of EEG manifestations of generalized epilepsy and most authors agree that the latter are of cortical origin since a) with or without cardiazol, generalized seizures may occur after ablation of cat thalamus; b) in the cat diffuse cortical application of dilute penicillin can reproduce signs of generalized epilepsy observed after systemic injection of penicillin to this animal; c) finally paroxysmal discharges which appear in subcortical structures in the photosensitive baboon are always preceded by frontal cortical spike-waves; similarly intermittent light stimulation-provoked TCC always arise from the frontal cortex and furthermore hemispheric synchronization of attacks disappears after callosotomy. These findings indicate that the origin of GSW and TCC, is not in the thalamus but that the latter nevertheless plays a role in their elaboration.

Animals↗
PubMed1980

The effect of intoxication by ceresan on the activity of phosphatases and esterases in the rat thalamus.

The effect of Ceresan (Methoxyethylmercury chloride) on the histoenzymatic pattern of the thalamus was studied. The experimental animals were treated intragastrically with 100 mg of Ceresan for 6 consecutive days, and the activity of various hydrolases of the thalamus was investigated histochemically. Ingestion of large doses of Ceresan caused widespread alterations in activity of the thalamic hydrolases. A generalized increase of activity was found with respect to TPPase, acP and NsE, while AChE, BuTJ and ATPase activities appeared distinctly reduced. The thalamic neuroglia of experimental rats demonstrated enzymic activities which could not be detected in control animals, and these were: AChE, NsE, acP and TPPase -- in astrocytes, and ATPase -- in oligodendroglia. The changes in the histoenzymatic pattern of the thalamus caused by Ceresan ingestion were topographically highly differentiated. The anterior and lateral nuclei of the thalamus seem to be more sensitive towards Ceresan intoxication than the posterior ones.

Acetylcholinesterase↗
PubMed1980

Unit activity in medial thalamus: comparative effects of caffeine an amphetamine.

The effects of caffeine and d-amphetamine sulfate were evaluated upon single unit activity of medial thalamus in chloral hydrate anesthetized rats. Single unit activity recorded extracellularly with platinum-iridium microelectrodes. It was found that caffeine, 0.1 to 0.5 mg/kg i.v., markedly suppressed and that amphetamine, 0.1 to 1 mg/kg i.v., markedly augmented the spontaneous firing rates of medial thalamic neurons. It was also demonstrated that amphetamine was capable of activating the medial thalamic neuronal activity while it was suppressed by caffeine. On the other hand, while the firing rate was increased by a previous amphetamine injection, administration of caffeine suppressed the amphetamine-induced augmentation of neuronal activity. The data imply that these two central nervous system (CNS) stimulants, caffeine and amphetamine, have different mechanisms of action at least at the medial thalamic site. Moreover, since medial thalamus participates in the recruitment phenomenon and exerts a stabilizing action on the cerebral cortex, our findings that caffeine suppressed this brain area suggest that the medial thalamus may be an important site of action for the arousal induced by caffeine. In addition, the demonstration of inhibitory effects of caffeine on the medial thalamus in this study and excitatory effects on brain stem reticular formation from our previous studies indicate that caffeine has differential actions on different brain areas. This observation broadens the generally held belief that caffeine excites at all levels of the CNS to specifically include inhibition of inhibitory influences in at least one functional system of the brain.

Action Potentials↗
PubMed1994

State-dependent release of acetylcholine in rat thalamus measured by in vivo microdialysis.

Mesopontine cholinergic neurons have long been thought to play a key role in behavioral state control. In particular, they have been implicated in the process of EEG desynchrony and in the generation of rapid eye movement (REM) sleep. However, the behavioral profile of identified mesopontine cholinergic neurons has not been unequivocally demonstrated. In an attempt to address this issue, in vivo microdialysis was used to monitor acetylcholine (ACh) release across behavioral state in the rat thalamus, a major projection site of mesopontine cholinergic neurons. Because REM periods in rats are of short duration, a method was developed to collect and accumulate sufficiently large samples from each of the individual states of wake, slow-wave sleep, and REM sleep to permit off-line analysis via (HPLC-ECD). Probe placement and the source of cholinergic innervation to the vicinity of the microdialysis probe were verified using retrograde tracing combined with ChAT immunohistochemistry. Finally, the sodium and calcium dependence of ACh measured in the thalamus were tested using TTX and calcium-free dialysates. The results showed that (1) extracellular ACh concentrations in the thalamus are high during both wake and REM sleep and significantly lower during slow-wave sleep, (2) the majority of cholinergic projections to the vicinity of the dialysis probes originate in the mesopontine tegmentum, and (3) ACh release in the thalamus is due to sodium- and calcium-dependent mechanisms. In contrast to predictions of some previous hypotheses, these results demonstrate that mesopontine cholinergic neurons are active during both wake and REM sleep.

Acetylcholine↗
PubMed1975

Stereotaxic coordinates for the Rhesus monkey thalamus and mesencephalon referencing visual afferents and cytoarchitecture.

When using a stereotaxic instrument for visual field stimulation we found that electrode placements in the thalamus and mesencephalon of prone rhesus monkeys with the aid of avaiable atlases showed considerable errors. As these animals are valuable for primate visual system reseach an atlas was constructed with methods that have not been used before for rhesus. In addition, the specific connections from the visual cortices, superior colliculus and retina to the thalamus and mesencephalon are also shown. Anesthetized monkeys of specific body dimensions had a matrix of pins inserted into the brain before fixation. A matrix was used so that the penetrations seen in the sectioned brain could be cross related as a control for accurate measurements of the stereotaxic planes throughout the brain. The surface of the whole brain frozen blocks were photographed on the microtome just before a cut section was taken. These calibrated pictures formed the "floor plan" of the atlas as they represent more accurately the brain geometry than individual sections which are distorted by cutting, staining and mounting. Cytoarchitectural (Nissl stain) and axonal connectional (Fink-Heimer stain) information was transferred and adjusted onto the block pictures from their corresponding stained sections. Follow up experiments showed that the present coordinates are accurate for these monkeys of restricted body dimensions. In addition, referencing visual axonal projections onto the same cytoarchitectural map in stereotaxic coordinates provides an atlas for localizing areas of the thalamus, on a basis other than cytoarchitecture, which receive combinations of visual inputs for further anatomical and physiological studies of the rhesus monkey visual system. The atlas further demonstrates that projections do not necessarily follow the cytoarchitectural definition of an area, but rather redefine the thalamus on the basis of specific axonal connections.

Animals↗
PubMed1997

Distribution of neurons immunoreactive for parvalbumin and calbindin in the somatosensory thalamus of the raccoon.

The aim of this study was to assess the distribution of neurons immunoreactive for parvalbumin (PV), calbindin (CaBP), glutamic acid decarboxylase (GAD), and gamma-aminobutyric acid (GABA) in the somatosensory thalamus of the raccoon and to compare these features to those of other species, especially primates. Immunohistochemistry was used to study the location of these neurons in the ventroposterior nucleus (VP), ventroposterior inferior nucleus (VPI), posterior group of nuclei (Po), and reticular nucleus (Rt). A consistent differential pattern of PV-positive (PV+) and CaBP-positive (CaBP+) cells was found in the somatosensory thalamus. Many PV+ neurons were observed in VP and Rt, but very few were found in VPI or Po. In contrast, CaBP+ neurons were distributed throughout VP, VPI, and Po but were very sparse or absent in Rt. In the VP nucleus, PV+ cells were distributed in clusters separated by interclusteral regions with a sparse distribution of PV+ cell bodies. The distributions of PV+ and CaBP+ cells tended to be complementary to each other in VP; regions with a high density of PV+ neurons had a low density of CaBP+ cell bodies. Double-labeling experiments revealed very few neurons in which PV and CaBP immunoreactivities were colocalized. Cells immunoreactive for GAD or GABA were found in PV-dense clusters of VP; fewer GABAergic neurons were present in the CaBP-dense interclusteral regions of VP and in VPI and Po. GAD+ and GABA+ neurons were most prominently distributed in Rt. We conclude that the distributions of PV+ and CaBP+ cell bodies in the raccoon somatosensory thalamus are very similar to those in primates. The density of GABAergic neurons in the somatosensory thalamus of the raccoon is less than that in the cat and monkey, but the relative distribution of GABAergic neurons in the different somatosensory nuclei is very similar to that in the cat and monkey. These results are discussed in relation to findings in other species and are related to the functions of lemniscal and nonlemniscal somatosensory pathways.

Animals↗
PubMed1999

Efficacy of unilateral deep brain stimulation of the VIM nucleus of the thalamus for essential head tremor.

Essential tremor is a common movement disorder. Deep brain stimulation of the VIM nucleus of the thalamus has been reported to be efficacious for reducing essential hand tremor. The effect of deep brain stimulation of the thalamus on essential head tremor has not been well studied. Therefore, we evaluated the effect of DBS of the thalamus in 38 patients with essential head tremor. Head tremor scores prior to surgery were compared with scores at 3, 6, and 12 months postimplant with stimulation "on" and "off." The 3-month evaluations were blinded for 24 patients and all others were open-label. There was a significant improvement in head tremor at all postimplant evaluations compared with baseline. Essential head tremor can be reduced with deep brain stimulation of the VIM nucleus of the thalamus and, pending the results of other controlled trials, should be considered as a treatment option for patients with disabling essential head tremor unresponsive to medication.

Aged↗
PubMed2001

Synaptic targets of thalamic reticular nucleus terminals in the visual thalamus of the cat.

A major inhibitory input to the dorsal thalamus arises from neurons in the thalamic reticular nucleus (TRN), which use gamma-aminobutyric acid (GABA) as a neurotransmitter. We examined the synaptic targets of TRN terminals in the visual thalamus, including the A lamina of the dorsal lateral geniculate nucleus (LGN), the medial interlaminar nucleus (MIN), the lateral posterior nucleus (LP), and the pulvinar nucleus (PUL). To identify TRN terminals, we injected biocytin into the visual sector of the TRN to label terminals by anterograde transport. We then used postembedding immunocytochemical staining for GABA to distinguish TRN terminals as biocytin-labeled GABA-positive terminals and to distinguish the postsynaptic targets of TRN terminals as GABA-negative thalamocortical cells or GABA-positive interneurons. We found that, in all nuclei, the TRN provides GABAergic input primarily to thalamocortical relay cells (93-100%). Most of this input seems targeted to peripheral dendrites outside of glomeruli. The TRN does not appear to be a significant source of GABAergic input to interneurons in the visual thalamus. We also examined the synaptic targets of the overall population of GABAergic axon terminals (F1 profiles) within these same regions of the visual thalamus and found that the TRN contacts cannot account for all F1 profiles. In addition to F1 contacts on the dendrites of thalamocortical cells, which presumably include TRN terminals, another population of F1 profiles, most likely interneuron axons, provides input to GABAergic interneuron dendrites. Our results suggest that the TRN terminals are ideally situated to modulate thalamocortical transmission by controlling the response mode of thalamocortical cells.

Animals↗
PubMed1993

Depression by nicotine of pain-related nociceptive activity in the rat thalamus and spinal cord.

To assess the possible role of nicotinergic control in nociception and pain, experiments were carried out on rats under urethane anesthesia in which nociceptive activity was elicited by electrical stimulation of afferent C fibers in the sural nerve and recorded from single neurones in the thalamus and from ascending axons in the spinal cord. Intravenous administration of nicotine (0.01-0.5 mg/kg) depressed the nociceptive activity evoked in the thalamus and the spinal cord in a dose-dependent way. The maximum depression in thalamus and spinal cord was 40% of control activity and obtained at a dose of 0.025 mg/kg. Likewise, local administration of nicotine to the spinal cord by intrathecal injection (5, 10, and 30 micrograms) reduced the nociceptive activity evoked in neurones of the thalamus and in ascending axons of the spinal cord, the maximum of the depression being 40% of control activity. The depressant effect of nicotine (0.05 mg/kg) was reduced by mecamylamine (1 mg/kg) but not by atropine (0.5 mg/kg). It is concluded that the antinociceptive effect of nicotine is due to a specific action of the alcaloid at the spinal level.

Afferent Pathways↗