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PubMed1995

Purinergic inhibition of GABA and glutamate release in the thalamus: implications for thalamic network activity.

Adenosine is a CNS depressant with both pre- and postsynaptic actions. Presynaptically, adenosine decreases neurotransmitter release in the hippocampus but only at excitatory terminals. In the thalamus, however, we show that, in addition to its actions at excitatory synapses, adenosine strongly suppresses monosynaptic inhibitory currents both in relay cells of the thalamic ventrobasal complex (VB) and in inhibitory neurons of the nucleus reticularis thalami (nRt). A concomitant increase in transmission failures and results coefficient of variation analysis are both consistent with a presynaptic mechanism. Pharmacological manipulations support an A1 receptor-mediated process. Slow thalamic oscillations induced in vitro by extracellular stimulation and recorded with extracellular multiunit electrodes in VB and nRt are dampened by adenosine without affecting their periodicity. We conclude that adenosine can presynaptically down-regulate inhibitory postsynaptic responses in thalamus and exert robust antioscillatory effects, likely by synergistic depression of both excitatory and inhibitory neurotransmitter release.

Adenosine↗
PubMed2006

Odour-place paired-associate learning and limbic thalamus: comparison of anterior, lateral and medial thalamic lesions.

Several subregions in the limbic thalamus have been suggested as the key locus for diencephalic amnesia, including the anterior thalamic nuclei, intralaminar nuclei and mediodorsal nuclei. There is, however, no consensus as to a single critical site and recent research has suggested instead that different thalamic areas may contribute to diencephalic amnesia in subtly different ways. This study compared the effects of lesions to anterior (AT), lateral (LT) and posteromedial (MT) aggregates of thalamic nuclei on Gilbert and Kesner's [Gilbert, PE, Kesner, RP. Role of the rodent hippocampus in paired-associate learning involving associations between a stimulus and a spatial location. Behav Neurosci 2002;116(1):63-71; Gilbert, PE, Kesner, RP. Localization of function within the dorsal hippocampus: the role of the CA3 subregion in paired-associate learning. Behav Neurosci 2003;117(6):1385-94] paired-associate task, in which rats were postoperatively trained to form an arbitrary association between odours and spatial locations in a circular open field. Both AT and LT lesions, but not MT lesions, severely impaired odour-place paired-associate learning. Probe trials revealed that the rats were not using specific location information after acquisition training. All groups were able to learn non-associative odour and place discrimination tasks quickly, with only the AT group showing delayed acquisition. This study provides the first direct comparison of different thalamic lesions on paired-associate learning and new evidence on the importance of the LT region in learning and memory. The results support the notion that injury to both the AT and LT subregions of the thalamus may each be major contributors to diencephalic amnesia. There is need for traditional models of memory function to take greater account of the contributions of thalamic nuclei.

Animals↗
PubMed2004

Differential expression of GABA(B(1b)) receptor mRNA in the thalamus of normal and monoarthritic animals.

GABA(B) receptors have been implicated in the plastic changes occurring in the spinal cord during the development of chronic inflammatory pain. In this study, we evaluated whether the expression of GABA(B(1b)) receptor mRNA is regulated supraspinally, namely in the thalamus, as part of the response to chronically enhanced noxious input arising from experimental monoarthritis (MA). In situ hybridization with [(35)S]-labelled oligonucleotide probes was performed in sections of control, 2, 4, 7 and 14 days MA rats' brains (n = 6/group). The distribution of GABA(B(1b)) mRNA was determined bilaterally in the ventrobasal complex (VB), posterior (Po), centromedial/centrolateral (CM/CL) and reticular (Rt) thalamic nuclei. The amount of GABA(B(1b)) mRNA was expressed as times fold of background values. In normal animals, values of mRNA expression were very similar in VB, Po and CM/CL, ranging from 2.2 +/- 0.2 to 2.7 +/- 0.4 (mean +/- S.E.M.) times higher than background levels. No expression of GABA(B(1b)) mRNA was found in the Rt of control or MA animals. A significant decrease of 26% at 4 days, and 37% at 7 days of MA, was observed in the VB contralateral to the affected joint. On the contrary, in the Po there was a significant bilateral increase at 2 days (38% contralaterally, 25% ipsilaterally), returning to basal levels at 4 days MA. No significant changes were observed in CM/CL. These results suggest that the expression of GABA(B(1b)) in the VB and Po is regulated by noxious input, and might contribute to the functional changes that occur in the thalamus during chronic inflammatory pain.

Animals↗
PubMed2005

Chronic daily intrathecal injections of a large volume of fluid increase mast cells in the thalamus of mice.

Mast cells are found in the central nervous system (CNS) as well as in the periphery. In the brain of mice, they are localized primarily in the thalamus and meninges. Although their numbers increase in response to stress, the mediator of their recruitment is not known. During studies in which drugs were delivered intrathecally in a volume sufficiently large to distribute to the brain, we discovered that repeated daily injections of this large volume increased the number of mast cells in the thalamus. The increase was not due to changes in electrolyte composition of the cerebrospinal fluid (CSF) as chronically administered artificial CSF produced similar effects. Repeated injections of even small volumes (2 mul) increased mast cells in the medial intralaminar (Med), ventral posterior (VP) and posterior (Po) nuclei. Increasing the volume injected daily to 20 mul increased mast cells in the lateral intralaminar (Lat), laterodorsal (LD), ventrolateral (VL) and lateral geniculate (LG) nuclei and further increased those in the lateral extension of the Po nucleus. Thus, small and large volumes augment distinct populations of mast cells. While stem cell factor (SCF) is abundant in the CNS and is chemotactic to mast cells in the periphery, thalamic mast cells in the rodent do not express c-kit, the SCF receptor, suggesting that this factor may not be responsible for the effect. Consistent with this, centrally injected SCF was incapable of increasing thalamic mast cell populations after either single or chronic (21 days) daily injections compared to the effect of saline alone. Although the mechanism is not known, repeated injections of a large volume of fluid dramatically increase mast cells in the CNS, a phenomenon that may be relevant to clinical conditions of increased CSF pressure or volume.

Analysis of Variance↗
PubMed2004

Neuronal activity in the basal ganglia and thalamus in patients with dystonia.

OBJECTIVE: To explore the role of abnormal neuronal activity in the basal ganglia and thalamus in the generation of dystonia. METHODS: Microelectrode recording was performed in the globus pallidus internus (GPi), ventral thalamic nuclear group ventral oral posterior/ventral intermediate, Vop/Vim) and subthalamic nucleus (STN) in patients with primary dystonia (n=11) or secondary dystonia (n=9) during surgery. Electromyogram (EMG) was simultaneously recorded in selected muscle groups. Single unit analysis and cross-correlations were carried out. RESULTS: Three hundred and sixty-seven neurons were obtained from 29 trajectories (GPi: 13; Vop/Vim: 12; STN: 4), 87% exhibited altered neuronal activity including grouped discharges in GPi (n=79) and STN (n=37), long-lasting neuronal activity (n=70) and rapid neuronal discharge (n=86) in Vop/Vim. There were neurons in Vop, GPi and STN firing at the same frequency as EMG during dystonia (mean: 0.39 Hz, range 0.12-0.84 Hz). Significant correlations between neuronal activity and EMG at the frequency of dystonia were obtained (GPi: r2=0.7 (n=31), Vop/Vim: r2=0.64 (n=18) and STN: r2=0.86 (n=17)). CONCLUSIONS: Consistent with previous findings of abnormalities observed in Vop/VIM and GPi in relation to dystonia, the present data further show that the altered activity in GPi, specifically in dorsal subregions of GPi, Vop/Vim and STN is likely to be directly involved in the production of dystonic movement. Dystonia-related neuronal activity observed in motor thalamus and basal ganglia nuclei of GPi and STN indicates a critical role of their interactions affecting both indirect and direct pathways in the development of either generalized or focal dystonia. SIGNIFICANCE: These data support a central role of the basal ganglia in producing dystonic movements.

Adolescent↗
PubMed2003

The role of the thalamus in motor control.

Two characteristics of the thalamus--its apparently simple relay function and its daunting multinuclear structure--have been customarily viewed as good reasons to study something else. Yet, now that many other brain regions have been explored and neurophysiologists are turning to questions of how larger circuits operate, these two characteristics are starting to seem more attractive. First, the relay nature of thalamic neurons means that recording from them, like tapping into a wire, can reveal the signals carried by specific circuits. Second, the concentration of like relay neurons into nuclei means that inactivating or stimulating them can efficiently test the functions of the circuits. Recent studies implementing these principles have revealed pathways through the thalamus that contribute to generating movements and to monitoring one's own actions (corollary discharge).

Animals↗
PubMed2005

Psychotogenic drugs and delirium pathogenesis: the central role of the thalamus.

Delirium is thought to be a temporary psychiatric disorder resulting from a reduced central cholinergic transmission, combined with an increased dopaminergic transmission. The cholinergic and the dopaminergic systems interact not only with each other but with glutamatergic and gamma-amino-butyric acid (GABA) pathways. Besides the cerebral cortex, critical anatomical substrates of psychosis pathophysiology would comprise the striatum, the substantia nigra/ventral tegmental area, and the thalamus. The thalamus acts as a filter, allowing only the relevant information to travel to the cortex. Drugs of abuse (e.g. PCP, Ecstasy), as well as psychoactive medications frequently prescribed to hospitalized patients (e.g. benzodiazepines, opioids) could compromise the thalamic gating function, leading to sensory overload and hyperarousal. We propose that drug-induced delirium would result from the transient thalamic dysfunction caused by exposure to medications that interfere with central glutamatergic, GABAergic, dopaminergic and cholinergic pathways at critical sites of action. This model provides directions for future studies in neurophysiology, in vivo brain imaging, and psychopharmacology investigating delirium neuropathophysiology.

Cerebral Cortex↗
PubMed2004

Growth arrest and DNA damage-inducible gene 153 increases transiently in the thalamus following focal cerebral infarction.

The thalamus degenerates following cerebral infarction in the territory supplied by the middle cerebral artery (MCA), and apoptosis is suspected to be the mechanism of this phenomenon. The author studied the role of the growth arrest and DNA damage-inducible gene (GADD) 153 in this thalamic degeneration. The MCA was occluded in stroke-prone spontaneously hypertensive rats. The expression of GADD 153 and Bcl-2, and the release of cytochrome c from the mitochondria to cytosol, were examined in the thalamus until 7 days after ischemia using in situ hybridization, immunoblot, immunohistochemistry and RT-PCR analyses. Gadd153 mRNA expression and GADD153 protein increased transiently at 2, 3, 5 and 7 days, and at 3 and 5 days after ischemia. Bcl-2 mRNA expression and Bcl-2 protein decreased at 3 and 5 days. The release of cytochrome c from the mitochondria was detected at 5 days. These results suggest that increased GADD 153 suppresses Bcl-2 expression, which causes the release of cytochrome c from the mitochondria and leads to thalamic degeneration.

Animals↗
PubMed2005

Neuronal nicotinic acetylcholine receptor subunits in autism: an immunohistochemical investigation in the thalamus.

The cholinergic system has been implicated in the development of autism on the basis of neuronal nicotinic acetylcholine receptor (nAChR) losses in cerebral and cerebellar cortex. In the present study, the first to explore nAChRs in the thalamus in autism, alpha4, alpha7 and beta2 nAChR subunit expression in thalamic nuclei of adult individuals with autism (n=3) and age-matched control cases (n=3) was investigated using immunochemical methods. Loss of alpha7- and beta2- (but not alpha4-) immunoreactive neurons occurred in the paraventricular nucleus (PV) and nucleus reuniens in autism. Preliminary results indicated glutamic acid decarboxylase immunoreactivity occurred at a low level in PV, co-expressed with alpha7 in normal and autistic cases and was not reduced in autism. This suggested loss of neuronal alpha7 in autism is not caused by loss of GABAergic neurons. These findings indicate nicotinic abnormalities that occur in the thalamus in autism which may contribute to sensory or attentional deficits.

Adult↗
PubMed2006

Successive neuron loss in the thalamus and cortex in a mouse model of infantile neuronal ceroid lipofuscinosis.

Infantile neuronal ceroid lipofuscinosis (INCL) is caused by deficiency of the lysosomal enzyme, palmitoyl protein thioesterase 1 (PPT1). We have investigated the onset and progression of pathological changes in Ppt1 deficient mice (Ppt1-/-) and the development of their seizure phenotype. Surprisingly, cortical atrophy and neuron loss occurred only late in disease progression but were preceded by localized astrocytosis within individual thalamic nuclei and the progressive loss of thalamic neurons that relay different sensory modalities to the cortex. This thalamic neuron loss occurred first within the visual system and only subsequently in auditory and somatosensory relay nuclei or the inhibitory reticular thalamic nucleus. The loss of granule neurons and GABAergic interneurons followed in each corresponding cortical region, before the onset of seizure activity. These findings provide novel evidence for successive neuron loss within the thalamus and cortex in Ppt1-/- mice, revealing the thalamus as an important early focus of INCL pathogenesis.

Aging↗
PubMed2004

Recording of ventral posterior lateral thalamus neuron response to contact heat evoked potential in patient with neurogenic pain.

Microrecording of single unit response to contact heat-evoked potential (CHEP) were performed in right ventral posterior lateral (VPL) thalamus during deep brain stimulation (DBS) surgery in a patient with chronic neurogenic pain. In our patient, neurons (n = 10) recorded in the ventral thalamus fired at a higher rate of 40 Hz compared to neurons recorded in Parkinsonian patients (24 Hz). Contact heat was applied by a fast heating and cooling probe of 5 cm2 area on the dermatome C6 territory of the left hand. One out of four thalamic cells located in the VPL responded repetitively 325 ms after the peak temperature was reached with a burst of action potential, suggesting A-delta fibre activation. This observation supports the use of CHEP for mapping nociceptive neurons location during DBS surgery for intractable pain.

Action Potentials↗
PubMed2004

The thalamus as the generator and modulator of EEG alpha rhythm: a combined PET/EEG study with lorazepam challenge in humans.

BACKGROUND: Purpose of this study was to investigate the functional relationship between electroencephalographic (EEG) alpha power and cerebral glucose metabolism before and after pharmacological alpha suppression by lorazepam. METHODS: Ten healthy male volunteers were examined undergoing two F18-fluorodeoxyglucose (18-FDG) positron emission tomography (PET) scans with simultaneous EEG recording: 1x placebo, 1x lorazepam. EEG power spectra were computed by means of Fourier analysis. The PET data were analyzed using SPM99, and the correlations between metabolism and alpha power were calculated for both conditions. RESULTS: The comparison lorazepam versus placebo revealed reduced glucose metabolism of the bilateral thalamus and adjacent subthalamic areas, the occipital cortex and temporo-insular areas (P < 0.001). EEG alpha power was reduced in all derivations (P < 0.001). Under placebo, there was a positive correlation between alpha power and metabolism of the bilateral thalamus and the occipital and adjacent parietal cortex (P < 0.001). Under lorazepam, the thalamic and parietal correlations were maintained, whereas the occipital correlation was no longer detectable (P < 0.001). The correlation analysis of the difference lorazepam-placebo showed the alpha power exclusively correlated with the thalamic activity (P < 0.0001). CONCLUSIONS: These results support the hypothesis of a close functional relationship between thalamic activity and alpha rhythm in humans mediated by corticothalamic loops which are independent of sensory afferences. The study paradigm could be a promising approach for the investigation of cortico-thalamo-cortical feedback loops in neuropsychiatric diseases.

Adult↗
PubMed2005

Voxel-based morphometry of the thalamus in patients with refractory medial temporal lobe epilepsy.

Previous research has suggested that patients with refractory medial temporal lobe epilepsy (MTLE) show gray matter atrophy both within the temporal lobes as well as in the thalamus. However, these studies have not distinguished between different nuclei within the thalamus. We examined whether thalamic atrophy correlates with the nuclei's connections to other regions in the limbic system. T1-weighted MRI scans were obtained from 49 neurologically healthy control subjects and 43 patients diagnosed with chronic refractory MTLE that was unilateral in origin (as measured by ictal EEG and hippocampal atrophy observed on MRI). Measurements of gray matter concentration (GMC) were made using automated segmentation algorithms. GMC was analyzed both voxel-by-voxel (preserving spatial precision) as well as using predefined regions of interest. Voxel-based morphometry revealed intense GMC reduction in the anterior portion relative to posterior thalami. Furthermore, thalamic atrophy was greater ipsilateral to the MTLE origin than on the contralateral side. Here we demonstrate that the thalamic atrophy is most intense in the thalamic nuclei that have strong connections with the limbic hippocampus. This finding suggests that thalamic atrophy reflects this region's anatomical and functional association with the limbic system rather than a general vulnerability to damage.

Adolescent↗
PubMed2004

The mGlu2/3 receptor agonist LY379268 injected into cortex or thalamus decreases neuronal injury in retrosplenial cortex produced by NMDA receptor antagonist MK-801: possible implications for psychosis.

The non-competitive NMDA receptor antagonists, including PCP (phencyclidine), ketamine, and MK-801 (dizocilpine) produce psychosis in humans and injure neurons in retrosplenial cortex in adult rodent brain. This study examined the effects of the metabotropic mGlu2/3 agonist LY379268 and antagonist LY341495 on cortical injury produced by systemic MK-801 (1 mg/kg i.p.) in adult female rats. Systemic injections of mGlu2/3 agonist LY379268, but not mGlu2/3 antagonist LY341495, decreased the injury in the retrosplenial cortex produced by systemic MK-801 as assessed by Hsp70 induction. Bilateral injections of LY379268, but not vehicle, into retrosplenial cortex or bilateral injections of LY379268 into anterior thalamus also decreased the injury in retrosplenial cortex produced by systemic MK-801. The data show that bilateral activation of mGlu2/3 glutamate receptors in cortex or anterior thalamus decreases the neuronal injury in retrosplenial cortex produced by systemic MK-801. Because antipsychotic medications decrease cortical injury produced by NMDA antagonists in rodents and decrease psychosis in humans, mGlu2/3 agonists that decrease cortical injury produced by NMDA antagonists in rodents might be evaluated for decreasing psychosis in people.

Amino Acids↗
PubMed2005

Glycinergic inhibition in thalamus revealed by synaptic receptor blockade.

Using juvenile rat brain slices, we examined the possibility that strychnine-sensitive receptors for glycine-like amino acids contributed to synaptic inhibition in ventrobasal thalamus, where gamma-aminobutyrate (GABA) is the prevalent inhibitory transmitter. Ventrobasal nuclei showed staining for antibodies against alpha1 and alpha2 subunits of the glycine receptor. Exogenously applied glycine, taurine and beta-alanine increased membrane conductance, effects antagonized by strychnine, indicative of functional glycine receptors. Using glutamate receptor antagonists, we isolated inhibitory postsynaptic potentials and currents (IPSPs and IPSCs) evoked by high-threshold stimulation of medial lemniscus. Like the responses to glycine agonists, these synaptic responses reversed near E(Cl). In comparative tests with GABA receptor antagonists, strychnine attenuated inhibition in a majority of neurons, but did not alter slow, GABA(B) inhibition. For complete blockade, the majority of fast IPSPs required co-application of strychnine with bicuculline or gabazine, GABA(A) receptor antagonists. Strychnine acting with an IC50 approximately = 33 nM, eliminated residual fast inhibition during selective GABA(A) receptor blockade with gabazine. The latency of onset for IPSPs was compatible with polysynaptic pathways or prolonged axonal propagation time. Strychnine lacked effects on monosynaptic, GABAergic IPSPs from zona incerta. The specific actions of strychnine implicated a glycine receptor contribution to fast inhibition in somatosensory thalamus.

Animals↗
PubMed2006

Pre-synaptic histamine H3 receptors regulate glutamate, but not GABA release in rat thalamus.

We have investigated the presence of histamine H(3) receptors (H(3)Rs) on rat thalamic isolated nerve terminals (synaptosomes) and the effect of their activation on glutamate and GABA release. N-alpha-[methyl-(3)H]histamine ([(3)H]-NMHA) bound specifically to synaptosomal membranes with dissociation constant (K(d)) 0.78+/-0.20 nM and maximum binding (B(max)) 141+/-12fmol/mg protein. Inhibition of [(3)H]-NMHA binding by histamine and the H(3)R agonist immepip fit better to a two-site model, whereas for the H(3)R antagonist clobenpropit the best fit was to the one-site model. GTPgammaS (30 microM) decreased [(3)H]-NMHA binding by 55+/-4% and made the histamine inhibition fit better to the one-site model. Immepip (30 nM) induced a modest, but significant increase (113+/-2% of basal) in [(35)S]-GTPgammaS binding to synaptosomal membranes, an effect prevented by clobenpropit (1 microM) and by pre-treatment with pertussis toxin. In thalamus synaptosomes depolarisation-induced, Ca(2+)-dependent glutamate release was inhibited by histamine (1 microM, 25+/-4% inhibition) and immepip (30 nM, 38+/-5% reduction). These effects were reversed by clobenpropit (1microM). Conversely, immepip (up to 1 microM) had no effect on depolarisation-evoked [(3)H]-GABA release. Extracellular synaptic responses were recorded in the thalamus ventrobasal complex by stimulating corticothalamic afferents. H(3)R activation reduced by 38+/-7% the glutamate receptor-mediated field potentials (FPs), but increased the FP2/FP1 ratio (from 0.86+/-0.03 to 1.38+/-0.05) in a paired-pulse paradigm. Taken together, our results confirm the presence of H(3)Rs on thalamic nerve terminals and show that their activation modulates pre-synaptically glutamatergic, but not GABAergic neurotransmission.

4-Aminopyridine↗
PubMed2004

Topographical memory impairments after unilateral lesions of the anterior thalamus and contralateral inferotemporal cortex.

Monkeys with crossed unilateral excitotoxic lesions of the anterior thalamus and unilateral inferotemporal cortex ablation were severely impaired at learning two tasks which required the integration of information about the appearance of objects and their positions in space. The lesioned monkeys were also impaired at learning a spatial task and a task which required the integration of information about the appearance of objects and the background on which the objects were situated. Monkeys with only one of the unilateral lesions were not impaired and previous work has shown that monkeys with bilateral lesions of the anterior thalamus were not impaired on these tasks. These results indicate that the whole of the inferotemporal cortex-anterior thalamic circuit, which passes via the hippocampus, fornix, mamillary bodies and mamillothalamic tract, is essential for the topographical analysis of information about specific objects in different positions in space. Together with previous work, the results show that a unilateral lesion may affect cognition in the presence of other brain damage when an equivalent bilateral lesion alone does not. The tasks required the slow acquisition of information into long term memory and therefore assessed semantic knowledge although other research has shown impairment on topographical processing within working or episodic memory following lesions of the hippocampal-diencephalic circuit. It is argued that the hippocampal-diencephalic circuit does not have a role in a specific form of memory such as episodic memory but rather is involved in topographical analysis of the environment in perception and across all types of declarative memory.

Animals↗
PubMed2006

Interactions among the medial prefrontal cortex, hippocampus and midline thalamus in emotional and cognitive processing in the rat.

The medial prefrontal cortex (mPFC) participates in several higher order functions including selective attention, visceromotor control, decision making and goal-directed behaviors. We discuss the role of the infralimbic cortex (IL) in visceromotor control and the prelimbic cortex (PL) in cognition and their interactions in goal-directed behaviors in the rat. The PL strongly interconnects with a relatively small group of structures that, like PL, subserve cognition, and together have been designated the 'PL circuit.' These structures primarily include the hippocampus, insular cortex, nucleus accumbens, basolateral nucleus of the amygdala, the mediodorsal and reuniens nuclei of the thalamus and the ventral tegmental area of the midbrain. Lesions of each of these structures, like those of PL, produce deficits in delayed response tasks and memory. The PL (and ventral anterior cingulate cortex) (AC) of rats is ideally positioned to integrate current and past information, including its affective qualities, and act on it through its projections to the ventral striatum/ventral pallidum. We further discuss the role of nucleus reuniens of thalamus as a major interface between the mPFC and the hippocampus, and as a prominent source of afferent limbic information to the mPFC and hippocampus. We suggest that the IL of rats is functionally homologous to the orbitomedial cortex of primates and the prelimbic (and ventral AC) cortex to the lateral/dorsolateral cortex of primates, and that the IL/PL complex of rats exerts significant control over emotional and cognitive aspects of goal-directed behavior.

Animals↗