SEARCH · PubMed Health

Results for “Subthalamic Nucleus”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 865 records · Page 48Linked to original sources

PubMed1980

Selective effects of kainic acid on diencephalic neurons.

Injections of kainic acid (KA) into the lateral hypothalamus (LH) produce neuronal loss in this region without apparent damage to medial forebrain bundle fibers passing through the area. Cellular destruction is not limited to the LH; the neuronal loss in the thalamic reticular nucleus, the subthalamic nucleus and zona incerta is more extensive than that in the LH. Since all of the nuclei of ventral thalamic origin except the ventral lateral geniculate nucleus (VLGN) were destroyed by LH injections of KA, we sought to determine whether this nucleus also is sensitive to KA. Injections directly into the VLGN produce total neuronal loss here as well as in the thalamic reticular nucleus, zona incerta and subthalamic nucleus. Other areas showing cell loss are the dorsal LGN, medial geniculate, lateral portion of the ventrobasal complex and midline thalamic nuclei. Injections of KA into medial hypothalamus adjacent to the suprachiasmatic nucleus produced no neuronal degeneration. In addition, no neuronal loss was noted in medial hypothalamic nuclei lying adjacent to areas of LH in which KA was injected. Therefore, the sensitivity of diencephalic nuclei appears to range from highly sensitive regions such as derivatives of ventral thalamus and midline thalamic nuclei to regions of moderate sensitivity such as the LH, geniculate nuclei and ventrobasal thalamic nucleus, to regions resistant to KA toxicity such as the suprachiasmatic nucleus and other nuclei and areas of medial hypothalamus.

Animals↗

PubMed2003

Deep brain stimulation for Parkinson's disease.

Deep brain stimulation at high frequency was first used in 1997 to replace thalamotomy in treating the characteristic tremor of Parkinson's disease, and has subsequently been applied to the pallidum and the subthalamic nucleus. The subthalamic nucleus is a key node in the functional control of motor activity in the basal ganglia. Its inhibition suppresses symptoms in animal models of Parkinson's disease, and high frequency chronic stimulation does the same in human patients. Acute and long-term results after deep brain stimulation show a dramatic and stable improvement of a patient's clinical condition, which mimics the effects of levodopa treatment. The mechanism of action may involve a functional disruption of the abnormal neural messages associated with the disease. Long-term changes, neural plasticity and neural protection might be induced in the network. Similar effects of stimulation and lesioning have led to the extension of this technique for other targets and diseases.

Electric Stimulation Therapy↗

PubMed1993

Toward an understanding of the role of glutamate in experimental parkinsonism: agonist-sensitive sites in the basal ganglia.

Increased glutamatergic transmission in the basal ganglia is implicated in the pathophysiology of Parkinson's disease. However, the mechanisms by which activation of glutamate receptors produce parkinsonism are unknown. Therefore, we examined whether the glutamate agonists N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA), kainate, and trans-(+/-)-1-amino-1,3-cyclopentanedicarboxylate produce parkinsonism in rats after microapplication into different subregions of the basal ganglia. Electromyographic activity was used as a measure of parkinsonian rigidity. We found that in the rostral striatum, excitation mediated by NMDA but not by non-NMDA receptors led to parkinsonism. In the substantia nigra pars reticulata, internal pallidal segment/entopeduncular nucleus, and subthalamic nucleus, activation of AMPA/kainate and metabotropic receptors but not of NMDA receptors led to parkinsonian rigidity. Rigidity occurred also in animals bearing ibotenate-induced lesions of the posterior part of the striatum and of the external pallidal segment, but not in animals with lesions of the anterior striatum, subthalamic nucleus, internal pallidal segment/entopeduncular nucleus, or substantia nigra pars reticulata. These observations suggest that the activation of glutamate receptor subtypes in the basal ganglia may be differentially involved in the expression of parkinsonian symptoms.

Animals↗

PubMed1990

Parameters of cholinergic neurotransmission in the thalamus in Parkinson's disease and Alzheimer's disease.

Loss of cholinergic cells in the basal forebrain is associated with commensurate reductions in cortical acetylcholine-related enzyme activities in both Alzheimer's disease (AD) and Parkinson's disease (PD). Nerve cell loss from the cholinergic pontine tegmental nuclei also occurs. As the latter nuclei project to the diencephalon, we used frozen tissue from 5 controls, 5 PD and 5 AD cases to study the distribution of ChAT, AChE and [3H]nicotine binding in the thalamus and subthalamic nucleus. The anterior nuclear group and the mediodorsal nucleus showed high activities of ChAT and AChE together with relatively high levels of [3H]nicotine binding. The centromedian nucleus and subthalamic nucleus contained equally high levels of ChAT but negligible levels of [3H]nicotine binding. There were no significant changes in the levels of ChAT, AChE and nicotine binding in the PD and AD groups indicating that involvement of the pedunculopontine tegmental nucleus is likely to be a secondary retrograde phenomenon rather than part of a systematic cholinergic fibre degeneration.

Acetylcholine↗

PubMed1983

Nucleus tegmenti pedunculopontinus: efferent connections with special reference to the basal ganglia, studied in the rat by anterograde and retrograde transport of horseradish peroxidase.

The efferent connections of the brain stem nucleus tegmenti pedunculopontinus were studied in the rat using the techniques of anterograde and retrograde transport of the enzyme horseradish peroxidase, laying particular emphasis on that part of pedunculopontinus which receives direct descending projections from the basal ganglia and related nuclei. In a preliminary series of experiments horseradish peroxidase was injected into either the entopeduncular nucleus or the subthalamic nucleus and, following anterograde transport of enzyme, terminal labelling was identified in nucleus tegmenti pedunculopontinus, surrounding the brachium conjunctivum in the caudal mesencephalon. In a subsequent series of experiments, horseradish peroxidase was injected into that region of nucleus tegmenti pedunculopontinus which receives entopeduncular and subthalamic efferents and its efferent projections were studied by anterograde transport of the enzyme. The results indicate that nucleus tegmenti pedunculopontinus gives rise to widely distributed efferent projections which terminate rostrally in mesencephalic, diencephalic and telencephalic structures and caudally in the pontine tegmentum. In the mesencephalon, terminal labelling was found in the pars compacta of the ipsilateral substantia nigra and sometimes in the adjoining ventral tegmental area. Labelling was also found in the ipsilateral half of the periaqueductal grey. In the diencephalon terminal labelling occurred bilaterally in the subthalamic nucleus and ipsilaterally in the intralaminar nuclei of the thalamus. Further rostrally, terminal labelling was particularly evident in the ipsilateral pallidal complex, especially in the caudal two-thirds of the entopeduncular nucleus and the ventral half of the caudal third of the globus pallidus. Caudal to pedunculopontine injection sites dense labelling was observed in the reticular formation of the pontine tegmentum. In a final series of experiments, confirmation of apparent pedunculopontine efferent projections was sought using the retrograde transport of horseradish peroxidase. Enzyme was injected into sites possibly receiving pedunculopontine efferents and the peribrachial area of the brain stem was examined for retrograde cell labelling. In this way, pedunculopontine projections were confirmed to the globus pallidus, entopeduncular nucleus, subthalamic nucleus, substantia nigra, parafascicular nucleus and pontine reticular formation. Injections into the globus pallidus or subthalamic nucleus gave rise to retrograde cell labelling bilaterally in pedunculopontinus. In addition, retrograde transport studies alone demonstrated projections from pedunculopontinus to the cerebral cortex and to the spinal cord. It is concluded that the nucleus tegmenti pedunculopontinus has reciprocal relationships with parts of the basal ganglia and some functionally related nuclei (in particular, the pallidal complex, subthalamic nucleus and substantia nigra).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2000

Functional anatomy of movement disorders.

Models of basal ganglia function are described which encapsulate the principal pathophysiological mechanisms underlying parkinsonian akinesia on the one hand and abnormal involuntary movement disorders (dyskinesias) on the other. In Parkinson's disease, degeneration of the nigrostriatal dopamine system leads to overactivity of the 'indirect' striatopallidal projection to the lateral (external) segment of the globus pallidus. This causes inhibition of lateral pallidal neurons, which in turn project to the subthalamic nucleus. Disinhibition of the subthalamic nucleus leads to abnormal subthalamic overactivity and, as a consequence, overactivity of medial (internal) pallidal output neurons. Dyskinesias, such as are observed in Huntington's disease, levodopa-induced dyskinesia and ballism, share mechanistic features in common and are associated with decreased neuronal activity in both the subthalamic nucleus and the medial globus pallidus.

Animals↗

PubMed1988

Alterations in local cerebral glucose utilization during electrical stimulation of the striatum and globus pallidus in rats.

Alterations in local cerebral glucose utilization (LCGU) in conscious rats during electrical stimulation of the striatum and the globus pallidus were investigated using the [14C]deoxyglucose method. Stimulation of the globus pallidus produced a marked contraversive circling behavior, while stimulation of the striatum led only to contraversive head turning. Unilateral stimulation of the striatum increased LCGU bilaterally in the globus pallidus and substantia nigra pars compacta, but only ipsilaterally in the entopeduncular nucleus, substantia nigra pars reticulata and subthalamic nucleus. Similar stimulation of the globus pallidus increased LGCU in the globus pallidus, substantia nigra pars reticulata and compacta, entopeduncular nucleus, subthalamic nucleus, lateral habenular nucleus, parafascicular nucleus of the thalamus, deep layers of the superior colliculus and pedunculopontine nucleus, exclusively on the ipsilateral side. These results indicate that the electrical stimulation induces LCGU changes in the respective structures having both monosynaptic and transsynaptic neuronal inputs. Some changes may also be mediated by antidromic activation. They also suggest that activation of a synaptic process whether excitatory or inhibitory results in increases in LCGU. The bilateral modulatory effects of striatal stimulation may cancel out the circling behavior seen during pallidal stimulation, and cause only head turning.

Animals↗

PubMed2000

Functional changes of the basal ganglia circuitry in Parkinson's disease.

The basal ganglia circuitry processes the signals that flow from the cortex, allowing the correct execution of voluntary movements. In Parkinson's disease, the degeneration of dopaminergic neurons of the substantia nigra pars compacta triggers a cascade of functional changes affecting the whole basal ganglia network. The most relevant alterations affect the output nuclei of the circuit, the medial globus pallidus and substantia nigra pars reticulata, which become hyperactive. Such hyperactivity is sustained by the enhanced glutamatergic inputs that the output nuclei receive from the subthalamic nucleus. The mechanisms leading to the subthalamic disinhibition are still poorly understood. According to the current model of basal ganglia organization, the phenomenon is due to a decrease in the inhibitory control exerted over the subthalamic nucleus by the lateral globus pallidus. Recent data, however, suggest that additional if not alternative mechanisms may underlie subthalamic hyperactivity. In particular, given the reciprocal innervation of the substantia nigra pars compacta and the subthalamic nucleus, the dopaminergic deficit might influence the subthalamic activity, directly. In addition, the increased excitatory drive to the dopaminergic nigral neurons originating from the hyperactive subthalamic nucleus might sustain the progression of the degenerative process. The identification of the role of the subthalamic nucleus and, more in general, of the glutamatergic mechanisms in the pathophysiology of Parkinson's disease might lead to a new approach in the pharmacological treatment of the disease. Current therapeutic strategies rely on the use of L-DOPA and/or dopamine agonists to correct the dopaminergic deficit. Drugs capable of antagonizing the effects of glutamate might represent, in the next future, a valuable tool for the development of new symptomatic and neuroprotective strategies for therapy of Parkinson's disease.

Animals↗

PubMed2000

Relationship of activity in the subthalamic nucleus-globus pallidus network to cortical electroencephalogram.

One of the functions of the excitatory subthalamic nucleus (STN) is to relay cortical activity to other basal ganglia structures. The response of the STN to cortical input is shaped by inhibition from the reciprocally connected globus pallidus (GP). To examine the activity in the STN-GP network in relation to cortical activity, we recorded single and multiple unit activity in STN and/or GP together with cortical electroencephalogram in anesthetized rats during various states of cortical activation. During cortical slow-wave activity (SWA), STN and GP neurons fired bursts of action potentials at frequencies that were similar to those of coincident slow ( approximately 1 Hz) and spindle (7-14 Hz) cortical oscillations. Spontaneous or sensory-driven global activation was associated with a reduction of SWA and a shift in STN-GP activity from burst- to tonic- or irregular-firing. Rhythmic activity in STN and GP neurons was lost when the cortex was inactivated by spreading depression and did not resume until SWA had recovered. Although rhythmic STN-GP activity was correlated with SWA, the phase relationships of activities of neurons within the STN and GP and between the nuclei were variable. Even when neurons displayed synchronous bursting activity, correlations on the millisecond time scale, which might indicate shared synaptic input, were not observed. These data indicate that (1) STN and GP activity is intimately related to cortical activity and hence the sleep-wake cycle; (2) rhythmic oscillatory activity in the STN-GP network in disease states may be driven by the cortex; and (3) activity of the STN-GP network is regulated in space in a complex manner.

Action Potentials↗

PubMed1981

The pallido-subthalamic projection in rat: anatomical and biochemical studies.

Horseradish peroxidase injected into the rat globus pallidus was transported retrogradely to subthalamic nucleus neuronal cell bodies and anterogradely to axon terminals in the subthalamic nucleus. Electron microscopic observations revealed that the labeled axon terminals made symmetrical axosomatic and axo-dendritic synaptic contacts with labeled subthalamic nucleus perikarya and dendrites. Injection of kainic acid in the globus pallidus several days prior to the horseradish peroxidase injection abolished the anterograde but not the retrograde transport of the tracer. This suggested the anterograde labeling observed in the subthalamic nucleus originated from neuronal cell bodies in the globus pallidus. Kainic acid lesions identical to those employed in the above anatomical studies resulted in a loss of neuronal cell bodies throughout the globus pallidus and caused a drop in glutamic acid decarboxsylase and choline acetyltransferase levels in the globus pallidus. Levels of these two enzymes were not changed in the subthalamic nucleus after the globus pallidus kainic acid lesions, but both showed small, statistically significant decreases in the substantia nigra. It was concluded that there is a massive pathway from the globus pallidus to the subthalamic nucleus, which terminates on subthalamic nucleus neurons projecting back to the globus pallidus. Neither gamma-aminobutyric acid nor acetylcholine is the major neurotransmitter in the massive pallido-subthalamic pathway.

Animals↗

PubMed1987

Experimental hemiplegia in the monkey: basal ganglia glucose activity during recovery.

Unilateral ablation of cerebral cortical areas 4 and 6 of Brodmann in the macaque monkey results in a dense contralateral hemiplegia that recovers partially with time. During the phase of dense hemiplegia, the local cerebral metabolic rate for glucose (lCMRGlc) is decreased significantly in the caudate nucleus, putamen, globus pallidus, subthalamic nucleus, substantia nigra, and red nucleus of the hemisphere ipsilateral to the lesion. In the present study, lCMRGlc in the basal ganglia was studied during the phase of partial recovery of motor activity. lCMRGlc was partially restored, and the greatest degree of restoration occurred in structures with direct connections to the cerebral cortex (caudate nucleus, putamen, subthalamic nucleus, substantia nigra, and red nucleus). Restoration was least in structures that do not receive direct connections from the cerebral cortex (the internal and external segments of the globus pallidus). The findings support the hypothesis that corticofugal activity accounts for a substantial degree of functional recovery.

Animals↗

PubMed1994

Excitatory amino acid receptor antagonists modify regional cerebral metabolic responses to levodopa in 6-hydroxydopamine-lesioned rats.

Excitatory amino acid receptor antagonists have been proposed as novel therapeutic agents to be used with levopoda in the treatment of Parkinson's disease. We examined the neural substrates for the interaction between levodopa and antagonists of either the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid or N-methyl-D-aspartate type of excitatory amino acid receptor using 2-deoxyglucose autoradiography. Thus, we compared the effects of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor antagonist 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline (10 mg/kg, i.v.) and the N-methyl-D-aspartate antagonist MK-801 (0.1 mg/kg, i.v.) on cerebral metabolic responses to levodopa (25 mg/kg, i.v., with 12.5 mg/kg benserazide) in rats with a unilateral nigrostriatal pathway lesion. Levodopa increased glucose utilization ipsilateral to the lesion in substantia nigra pars reticula (up to 104%), entopeduncular nucleus (up 90%) and subthalamic nucleus (up 30%), indicating that levodopa alters striatal output through the striatonigral, striatoentopeduncular and striatopallidal pathways. Levodopa also decreased metabolic rate in lateral habenula (down 39%), a target of projections from entopeduncular nucleus, implying a reduction in basal ganglia output. 2,3-Dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline and MK-801 by themselves did not affect glucose utilization in any of these regions. Pretreatment with 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline reduced the effect of levodopa in substantia nigra pars reticulata but not in entopeduncular nucleus or subthalamic nucleus, while MK-801 attenuated the effect of levodopa in all three of these structures; neither 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline nor MK-801 altered the effect of levodopa in lateral habenula. When given at the same doses to a separate group of lesioned animals, neither 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline nor MK-801 affected rotational behavior elicited by levodopa. These findings indicate that alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid and N-methyl-D-aspartate receptor antagonists differentially modify dopamine receptor-mediated striatal output. alpha-Amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor blockade may preferentially attenuate the effect of dopamine receptor activation on the striatonigral pathway, while N-methyl-D-aspartate blockade appears to reduce the actions of dopamine on the striatonigral, striatoentopeduncular and striatopallidal pathways.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2003

Modeling facilitation and inhibition of competing motor programs in basal ganglia subthalamic nucleus-pallidal circuits.

The motor symptoms of Parkinson's disease (PD) implicate the basal ganglia (BG) in some aspect of motor control, although the role the BG play in regulation of motor behavior is not completely understood. The modeling study presented here takes advantage of available cellular, systems, and clinical data on BG and PD to begin to build a biophysically based network model of pallidosubthalamic circuits of BG, to integrate this information and better understand the physiology of the normal BG and PD pathophysiology. The model reflects the experimentally supported hypothesis that the BG are involved in facilitation of the desired motor program and inhibition of competing motor programs that interfere with the desired movement. Our model network consists of subthalamic and pallidal (both external and internal segments) neural assemblies, with inputs from cortex and striatum. Functional subsets within each of the BG nuclei correspond to the desired motor program and the unwanted motor programs. A single compartment conductance-based model represents each subset. This network can discriminate between competing signals for motor program initiation, thus facilitating a single motor program. This ability depends on metabotropic gamma-aminobutyric acid B projections from the external pallidum to subthalamic nucleus and rebound properties of subthalamic cells, as well as on the structure of projections between pallidum and subthalamus. The loss of this ability leads to hypokinesia, known PD motor deficits characterized by a slowness or inability to switch between motor programs.

Animals↗

PubMed2002

Move to the rhythm: oscillations in the subthalamic nucleus-external globus pallidus network.

Recent anatomical, physiological and computer modeling studies have revealed that oscillatory processes at the levels of single neurons and neuronal networks in the subthalamic nucleus (STN) and external globus pallidus (GPe) are associated with the operation of the basal ganglia in health and in Parkinson's disease (PD). Autonomous oscillation of STN and GPe neurons underlies tonic activity and is important for synaptic integration, whereas abnormal low-frequency rhythmic bursting in the STN and GPe is characteristic of PD. These recent findings provide further support for the view that the basal ganglia use both the pattern and the rate of neuronal activity to encode information.

Animals↗

PubMed2000

Intrasubthalamic nucleus metabotropic glutamate receptor activation: a behavioral, Fos immunohistochemical and [14C]2-deoxyglucose autoradiographic study.

Metabotropic glutamate receptors are a major class of excitatory amino acid receptors. Eight metabotropic glutamate receptor subtypes have been cloned, and are classified into three groups (I, II and III) based on amino acid sequence identity, effector systems and pharmacological profile. Previous results have shown that unilateral stimulation of metabotropic glutamate receptors in the subthalamic nucleus with the non-subtype-selective metabotropic glutamate receptor agonist 1S,3R-1-amino-1,3-cyclopentane dicarboxylate results in contralateral rotation in rats and Fos expression in the subthalamic nucleus. This suggests that metabotropic glutamate receptor stimulation results in altered subthalamic nucleus activity with consequent altered basal ganglia activity on the injected side. We sought to determine the metabotropic glutamate receptor subtype(s) involved and the functional neuroanatomy underlying the rotational behavior. Unilateral intrasubthalamic nucleus injection of group II or group III metabotropic glutamate receptor agonists induced contralateral rotation. In addition to producing rotation, group II and group III metabotropic glutamate receptor agonists induce toxicity in the subthalamic nucleus and overlying thalamus. Following group II or group III subthalamic nucleus metabotropic glutamate receptor stimulation, there is Fos-like immunoreactivity in the globus pallidus, subthalamic nucleus, substantia nigra pars reticulata and entopeduncular nucleus, suggesting altered activity in subthalamic nucleus target regions. However, examination of [14C]2-deoxyglucose uptake suggests that the alterations in basal ganglia activity are different following group II versus group III metabotropic glutamate receptor stimulation, suggesting that rotation is occurring via different mechanisms. It appears that stimulation of subthalamic nucleus group II metabotropic glutamate receptors induces rotation by increasing subthalamic nucleus activity. These results suggest that group II metabotropic glutamate receptor antagonists may be useful for alleviating subthalamic nucleus overactivity in Parkinson's disease.

4-Aminopyridine↗

PubMed2005

Bilateral stimulation of nucleus subthalamicus in advanced Parkinson's disease: no effects on, and of, autonomic dysfunction.

It is not known whether bilateral stimulation of the subthalamic nucleus, performed to improve skeletal motor control in advanced Parkinson's disease, also affects central autonomic regulation of cardiovascular motor function. Furthermore, reduced treatment with dopaminergic and other drugs after bilateral stimulation of the subthalamic nucleus could affect cardiovascular autonomic reflexes and/or other factors controlling blood pressure level. The primary aim of this study was to investigate putative effects of bilateral stimulation of the subthalamic nucleus on the autonomic nervous system, using respiratory heart rate variability and blood pressure responses to tilt as indices. Baseline autonomic tests were performed in 19 patients with Parkinson's disease and 10 matched healthy subjects. Patients were divided in two groups and re-investigated after 1 year of optimized pharmacological treatment (n = 8) or 1 year of bilateral subthalamic nucleus stimulation (n = 11). Both skeletal motor dysfunction and dopaminergic drug treatment were significantly reduced after 1 year of bilateral subthalamic nucleus stimulation. However, heart rate variability as well as blood pressure during tilt was reduced compared to baseline to a similar extent in both patient groups. The number of individual patients showing pathological autonomic test results at 1-year follow-up increased only in the subthalamic nucleus stimulation group. Despite reduced pharmacological treatment and reduced motor disability, bilateral subthalamic nucleus stimulation does not improve cardiovascular autonomic reflex function or protect against development of cardiovascular autonomic failure in Parkinson's disease. Preoperative cardiovascular autonomic reflex dysfunction, conversely, does not exclude an excellent stimulation effect.

Aged↗

PubMed1993

Organization of the output of the ventral striatopallidal system in the rat: ventral pallidal efferents.

The efferent projections of the ventral pallidum in the rat were studied using anterograde tracing of Phaseolus vulgaris-leucoagglutinin and retrograde tracing of choleratoxin subunit B. The main aim of this study was to determine the degree of topographical organization in the outputs of the ventral pallidum. In the telencephalon, ventral pallidal fibers reach the prefrontal cortex, the ventral striatum, the lateral septum, the basolateral, lateral, and central amygdaloid nuclei, and the lateral entorhinal area. Diencephalic targets of ventral pallidal fibers are the lateral hypothalamus, the reticular nucleus of the thalamus, the mediodorsal thalamic nucleus, the dorsomedial part of the subthalamic nucleus, the medial part of the parafascicular nucleus and the lateral habenula. In the mesencephalon, ventral pallidal fibers terminate in the ventral tegmental area, the substantia nigra, the retrorubral area, the median raphe nucleus, the nucleus raphe magnus, the peribrachial area, the ventromedial part of the central gray substance and the locus coeruleus. The results of the experiments in which retrograde tracers were injected in different nuclei in the mesencephalon allow the distinction of two main areas in the ventral pallidum. Deposits of retrograde tracers in the substantia nigra, pars reticulata result in labeling of cells in the dorsolateral part of the ventral pallidum, located immediately ventral to the anterior limb of the anterior commissure. Retrograde tracer injections in other targets of the ventral mesencephalon, i.e. the dopaminergic cell groups A10, A9 or A8, or nuclei in the peribrachial area result in labeling of neurons in an extensive ventromedial and ventrolateral zone of the ventral pallidum. The medial part of this ventral pallidal zone projects to the ventral tegmental area, whereas ventral and lateral parts connect with more lateral and caudal mesencephalic targets. The projections from the ventral pallidum to the ventral striatum, the subthalamic nucleus and adjacent lateral hypothalamic area, and the mediodorsal thalamic nucleus are distinctly topographically organized. The ventral pallidostriatal projections preserve a medial-to-lateral, a dorsal-to-ventral and, to a lesser degree, a rostral-to-caudal topography. With respect to the subthalamic region, the dorsolateral part of the ventral pallidum projects to the dorsomedial part of the subthalamic nucleus, whereas the ventromedial and ventrolateral parts of the ventral pallidum are topographically connected with the area of the lateral hypothalamus medially adjacent to the subthalamic nucleus.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1992

Afferent projections to the cholinergic pedunculopontine tegmental nucleus and adjacent midbrain extrapyramidal area in the albino rat. I. Retrograde tracing studies.

The afferent connections of the pedunculopontine tegmental nucleus (PPT) and the adjacent midbrain extrapyramidal area (MEA) were examined by retrograde tracing with wheat germ agglutinin-conjugated horseradish peroxidase (WGA-HRP). Major afferents to the PPT originate in the periaqueductal gray, central tegmental field, lateral hypothalamic area, dorsal raphe nucleus, superior colliculus, and pontine and medullary reticular fields. Other putative inputs originate in the paraventricular and preoptic hypothalamic nuclei, the zona incerta, nucleus of the solitary tract, central superior raphe nucleus, substantia innominata, posterior hypothalamic area, and thalamic parafascicular nucleus. The major afferent to the medially adjacent MEA originates in the lateral habenula, while other putative afferents include the perifornical and lateral hypothalamic area, periaqueductal gray, superior colliculus, pontine reticular formation, and dorsal raphe nucleus. MEA inputs from basal ganglia nuclei include moderate projections from the substantia nigra pars reticulata, entopeduncular nucleus, and a small projection from the globus pallidus, but not the subthalamic nucleus. Dense anterograde labeling was observed in the substantia nigra pars compacta, entopeduncular nucleus, subthalamic nucleus, globus pallidus, and caudate-putamen only following WGA-HRP injections involving the MEA. The results of this study demonstrate that the PPT and MEA share many potential afferents. Remarkable differences were found that support distinguishing between these two nuclei in future studies regarding the functional organization of the midbrain and pons. The results, for example, confirm our previous observations that the largely reciprocal connections between the midbrain and basal ganglia distinguish the MEA from the PPT. Afferents from the lateral habenula and contralateral superior colliculus represent extensions of more traditional basal ganglion circuitry which further delineate the MEA from the PPT. The results are discussed with respect to the important role of the midbrain and pons in behavioral state control and locomotor mechanisms.

Afferent Pathways↗