Ventrolateral Thalamic Nucleus Research Articles

Neural firing in ventrolateral thalamic nucleus during conditioned vocal behavior in cats.

The ventrolateral (VL) thalamus in mammals is a site well-situated to show vocalization-related neural activity if there is general or classical motor system involvement in vocal production. It receives input from both the basal ganglia and cerebellum, and forms reciprocal connections with motor cortical areas. The current study examined the activity in cat VL thalamus neurons during instrumentally conditioned vocalization. Units in our sample showed irregular spontaneous firing which could be modulated by slowly occurring fluctuations in intensity of vocalization task performance. Two main types of behavioral events were associated with changes in neural firing rate. The first of these was the ingestion of food reward. More than half of all recordings showed phasic bursting patterns during licking; a similar number had increases in firing preparatory to this phasic activity. The second behavioral event modulating unit responses was vocalization. Approximately 60% of recordings showed activity changes time-locked to vocalization. These responses were almost always excitatory, and often involved changes in firing that preceded vocalization onset. No spatial organization of differences in firing pattern between neurons could be distinguished. Our results suggest that VL thalamus may well be involved in mediating vocal behavior, although its functional role remains an object of speculation. Results are compared with previous studies of vocalization-related activity and of VL thalamus activity.

Neuropeptide Y and enkephalin immunoreactivity in retinorecipient nuclei of the hamster pretectum and thalamus.

This investigation was stimulated by the historical confusion concerning the identity of certain pretectal nuclei and by large differences reported between species with respect to which nuclei receive retinal innervation. Subcortical visual nuclei were studied using immunohistochemistry to identify retinal projections labeled following intraocular injection of cholera toxin, b fragment. In addition, neuropeptide Y (NPY) or enkephalin (ENK) immunoreactive cells and fibers were also evaluated in the retinorecipient pretectal and thalamic areas. The results confirm the established view that the retina directly innervates the nucleus of the optic tract (NOT), posterior (PPT), and olivary pretectal (OPT) nuclei. However, the retina also innervates the hamster medial (MPT) and anterior (APT; dorsal division) pretectal nuclei, results not previously reported in rodents. A commissural pretectal area (CPT) sparsely innervated by retina is also described. The data show for the first time that the posterior limitans nucleus (PLi) receives a moderately dense, direct retinal input. The PLi does not project to the cortex and appears to be a pretectal, rather than thalamic, nucleus. All retinal projections are bilateral, although predominantly contralateral. The PLi contains a moderately dense plexus of NPY- and ENK-IR fibers and terminals. However, peptidergic fibers also traverse the ATP and connect with the dorsomedial pretectium. The OPT contains ENK- and NPY-IR neurons and fibers, but is specifically identifiable by a moderately dense plexus of ENK-IR terminals. Numerous ENK-IR neurons are found in the NOT and PPT. The latter also has moderate numbers of ENK-IR fibers and terminals, but few NPY-IR neurons or fibers. The MPT contains modest numbers of ENK-IR fibers. The APT has no NPY-IR neurons or terminals, but an occasional ENK-IR neuron is seen and there is sparse ENK-IR innervation. Peptidergic innervation of the visual nuclei does not appear to be derived from the retina. The results show a set of retinally innervated, contiguous nuclei extending from the thalamic ventrolateral geniculate nucleus dorsomedially to the midbrain CPT. These nuclei plus the superior colliculus comprise a dorsal "visual shell" embracing a central core of caudal thalamus and rostral midbrain.

Efferent connections of the internal globus pallidus in the squirrel monkey: I. topography and synaptic organization of the pallidothalamic projection

The objectives of this study were, on one hand, to better understand how the segregated functional pathways from the cerebral cortex through the striatopallidal complex emerged in the projections to the thalamus and, on the other hand, to compare the ultrastructure and synaptic organization of the pallidal efferents to the ventrolateral (VL) and centromedian (CM) thalamic nuclei in primates. These aims were achieved by injections of the retrograde-anterograde tracer, biotinylated dextran amine (BDA), in different functional regions of the internal pallidum (GPi) in squirrel monkeys. The location of retrogradely labelled cells in the striatum was determined to ascertain the functional specificity of the injection sites. Injections in the ventrolateral two-thirds of the GPi (group 1) led to retrograde labelling in the postcommissural region of the putamen ("sensorimotor striatum") and plexuses of labelled fibers in the rostral one-third of the principal ventrolateral nucleus (VLp) and the central part of the CM. On the other hand, injections in the dorsal one-third (group 3) and the rostromedial pole (group 4) of the GPi led to retrogradely labelled cells in the body of the caudate nucleus ("associative striatum") and the ventral striatum ("limbic striatum"), respectively. After those injections, dense plexuses of anterogradely labelled varicosities were found in common thalamic nuclei, including the parvocellular ventral anterior nucleus (VApc), the dorsal VL (VLd), and the rostrodorsal part of the parafascicular nucleus (PF). In the caudal two-thirds of the CM/PF, the labelled fibers formed a band that lay along the dorsal border of the complex in a region called the dorsolateral PF (PFdl) in this study. The ventromedial nucleus (VM) was densely labelled only after injections in the rostromedial GPi, whereas the dorsal part of the zona incerta was labelled in both groups. At the electron microscopic level, the BDA-positive terminals in the VLp were larger and more elongated than those in the CM but, overall, displayed the same pattern of synaptic organization. Our findings indicate 1) that some associative and limbic cortical information, which is largely processed in segregated corticostriatopallidal channels, converges to common thalamic nuclei and 2) that the PF is a major target of associative and limbic GPi efferents in monkeys.

Efferent connections of the internal globus pallidus in the squirrel monkey: I. topography and synaptic organization of the pallidothalamic projection

The objectives of this study were, on one hand, to better understand how the segregated functional pathways from the cerebral cortex through the striatopallidal complex emerged in the projections to the thalamus and, on the other hand, to compare the ultrastructure and synaptic organization of the pallidal efferents to the ventrolateral (VL) and centromedian (CM) thalamic nuclei in primates. These aims were achieved by injections of the retrograde-anterograde tracer, biotinylated dextran amine (BDA), in different functional regions of the internal pallidum (GPi) in squirrel monkeys. The location of retrogradely labelled cells in the striatum was determined to ascertain the functional specificity of the injection sites. Injections in the ventrolateral two-thirds of the GPi (group 1) led to retrograde labelling in the postcommissural region of the putamen (“sensorimotor striatum”) and plexuses of labelled fibers in the rostral one-third of the principal ventrolateral nucleus (VLp) and the central part of the CM. On the other hand, injections in the dorsal one-third (group 3) and the rostromedial pole (group 4) of the GPi led to retrogradely labelled cells in the body of the caudate nucleus (“associative striatum”) and the ventral striatum (“limbic striatum”), respectively. After those injections, dense plexuses of anterogradely labelled varicosities were found in common thalamic nuclei, including the parvocellular ventral anterior nucleus (VApc), the dorsal VL (VLd), and the rostrodorsal part of the parafascicular nucleus (PF). In the caudal two-thirds of the CM/PF, the labelled fibers formed a band that lay along the dorsal border of the complex in a region called the dorsolateral PF (PFdl) in this study. The ventromedial nucleus (VM) was densely labelled only after injections in the rostromedial GPi, whereas the dorsal part of the zona incerta was labelled in both groups. At the electron microscopic level, the BDA-positive terminals in the VLp were larger and more elongated than those in the CM but, overall, displayed the same pattern of synaptic organization. Our findings indicate 1) that some associative and limbic cortical information, which is largely processed in segregated corticostriatopallidal channels, converges to common thalamic nuclei and 2) that the PF is a major target of associative and limbic GPi efferents in monkeys. J. Comp. Neurol. 382:323-347, 1997. © 1997 Wiley-Liss, Inc.

Alterations in N-methyl- d-aspartate receptor binding in dystonic hamster brains

The genetically dystonic hamster is an animal model of idiopathic dystonia that displays sustained abnormal movements and postures either spontaneously or in response to mild environmental stimuli. Previous pharmacological studies have shown that competitive and non-competitive N-methyl- d-aspartate (NMDA) receptor antagonists exert potent antidystonic activity in this model, indicating that abnormal NMDA receptor function may be involved in the pathophysiology of this movement disorder. Autoradiographic analysis of NMDA receptor density in 67 brain regions, using the ligand [ 3H] N-(1-[2-thienyl]cyclohexyl)3,4-piperidine, which binds to the phencyclidine (PCP) site in the ion channel of the NMDA receptor channel complex, revealed that NMDA receptor binding is not substantially altered in dystonic hamster brains compared to age-matched controls. Nevertheless, there was a tendency towards enhanced binding during a dystonic attack in several regions, including a 25% increase in the ventrolateral thalamic nucleus ( P<0.05), which may be associated with altered basal ganglia output. While the data do not indicate widespread abnormalities in the PCP site of the NMDA complex, they do not exclude the possibility of more pronounced changes at other regulatory binding sites of the NMDA complex or other types of glutamate receptors in dystonia.

Ontogeny of vasoactive intestinal peptide gene expression in rat brain

Vasoactive intestinal peptide (VIP) expression was studied during rat brain development using in situ hybridization histochemistry with a 48mer, S35-ATP-labeled probe. First expression of VIP was found in the lateral thalamus at E17, in a region later recognized as the reticular nucleus. At E19, VIP mRNA was also found in the hypothalamus, especially the suprachiasmatic nucleus. The only other prenatal localizations were the cortex and the brainstem. VIP expression continously matured during the first three postnatal weeks, and adult-like patterns were found at P22, when cerebral cortex, ventrolateral and reticular thalamic nuclei, suprachiasmatic nucleus were the regions with most prominent VIP expression. These results demonstrate the relatively late appearance of VIP gene expression in the rat forebrain as compared with peptides like SRIF and CCK, suggesting it does not have a major role in early brain maturation.

Retrograde transport of brain-derived neurotrophic factor (BDNF) following infusion in neo- and limbic cortex in rat: relationship to BDNF mRNA expressing neurons.

Brain-derived neurotrophic factor (BDNF) was the second member of the nerve growth factor (NGF) family to be isolated. The ability of BDNF to be retrogradely transported following intraparenchymal infusion represents a unique neurobiological tool to determine the location of putative neuron-specific BDNF-responsive neuronal systems. In the present study, we infused recombinant human (rh) BDNF into the rodent neo- and limbic cortex and used a turkey anti-BDNF antibody to determine specific populations of neurons which retrogradely transport this neurotrophin. Frontal cortex infusion retrogradely labeled neurons within the ipsilateral and contralateral frontal cortex, basal forebrain, lateral hypothalamus, centrolateral, mediodorsal, ventrolateral, ventromedial, ventral posterior, rhomboid, reuniens, and medial geniculate thalamic nuclei, and locus coeruleus. Occipital cortex infusion retrogradely labeled neurons in the frontal, temporal, occipital, and perirhinal cortices as well as the claustrum, basal forebrain, thalamus, epithalamus, hypothalamus, and raphe nuclei. Dorsal hippocampal infusion retrogradely labeled neurons within the septal diagonal band, supramammillary nucleus, and entorhinal cortex and was also transported within various hippocampal subfields. Entorhinal cortex infusion retrogradely labeled neurons within the perirhinal cortex, endopiriform nucleus, piriform cortex, dentate gyrus, presubiculum, parasubiculum, CA1-CA4 fields, amygdaloid nuclei, basal forebrain, thalamus, hypothalamus, periaqueductal gray, raphe nuclei, and locus coeruleus. Amygdala infusion labeled neurons in the endopiriform nucleus, temporal cortex, piriform cortex, paralimbic cortex, hippocampus, subiculum, entorhinal cortex, amygdala, basal forebrain, thalamus, hypothalamus, substantia nigra, pars compacta, raphe, and pontine parabrachial nuclei. In situ hybridization experiments demonstrated that virtually all areas which retrogradely transport BDNF also express its message. Neuroanatomical distributional studies of BDNF will unravel specific central nervous system neurotrophic-responsive systems.

Microglial reactions to retrograde degeneration of tracer-identified thalamic neurons after frontal sensorimotor cortex lesions in adult rats.

Thalamic neuronal degeneration after neocortical lesions involve both anterograde and retrograde components. This study deals with the thalamic microglial response after neocortical aspiration lesions, using fluorogold fluorescent prelabeling, to identify retrogradely degenerating thalamocortical neurons, combined with histochemical or immunohistochemical staining of microglial cells. Adult male Wistar rats were injected with the retrograde fluorescent tracer fluorogold, in the right sensorimotor cortex (forepaw area) in order to retrogradely label thalamic neurons projecting to this area. After 1 week, the fluorogold injection site was removed by aspiration, axotomizing at the same time the thalamic projection neurons now retrogradely labeled with fluorogold. After 3, 7, 14, and 28 days the animals were killed and processed for nucleoside diphosphatase histochemistry or complement type 3 receptor immuno-histochemistry and class I and II major histocompatibility complex immunohistochemistry using OX42, OX18, and OX6 antibodies. The histological analysis showed a prominent and progressive nucleoside diphosphatase-, OX42-, and OX6-positive microglial cell response in the ventrolateral, posterior, and ventrobasal thalamic nuclei with ongoing retrograde and anterograde neuronal degeneration. Initially the reactive microglia had a bushy morphology and were succeeded by ameboid microglia and microglial cluster cells as the reaction progressed. However, in the reticular thalamic nucleus, which suffered exclusively anterograde neuronal degeneration, a different picture was seen with only bushy microglia. The neurons undergoing retrograde degeneration in the ventrolateral, posterior, and ventrobasal thalamic nuclei were retrogradely labeled by the fluorogold tracer. Individual nucleoside diphosphatase-, OX42-, or OX6-positive microglial cells extended long cytoplasmic processes surrounding fluorogold-labeled neurons and had in some cases apparently phagocytized these. Several microglial cells were thus double-labeled with nucleoside diphosphatase or OX42 and fluorogold. In addition, small nucleoside diphosphatase-positive, fluorogold-labeled perivascular cells were observed in the neocortex near the fluorogold-injected and ablated neocortical areas and in the ipsilateral thalamus. This study demonstrates: (1) that the microglial response to thalamic degeneration after neocortical lesion is graded with a limited reaction to the well-known massive anterograde axonal degeneration and a more extended reaction to the axotomy-induced retrograde cell death; and (2) that also perivascular cells and possibly macrophages may contribute to this reaction, as seen by uptake of fluorogold from axotomized neurons in the degenerating thalamic nuclei.

The relationship between monkey ventrolateral thalamic nucleus activity and kinematic parameters of wrist movement

Extracellular recordings were made from single neurones in the cerebellar thalamus (75 neurones) and the VPLc (44 neurones) of four conscious moving monkeys. The experiment was designed to establish whether the discharge of ventrolateral thalamic neurones encodes information about kinematic parameters. The animals were trained to resist unexpected perturbations of the wrist and to perform skilled, voluntary wrist movements, producing stereotyped reflex and active movements with a wide range of durations and amplitudes. Statistical analysis of the discharge pattern associated with individual trials of movement was performed. In various maintained wrist positions there was a significant correlation (P < 0.05) between frequency of tonic discharge and joint position in 40% of the cerebellar thalamic neurones and in 54% of VPLc neurones. The phasic neuronal discharge associated with stereotyped movement often appeared ‘velocity or acceleration-like’. However, statistical analyses revealed that the phasic discharge of only a small percentage of cerebellar thalamic and VPLc neurones was correlated with duration of movement, peak velocity or acceleration. The percentage of cerebellar thalamic neurones with discharge correlated to kinematic parameters was much greater when an unexpected change in the gain between joint angle and screen display led to errors in tracking the target. It is concluded that the cerebelao-thalamo-cortical (CTC) pathway carries information regarding maintained joint position but not velocity or acceleration of movement during a stereotyped task. However, the CTC pathway has a greater capacity to signal information about movement velocity and acceleration when there is a mismatch between the intended and actual movement.

The relationship between monkey ventrolateral thalamic nucleus activity and kinematic parameters of wrist movement

Extracellular recordings were made from single neurones in the cerebellar thalamus (75 neurones) and the VPLc (44 neurones) of four conscious moving monkeys. The experiment was designed to establish whether the discharge of ventrolateral thalamic neurones encodes information about kinematic parameters. The animals were trained to resist unexpected perturbations of the wrist and to perform skilled, voluntary wrist movements, producing stereotyped reflex and active movements with a wide range of durations and amplitudes. Statistical analysis of the discharge pattern associated with individual trials of movement was performed. In various maintained wrist positions there was a significant correlation ( P < 0.05) between frequency of tonic discharge and joint position in 40% of the cerebellar thalamic neurones and in 54% of VPLc neurones. The phasic neuronal discharge associated with stereotyped movement often appeared ‘velocity or acceleration-like’. However, statistical analyses revealed that the phasic discharge of only a small percentage of cerebellar thalamic and VPLc neurones was correlated with duration of movement, peak velocity or acceleration. The percentage of cerebellar thalamic neurones with discharge correlated to kinematic parameters was much greater when an unexpected change in the gain between joint angle and screen display led to errors in tracking the target. It is concluded that the cerebelao-thalamo-cortical (CTC) pathway carries information regarding maintained joint position but not velocity or acceleration of movement during a stereotyped task. However, the CTC pathway has a greater capacity to signal information about movement velocity and acceleration when there is a mismatch between the intended and actual movement.

A comparison of the ultrastructure of synapses in the cerebello-rubral and cerebello-thalamic pathways in the rat

The aim of this study was to compare the ultrastructure of anterogradely labelled cerebellar terminals in the red nucleus (RN), ventrolateral (VL), parafascicular (PF) and central medial (CM) thalamic nuclei, as well as in the zona incerta (ZI). No differences were found in the morphology of synapses in any of the nuclei. Terminals in RN and VL were larger than those in PF, CM and ZI and synapsed proximally. In contrast, synapses in PF, CM and ZI formed mainly on distal dendrites. These findings indicate that cerebellar output neurones (a) form morphologically similar synapses (Gray's type I) on neurones in functionally different nuclei, and (b) form larger, more proximal synapses in RN and VL than in PF, CM and ZI.

Involvement of the ventrolateral thalamic nucleus in rabbit classical eyeblink conditioning

The involvement of the ventrolateral nucleus of the thalamus in relaying learning-related activity to higher brain structures during classical conditioning of the rabbit eyelid response was examined in two experiments. In the first study, multiple-unit ventrolateral thalamic nucleus activity was monitored before and after lesions of either the cerebellar interpositus nucleus or red nucleus were given. Before the lesions were given, conditioned response-related activity was observed in the ventrolateral thalamic nucleus. Lesions of the interpositus nucleus, but not the red nucleus, disrupted the conditioning-related activity in the ventrolateral thalamic nucleus, thus suggesting that an efferent copy to conditioned response-related activity is projected directly from the interpositus nucleus to higher brain areas by way of the ventrolateral thalamic nucleus. In the second study, multiple unit activity in the hippocampus was monitored before and after lesions were placed in the ventrolateral thalamic nucleus or red nucleus. Conditioning-related activity in the hippocampus was not affected by either lesion, thus suggesting that maintenance of training-related activity in the hippocampus is not critically dependent on cerebellar information relayed through the ventrolateral thalamic nucleus or red nucleus.

Parietal kinetic ataxia without proprioceptive deficit.

A patient with acute onset "classic" cerebellar ataxia of the right arm without clinically detectable deep sensory loss is reported, in relation to an acute posterior parietal infarct. Wild back and forth swaying of the arm, giving away, or worsening by suppression of vision were not seen. The lesion involved area 5, parts of area 7, the angular gyrus, the middle and posterior parieto-occipital gyri, and posterior parts of the superior and middle temporal gyri. The paracentral lobule, commonly thought to be responsible for parietal ataxia, was spared. Thus posterior parietal lesions can mimick cerebellar ataxia, possibly by severing specific projections to the ventrolateral thalamic nuclei. On the basis of previous studies in primates, the superior parietal gyrus may play a major part in the ataxia presented by this patient.

Functional anatomy of the thalamic reticular nucleus as revealed with the [14C]deoxyglucose method following electrical stimulation and electrolytic lesion.

The [14C]-deoxyglucose quantitative autoradiographic method was used to map the metabolic changes induced by electrical stimulation and electrolytic lesion of the rostral pole of the thalamic reticular nucleus in the rat brain. Unilateral electrical stimulation of the thalamic reticular nucleus induced the following changes in glucose utilization: (i) local enhancement of metabolic activity within the stimulated thalamic reticular nucleus, (ii) increase in glucose consumption in the ipsilateral thalamic mediodorsal, centrolateral, ventromedial and ventrolateral nuclei, as well as in the nucleus accumbens, (iii) bilateral depression of metabolism in the locus coeruleus, periaqueductal gray, ventral tegmental area, and medial habenula, as well as contralateral metabolic depression in the substantia nigra reticulata, compacta and in the ventral pallidum. Unilateral electrolytic lesion of thalamic reticular nucleus elicited metabolic depression in the ipsilateral thalamic mediodorsal, centrolateral, ventrolateral and ventromedial nuclei, and metabolic activation in the dorsal tegmental nucleus bilaterally. The existence of a descending thalamic reticular nucleus input to the periaqueductal gray is supported by the depressed activity measured in brain stem structures after thalamic reticular nucleus stimulation. The similar effects observed in the periaqueductal gray and substantia nigra contralateral to the stimulated thalamic reticular nucleus indicate a possible flow of information from one thalamic reticular nucleus to the contralateral basal ganglia via the periaqueductal gray. The opposite effects induced in the dorsal thalamic nuclei by thalamic reticular nucleus stimulation and lesion support the gating role of the thalamic reticular nucleus in the information flow between thalamus and cortex.

Functional anatomy of the thalamic centrolateral nucleus as revealed with the [14C]deoxyglucose method following electrical stimulation and electrolytic lesion.

The effects of electrical stimulation and electrolytic lesion of the thalamic intralaminar centrolateral nucleus were studied in the rat brain by means of the quantitative autoradiographic [14C]deoxyglucose method. Unilateral electrical stimulation of the centrolateral nucleus induced: (i) local increase in metabolic activity within the stimulated centrolateral nucleus and the ipsilateral thalamic mediodorsal nucleus, (ii) metabolic depression in all layers of the ipsilateral frontal cortex, (iii) bilateral increase in glucose consumption within the periaqueductal gray, pedunculopontine nucleus, and pontine reticular formation, and (iv) contralateral metabolic activation in the deep cerebellar nuclei. The unilateral electrolytic lesion of the thalamic centrolateral nucleus elicited metabolic depressions in several distal brain areas. The metabolic depression elicited in the mediodorsal, ventrolateral, and lateral thalamic nuclei, as well as in the caudate nucleus, the cingulate, and the superficial layers of forelimb cortex were ipsilateral to the lesioned side. The metabolic depression measured in the medulla and pons (medullary and pontine reticular formation, periaqueductal gray, locus coeruleus, dorsal tegmental, cuneiformis, raphe and pedunculopontine tegmental nuclei), the cerebellum (molecular and granular layers of the cerebellar cortex, interpositus and dentate nuclei), the mesencephalon (substantia nigra reticulata, ventral tegmental area and deep layers of the superior colliculus), the diencephalon (medial habenula, parafascicular, ventrobasal complex, centromedial and reticular thalamic nuclei), the rhinencephalon (dentate gyrus and septum), the basal ganglia (ventral pallidum, globus pallidus, entopeduncular and accumbens nuclei) and the cerebral cortex (superficial and deep layers of the frontal and parietal cortex, deep layers of the forelimb cortex) were bilateral. These functional effects are discussed in relation to known anatomical pathways. The bilateral effects induced by the centrolateral nucleus lesion reflect an important role of the centrolateral nucleus in the processing of reticular activating input and in the interhemispheric transfer of information. The cortical metabolic depression induced by centrolateral nucleus stimulation indicates the participation of this nucleus in attentional functions.

Expression of cholecystokinin mRNA in corticothalamic projecting neurons: a combined fluorescence in situ hybridization and retrograde tracing study in the ventrolateral thalamus of the rat.

Cholecystokinin (CCK), a well-known neuroactive peptide, has been observed in the axon endings within the thalamic reticular nucleus and the adjacent ventrolateral nucleus of the thalamus. The origin of this CCK innervation remains undefined. In this study, a fluorescence in situ hybridization (FISH) technique was used in conjunction with latex microsphere retrograde tracing to investigate whether cortical neurons may provide a source of CCK afferents to the ventrolateral thalamic nucleus. Rhodamine latex beads were injected into the ventrolateral thalamic nucleus of adult male rats to retrogradely label corticothalamic cells. After 7 days, tissues were processed for FISH using a 24-base oligonucleotide probe complementary to the 3' coding region of rat preprocholecystokinin mRNA. It was found that CCK transcripts are expressed in about 80% of identified corticothalamic projecting neurons. We therefore conclude that the descending cortical projections to the ventrolateral thalamus may provide an important source of CCK innervation to this region of the brain.

Trans-synaptic modulation of striatal ACh release in vivo by the parafascicular thalamic nucleus.

Electrical stimulation of the parafascicular but not the ventrolateral or dorsomedial thalamic nucleus (ten 0.5 ms, 10 V pulses, 140 microA) of freely moving rats induced a frequency-dependent (2.5, 5, 10 and 20 Hz) increase in the extracellular acetylcholine (ACh) content of the dorsal striatum, assessed by trans-striatal microdialysis. The time-dependent effect of 10 Hz stimulation was studied. The peak increase, 39% above baseline, was attained during 4 min of stimulation. This was blocked by coperfusion with 5 microM tetrodotoxin, indicating that the release we measured represents a physiological process. The facilitatory effect of parafascicular nucleus stimulation does not appear to be associated with indirect action through the cerebral frontal cortex because acute lesion of the excitatory corticostriatal afferents, which by itself reduced basal ACh release by 40%, did not modify the effect of 10 Hz stimulation. The possible involvement of the fasciculus retroflexus in the facilitation of ACh release was also ruled out. The non-competitive NMDA-type receptor antagonist MK-801, applied by reversed dialysis (30 microM) or systemically injected (0.2 mg/kg), significantly reduced the basal ACh output and prevented the tetanus-evoked increase in ACh release. The results provide in vivo evidence that the activity of the cholinergic neurons in the dorsal striatum is trans-synaptically modulated by parafascicular nucleus excitatory afferents through activation of the NMDA subtype of glutamate receptors that is probably located in the striatum.

Interaction of direct afferent and recurrent signals in cat motor cortex neurons

Intracellular activity was recorded from the functionally identified motor cortex neurons (MI, area 4γ) in acute experiments on myorelaxin-immobilized cats under calypsol anesthesia. Changes in neuronal responses to testing stimulation of the ventrolateral thalamic nucleus or pyramidal tract fibers were studied; the same or another input was used for a conditioning stimulation. Excitatory and inhibitory components of test responses of variousMI neurons were found to be either facilitated or depressed. The facilitation of orthodromic excitation was more frequent in the case of thalamic testing stimulation. The depression of both excitatory and inhibitory components of the response was more pronounced with paired stimulation of the pyramidal tract fibers. The peculiarities of interaction between direct afferent and recurrent signals in theMI neurons are thought to be determined by different distribution of thalamocortical fiber terminals and recurrent collaterals of corticofugal axons in the cortex and nonuniform localization of their synapses on dendrites and somata of the studied cells. It seems possible that these peculiarities also are connected with different chemical mechanisms of synaptic transmission in the above synapses and different properties of postsynaptic membrane receptors.

The forebrain of gnathostomes: in search of a morphotype.

A morphotype of the forebrain of gnathostomes, i.e. those characters that must have been present in the forebrain of ancestral gnathostomes, was generated by using out-group analysis to identify the shared primitive characters present in the forebrains of extant gnathostomes. The nature of morphotypes and the steps in generating a morphotype are described. Because hypotheses of phylogenetic relationships profoundly affect the resulting morphotype, current hypotheses of gnathostome interrelationships are reviewed, and particular attention is paid to the problematic relationships of lobe-finned fishes. Ontogenetic studies provide the most common basis for how neural characters are grouped, and a review of the developmental literature indicates that gnathostome forebrains are segmented, with the diencephalon arising from a rostral parencephalic neuromere, which subsequently forms anterior and posterior divisions, and a more caudal synencephalic neuromere. Unfortunately, there is no agreement concerning the number of segments that form the secondary prosencephalon (telencephalon and hypothalamus). For this reason, the characters of the secondary prosencephalon must be analyzed in a topological manner. An out-group analysis of the characters of the diencephalon of extant gnathostomes reveals that the diencephalon of ancestral gnathostomes must have arisen from three segments: an anterior parencephalic segment, which gave rise to intermediate, ventrolateral and ventromedial thalamic nuclei; a posterior parencephalic segment, which gave rise to dorsal and ventral habenular nuclei, anterior, dorsal posterior, dorsal central, and, possibly, lateral posterior thalamic nuclei, and posterior tubercular nuclei; a synencephalic segment, which gave rise to pretectal nuclei, accessory optic nuclei and the nucleus of the medial longitudinal fascicle. The pretectal and posterior tubercular regions of ray-finned fishes appear to be highly derived, due to extensive cellular proliferations that give rise to numerous nuclei. The secondary prosencephalon of ancestral gnathostomes was probably divided rostrally into inverted and evaginated cerebral hemispheres, with paired olfactory bulbs arising directly from the hemispheres, and caudally into preoptic and hypothalamic areas. The cerebral hemispheres likely comprised a dorsally situated pallium divided into medial, dorsal and lateral pallial formations, as well as an intercalated pallial nucleus situated ventrolateral to the lateral pallium, and a ventrally situated subpallium divided medially into septal nuclei and a medial amygdalar nucleus and laterally into a corpus striatum. Both pallial and subpallial centers of ancestral gnathostomes probably received ascending thalamic and posterior tubercular inputs, with telencephalic efferent pathways terminating primarily in the hypothalamus, posterior tubercle and midbrain tegmentum. An out-group analysis further indicates that some taxa in each gnathostome radiation exhibit highly derived telencephalic characters due to the independent expansion of one or more pallial formations.

The Forebrain of Gnathostomes: In Search of a Morphotype; pp. 289–303

A morphotype of the forebrain of gnathostomes, i.e. those characters that must have been present in the forebrain of ancestral gnathostomes, was generated by using out-group analysis to identify the shared primitive characters present in the forebrains of extant gnathostomes. The nature of morphotypes and the steps in generating a morphotype are described. Because hypotheses of phylogenetic relationships profoundly affect the resulting morphotype, current hypotheses of gnathostome interrelationships are reviewed, and particular attention is paid to the problematic relationships of lobe-finned fishes. Ontogenetic studies provide the most common basis for how neural characters are grouped, and a review of the developmental literature indicates that gnathostome forebrains are segmented, with the diencephalon arising from a rostral parencephalic neuromere, which subsequently forms anterior and posterior divisions, and a more caudal synencephalic neuromere. Unfortunately, there is no agreement concerning the number of segments that form the secondary prosencephalon (telencephalon and hypothalamus). For this reason, the characters of the secondary prosencephalon must be analyzed in a topological manner. An out-group analysis of the characters of the diencephalon of extant gnathostomes reveals that the diencephalon of ancestral gnathostomes must have arisen from three segments: an anterior parencephalic segment, which gave rise to intermediate, ventrolateral and ventromedial thalamic nuclei; a posterior parencephalic segment, which gave rise to dorsal and ventral habenular nuclei, anterior, dorsal posterior, dorsal central, and, possibly, lateral posterior thalamic nuclei, and posterior tubercular nuclei; a synencephalic segment, which gave rise to pretectal nuclei, accessory optic nuclei and the nucleus of the medial longitudinal fascicle. The pretectal and posterior tubercular regions of ray-finned fishes appear to be highly derived, due to extensive cellular proliferations that give rise to numerous nuclei. The secondary prosencephalon of ancestral gnathostomes was probably divided rostrally into inverted and evaginated cerebral hemispheres, with paired olfactory bulbs arising directly from the hemispheres, and caudally into preoptic and hypothalamic areas. The cerebral hemispheres likely comprised a dorsally situated pallium divided into medial, dorsal and lateral pallial formations, as well as an intercalated pallial nucleus situated ventrolateral to the lateral pallium, and a ventrally situated subpallium divided medially into septal nuclei and a medial amygdalar nucleus and laterally into a corpus striatum. Both pallial and subpallial centers of ancestral gnathostomes probably received ascending thalamic and posterior tubercular inputs, with telencephalic efferent pathways terminating primarily in the hypothalamus, posterior tubercle and midbrain tegmentum. An out-group analysis further indicates that some taxa in each gnathostome radiation exhibit highly derived telencephalic characters due to the independent expansion of one or more pallial formations.