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Reciprocal interactions between intralaminar and lateral thalamic nuclei in rats.

Reciprocal interactions between intralaminar thalamic nuclei (ncl. centralis lateralis, CL, and ncl. parafascicularis, Pf), the pretectal area (Pt) and lateral thalamic nuclei (ventrobasal complex, VB, ncl. anterior ventralis, AV, and ncl. ventralis anterior, VA) have been observed in ketamine-anaesthetized rats. Extracellular single unit activity has been recorded after single electrical stimuli. Electrical stimulation of the VB evoked a short latency orthodromic response followed by a pause in spontaneous activity in neurones of medial thalamic nuclei. Lateral thalamic neurones responded to electrical stimulation of the intralaminar nuclei or the pretectal area with the same pattern of response. Striatal, sensorimotor cortical or peripheral electrical stimulation also evoked similar responses. The pauses in spontaneous activity were shown to be the result of inhibition since the responsiveness of the intralaminar nuclei or the lateral thalamic neurones to all inputs was abolished or reduced after a conditioning electrical single-shock stimulation in the VB or in the intralaminar nuclei, respectively. The two components of the response were of a different origin, since most of the short latency responses disappeared after medullary, upper cervical sections or large decortications, while the inhibitions persisted. These inhibitions were shown to be of thalamic origin since their duration was decreased after extensive decortications increased after medullary section. It is concluded that the neuroneal properties studied in this report are probably broadly represented throughout the thalamus and that thalamic neurones are under inhibitory control elicited by afferent volleys. This inhibitory control includes a relay in the nucleus reticularis thalami (nRT). The mechanisms of sensory interaction can be purely thalamic, but they can be modulated by suprathalamic and/or mesencephalic loops.

Animals↗

Electrophysiology of neurons of lateral thalamic nuclei in cat: resting properties and burst discharges.

Intracellular and extracellular recordings were performed in lateral thalamic nuclei (ventroanterior-ventrolateral, ventroposterolateral, centralis, lateralis, and reticularis) of cats under barbiturate anesthesia. Neurons were driven antidromically and/or synaptically by stimulating cortical projection areas and prethalamic afferent pathways. Three neuronal populations were identified on the basis of electrophysiological and anatomical criteria: thalamic relay neurons, local interneurons, and reticularis thalami neurons. At rest, two coexistent rhythms were observed in thalamic neurons. Brief episodes (1-2 s) of membrane-potential oscillations at frequencies of 8-12 Hz appeared with a periodicity of about 10 s. In relay neurons, each episode was characterized by a sequence of hyperpolarizations and burst discharges. These rhythmic episodes of hyperpolarization recurring about every 10 s could be reversed in sign by hyperpolarizing currents or by Cl injection, hence suggesting that they were mainly composed of rhythmic inhibitory postsynaptic potentials (IPSPs). This result also indicated that the slow 0.1-Hz rhythm was imposed on relay neurons by other neuronal pools. Following a complete isolation of the thalamus by cortical and high brain stem lesions, the slow 0.1-Hz rhythm was still present, and it was concluded that this rhythm was generated within the thalamus by inhibitory elements. In thalamic interneurons (identified by electrophysiological criteria) brief episodes (1-2 s) of repetitive depolarizations (8-12 Hz) and burst discharges recurred every 10 s. In the interval, the membrane potential of interneurons slowly hyperpolarized, contrasting with the rhythmic phasic hyperpolarizations observed in relay neurons. Electrophysiological properties shared by most relay neurons included a) afterspike hyperpolarizing potentials of long duration, which were blocked by injections of a Ca chelator; b) a pacemaker potential in the vicinity of the spike trigger level; and c) a low-threshold somatic Ca conductance that underlies burst discharges. As a general rule, prethalamic volleys induced faster rising and shorter lasting EPSPs than cortical volleys. Moreover prethalamic afferent-evoked responses could be associated with production of fast prepotentials, some of which appeared to result from dendritic spiking. It appears that synaptic and intrinsic membrane properties of thalamic neurons allow them to function under two modes: a relay mode and an oscillatory mode; the oscillatory mode being intrinsic to the thalamus and the relay mode being commanded and maintained by cortical and brain stem structures.

Animals↗

Electrophysiology of neurons of lateral thalamic nuclei in cat: mechanisms of long-lasting hyperpolarizations.

Intracellular recordings were performed in the lateral thalamic nuclei of cats under barbiturate anesthesia. The nature of cyclic hyperpolarizations triggered in relay cells by cortical stimulation was analyzed. These long-lasting hyperpolarizations were made of three different components. The early component, which was reversed by current and Cl injections, was identified as a Cl-dependent inhibitory postsynaptic potential (IPSP). A depolarizing hump was usually present in the depth of the long-lasting hyperpolarization. This intermediate component was identified as a voltage-dependent dendritic Ca conductance on the basis of recordings and ethylene glycol tetraacetic acid (EGTA) injections performed in relay cell dendrites. The late phase of hyperpolarization was dissociated from the early IPSP by its differential sensitivity to current and Cl injections and to conditioning tetanic stimulation. This late component was abolished by EGTA and, thus, was interpreted as a Ca-dependent K conductance increase. Activation of intrinsic somatic or dendritic conductances by current pulses never generated rhythmic hyperpolarizations in thalamic relay neurons. Oscillations appear to be imposed on these cells by synaptic inputs. It is then proposed that other thalamic neurons would have pacemaker properties and/or that oscillations would be produced in thalamic cellular pools by feedback interconnections.

Animals↗

Ascending projections to the lateral thalamic nuclei from the substantia grisea centralis in the rat: a retrograde WGA-HRP study.

Ascending projections to the lateral thalamic nuclear group from the substantia grisea centralis (SGC) were studied by injections of wheat germ agglutinin-conjugated with HRP (WGA-HRP) into the laterodorsal (LD) and lateroposterior (LP) thalamic nuclei. The present study demonstrated that the pars ventralis of the SGC at the levels of the intercollicular region and of the locus ceruleus sent fibers to both the LD and LP on both sides with homolateral predominance. Distribution pattern and morphological characteristics of the LD-projection neurons in the SGC were similar to those of SGC-LP projection cells. WGA-HRP injections into the LD or LP labeled also a considerable number of neurons in the dorsal raphe nucleus and the dorsal tegmental nucleus bilaterally with homolateral predominance, but the nucleus of Darkschewitsch contained labeled neurons only after the LD injection.

Animals↗

Electrophysiology and Pharmacology of the Corticothalamic Input to Lateral Thalamic Nuclei: an Intracellular Study in the Cat.

Though most experimental evidence indicates that the corticothalamic (CT) pathway would exert a direct excitatory action on thalamic relay neurons, the electrophysiological features of this excitation have never been clearly described. A methodological problem in previous electrophysiological studies was that direct corticofugal effects on relay cells could not be separated from those mediated by collateral activation of reticular thalamic neurons. In the present study, the reticular complex was lesioned by kainic acid and the CT response of relay neurons of the ventral lateral nucleus was recorded intracellularly in cats under pentobarbital or urethane anaesthesia. Following reticular thalamic lesions, a prominent depolarization was triggered in thalamic relay cells by stimulation of the CT pathway. This depolarization strongly drove spike discharges, and its amplitude augmented when the stimulation rate exceeded 2 Hz. Tetanizing the CT input with short trains (100 - 200 Hz for 200 - 300 ms) produced a similar augmentation to test volleys for 15 - 30 s after the tetanos. The CT excitation and its frequency-dependent augmentation were depressed by ketamine injection or by local application of N-methyl-D-aspartate (NMDA) antagonists. The augmenting phenomenon appeared strictly homosynaptic. For instance, it did not appear during repetitive stimulation of the cerebellar input, nor did the CT input potentiate subthreshold synaptic potentials of cerebellar origin during a conditioning procedure. Conversely, the cerebellar excitation was depressed when it occurred during the CT depolarization. It is concluded that the direct synaptic responses induced by CT fibres in relay neurons are mediated at least partly by the activation of NMDA receptors. Moreover, the marked non-linear additivity of cerebellar and CT synaptic potentials raises questions concerning the presumed improvement of thalamic transmission of peripheral informations ensured by the CT input. Instead, both inputs could compete for control of the firing of thalamic neurons. The numerical importance of CT fibres and the strong augmenting mechanism operating at synaptic sites in the thalamus suggest that the role of the thalamus is not only to transfer peripheral informations toward the cortex, but also and mainly to feed back to the cortex a modified copy of its own neuronal constructs.

Journal Article↗

[Neuronal organization of human ventral anterior and ventral lateral thalamic nuclei].

Neuronal composition was studied in two human thalamic nuclei--nucleus ventralis anterior and nucleus ventralis lateralis using serial horizontal and frontal sections stained using Kluver-Barrera and Golgi silver impregnation methods. It was found that the number of neuronal types, composing the nuclei (equal to eight) is greater than previously reported. Proposed neuronal classification based on the characteristics of their processes, in comparison with a similar study performed in dogs (pups) permitted to distinguish two types of neurons--long-axon and short-axon. Long-axon neurons are subdivided into sparsely-branched (reticular and short-dendritic) and densely-branched (arborescent, giant and medium bush-like, penicillar varieties). Short-axon neuronal type includes smooth-dendritic and "shaggy" cells.

Axons↗

[Reactions of neurons of the parietal associative cortex field 7 to electric stimulation of the latero-dorsal and postero-lateral thalamic nuclei].

Neuronal responses of the parietal associative cortex (PAC) field 7 to the electrical stimulation of laterodorsal (LD) and posterolateral (PL) thalamic nuclei were studied in calypsol-narcotized cats. A correlation between depth, duration of the background activity inhibition and latent periods was determined for distribution of neurons responding to stimulation of associative nuclei by impulses. It is shown that there are functional relations between LD and field 7 of PAC. Common and specific peculiarities of neuronal responses of the associative cortex were found when a volley of impulses came from LD- and PA-nuclei of the thalamus.

Action Potentials↗

Distribution of mRNAs coding for liver and heart gap junction proteins in the rat central nervous system.

The present study examined the distributions of connexin43 mRNA and connexin32 mRNA in the central nervous system (CNS) of the rat by using in situ hybridization histochemistry. These connexins are the best studied gap junction proteins; connexin32 forms direct cell-cell channels in the liver, as does connexin43 in the heart. There was a differential distribution of cells containing connexin32 mRNA compared with the population of cells which contained connexin43 mRNA, thus implying a regional specificity in the expression of connexins in the CNS. Cells containing connexin43 mRNA were uniformly distributed throughout the gray matter of the neuraxis. Several areas had a higher concentration of cells that express connexin43, such as layer IA of the piriform cortex, supraoptic and paraventricular nuclei of the hypothalamus, anterior cortical amygdaloid nucleus, the reticular part of the substantia nigra, lateral habenula, mesencephalic trigeminal nucleus. Purkinje cell layer of the cerebellum, facial nucleus, prepositus hypoglossal nucleus, and dorsal cochlear nucleus. The pattern of connexin43 hybridization and the morphology of connexin43 mRNA containing cells suggest that this gap junction forming protein is found predominantly in astrocytes. Connexin32 mRNA was detected in discrete cell groups of the gray matter that appeared to be neurons, including cells in layer 2 of the neocortex, layer II of the piriform cortex, pyramidal cell layer of the hippocampus, granule and polymorphic cell layers of the dentate gyrus, islands of Calleja, olfactory tubercle, lateral thalamic nuclei, lateral habenula, and Purkinje cell layer of the cerebellar cortex. A large population of cells in white matter tracts that were labelled with the connexin32 riboprobe appeared to be oligodendrocytes. These studies suggest that neurons and glial cells express connexin32 mRNA, but only astrocytes express connexin43 mRNA. Many of the areas in which connexin mRNAs were demonstrated have electrically coupled cells, morphologically distinct gap junction plaques, and/or have immunocytochemically identifiable connexin proteins. These results indicate that cells with mRNAs coding for intercellular channels have a widespread distribution in the mammalian CNS.

Animals↗

Afferent connections of the substantia innominata/basal nucleus of Meynert in carnivores and primates.

Afferent connections to the substantia innominata/nucleus basalis complex of monkeys and cats were traced by using the method of retrograde transport of horseradish peroxidase (HRP). Altogether ten injections of HRP were performed in four monkeys (Saimiri sciureus, Callithrix jacchus, Galago senegalensis) and in four cats, with either vertical or oblique needle approaches. The entire brains excluding the olfactory bulbs and the cerebellum were then screened for labeled neurons. In both monkey and cat brains, many retrogradely labeled neurons could be detected in the amygdala, hypothalamus, midline thalamus, zona incerta, and the fields of Forel. Further but weaker labeling occurred in the medial septal nucleus, diagonal band of Broca, olfactory tubercle, paraventricular, anterior, mediodorsal, and central lateral thalamic nuclei, lateral habenula, ventral tegmental area of Tsai, interpeduncular nucleus, parabrachial, raphe, dorsal tegmental nucleus and the locus caeruleus. Cortically, prefrontal, insular, entorhinal, prepiriform, and periamygdaloid areas of both species showed considerable labeling as well as the whole temporal lobe of the monkeys used. The perirhinal and basal temporal cortex of all cats showed moderate labeling. In both monkeys and cats, extremely scarce labeling occurred within the cingulate, retrosplenial, and subicular cortex. From an anatomical point of view, the manifold connections of the substantia innominata/basal nucleus of Meynert found in this study underscore the participation of these nuclear groups in motivational, emotional, and cognitive (e.g. mnemonic) functions. Considering the widespread cortical efferents of this complex, it is suggested that the substantia innominata/nucleus basalis of Meynert serves the transmission of information arising within the limbic system to the whole neocortex.

Afferent Pathways↗

Connections to the lateral posterior-pulvinar thalamic complex from the reticular and ventral lateral geniculate thalamic nuclei: a topographical study in the cat.

The projections from the reticular thalamic nucleus and the ventral lateral geniculate nucleus to the lateral posterior-pulvinar thalamic complex were studied in the adult cat using the retrograde transport of horseradish peroxidase. Small, stereotaxically guided injections of the enzyme were placed in the various nuclei of this complex, including the pulvinar, lateralis intermedius oralis, lateralis intermedius caudalis, lateralis posterior lateralis, lateralis posterior medialis and lateralis medialis nuclei. The distribution of labeled neurons indicates that these nuclei receive topographically organized projections from the reticular and ventral lateral geniculate nuclei. The pulvinar nucleus receives only very scarce projections from the reticular thalamic nucleus originating in its posterodorsal and posteroventral sectors. The reticular projection to the nucleus lateralis intermedius oralis is even sparser. The nuclei lateralis intermedius caudalis, lateralis posterior lateralis and lateralis posterior medialis receive substantial projections from the suprageniculate sector of the reticular thalamic nucleus. The nucleus lateralis medialis receives an abundant projection from the three sectors (suprageniculate, pregeniculate and infrageniculate) of the reticular thalamic nucleus. Except for the lateralis intermedius caudalis, all nuclei of the lateral posterior-pulvinar complex receive consistent projections from the ventral lateral geniculate nucleus, the nucleus lateralis medialis receiving the densest one. Our findings suggest that visual, auditory, somatosensory, motor and limbic impulses from thalamic nuclei and from primary sensory and association cortical areas modulate the activity of the nucleus lateralis medialis via the reticular thalamic nucleus. The remaining nuclei of the lateral posterior-pulvinar complex are mainly modulated by sectors of the reticular thalamic nucleus that receive afferent connections from visual structures. The intrathalamic projections arising from the ventral lateral geniculate nucleus may be the way through which visuomotor inputs reach the different components of the lateral posterior-pulvinar thalamic complex.

Animals↗

Afferent and efferent connections of the dorsolateral precentral gyrus (area 4, hand/arm region) in the macaque monkey, with comparisons to area 8.

The afferent and efferent connections of the dorsolateral precentral gyrus, the primary motor cortex for control of the upper extremity, were studied by using the retrograde and anterograde capabilities of the horseradish peroxidase (HRP) technique in three adult macaque monkeys that had received HRP gel implants in this cortical region. Reciprocal corticocortical connections were observed primarily with the supplementary motor area (SMA) in medial premotor area 6 and dorsal bank of the cingulate sulcus, postarcuate area 6 cortex, dorsal cingulate cortex (area 24), superior parietal lobule (area 5, PE/PEa), and inferior parietal lobule (area 7b, PF/PFop, including the secondary somatosensory SII region). In these heavily labeled regions, the associational intrahemispheric afferents originated primarily from small and medium sized pyramidal cells in layer III, but also from layer V. The SMA projections were columnar in organization. Intrahemispheric afferents from contralateral homologous and nonhomologous frontal and cingulate cortices also originated predominantly from layer III, but the connections from contralateral area 4 were almost exclusively from layer III. The bilateral connections with premotor frontal area 6 and cingulate cortices were not observed with parietal regions; i.e., only ipsilateral intrahemispheric parietal corticocortical connections were observed. There were no significant connections with prearcuate area 8 or the granular frontal (prefrontal) cortex. Subcortical afferents originated primarily from the nucleus basalis of Meynert, dorsal claustrum, ventral lateral (VLo and VLc), area X, ventral posterolateral pars oralis (VPLo), central lateral and centromedian thalamic nuclei, lateral hypothalamus, pedunculopontine nucleus, locus ceruleus and subceruleus, and superior central and dorsal raphe nuclei. Lesser numbers of retrogradely labeled neurons were observed in the nucleus of the diagonal band, mediodorsal (MD), paracentral, and central superior lateral thalamic nuclei, nucleus limitans, nucleus annularis, and the mesencephalic and pontine reticular formation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Potentiation of electroencephalographic spindles by ibotenate microinjections into nucleus reticularis thalami of cats.

It is well known that the electroencephalogram of the cat in the early stages of slow wave sleep is mainly characterized by rhythmic wave activity at 7-14 Hz, termed spindles, which recur periodically with a slow rhythm of 0.1-0.2 Hz. From early stimulation, decortication and transection studies (see Ref. 14), spindle oscillations were thought to originate in the thalamus. The search for the anatomical substrate of thalamic spindling, however, moved from medial (intralaminar nuclei) to lateral thalamic nuclei, and recently focused on the extreme shell-shaped collection of GABA-ergic cells, the nucleus reticularis thalami. This proposition was based on its structural, hodological, and physiological aspects. There is accumulating evidence that the nucleus reticularis may act as a conditional pacemaker, synchronizing the activity of cortically projecting thalamic neurons. The introduction of glutamate analogues with excitotoxic properties such as ibotenic acid provided the opportunity of studying the immediate effects of chemical excitation of this nucleus on synchronized electroencephalographic activity. We found that, in cats, spindle density was dramatically increased following infusion of ibotenic acid into the rostral pole of the nucleus, supporting the role of this sector in spindle-related rhythmicity.

Animals↗

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↗

Alterations in t-butylbicyclophosphorothionate binding in the brains of lidocaine-kindled rats.

This autoradiographic study examines regional GABAA receptors in lidocaine-kindled rats. [35S]t-Butylbicyclophosphorothionate (TBPS), which binds in or near the chloride channel, was used to radiolabel GABAA complexes. Male Sprague-Dawley rats were injected daily with lidocaine (65mg/kg, i.p.). Seizure activity was evaluated using the Racine Scale (Racine, 1972). The animals displayed a gradual increase in the indices and by day 20 greater than 50% were in stage 4 or 5. Regression of behavior was seen in half of the experimental group and this subgroup was considered 'compensated'. Autoradiographs were analyzed using a computer-based image analysis system. Several regions within the kindled group display a decrease in TBPS binding, including the subiculum, posterior lateral thalamic nuclei, the lateral hippocampus CA1, and the lateral hippocampus CA3. Conversely, within the compensated group these regions display normal or heightened TBPS binding. The data support the theory that alterations in the GABAA receptors are involved in the kindling model of epilepsy.

Animals↗

Immunocytochemical localization of angiotensinogen in the fetal and neonatal rat brain.

The aim of this study was to define the temporal appearance and regional distribution of angiotensinogen in the fetal and neonatal rat brain. This was done by immunocytochemical localization of angiotensinogen in brains from embryonic day 16 to postnatal day 12. Immunostaining was first observed on embryonic day 18, and persisted to postnatal day 2, in the choroid plexus and ependymal cells lining the third ventricle. This initial expression of angiotensinogen at embryonic day 18 was followed at postnatal day 20 by a rapid progression of angiotensinogen staining appearing in astrocytes in the paraventricular nucleus, medial preoptic area, ventromedial and arcuate hypothalamic nuclei; these areas showed the highest astrocyte staining intensity in the brain. This was followed sequentially by staining in areas of the thalamus, midbrain, forebrain and brainstem. In general, neuroglial staining was higher in regions proximal to the cerebral ventricles and cerebral aqueduct. Neuronal angiotensinogen was observed at day postnatal day 0 and later. The most consistent immunopositive areas were in the forebrain and thalamus; in particular, the hippocampus, anterior and posterior cingulate cortex, basal and lateral amygdala, the caudate-putamen, globus pallidus, lateral septum, medial habenular nuclei and lateral thalamic nuclei. Most of the immunopositive cells in the hypothalamus and brainstem were astrocytes, while those in the cortex were almost exclusively neurons. Staining in thalamic regions was both neuronal and neuroglial. From the intensity of staining and cell density, it was determined that a rapid increase in angiotensinogen occurs between embryonic day 20 and postnatal day 0, followed by further, smaller increases postnatally. In conclusion, this study has shown that angiotensinogen, the protein from which angiotensin II is generated, is present in the rat fetal brain. The timing of its appearance supports the establishment of a renin-angiotensin system by late gestation. Its predominance in fetal hypothalamic nuclei and in thalamic, cerebellar and cortical neurons suggests major roles in prenatal fluid and electrolyte balance, in sensorimotor development and in brain maturation.

Angiotensinogen↗