Direct projection of catecholamine (presumably dopamine)-containing neurons from hypothalamus to spinal cord

doi:10.1016/0304-3940(79)90052-1

Neuroscience Letters

Volume 11, Issue 1, January 1979, Pages 35-40

https://doi.org/10.1016/0304-3940(79)90052-1 Get rights and content

Abstract

A procedure for combining catecholamine (CA) and horseradish peroxidase (HRP) histochemistry was used to demonstrate that some of the catecholamine-containing cells in the rabbit dorsal hypothalamus project directly to the thoracic spinal cord. These cells, which are probably dopaminergic, may be involved in the integration of pituitary hormonal secretion and peripheral autonomic nervous regulation.

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Cited by (115)

Origins of a repetitive and co-contractive biphasic pattern of muscle activation in Parkinson's disease
2011, Neural Networks
Citation Excerpt :
Second, the model assumed that both model cortical and spinal cord cells are innervated by dopamine. Such widespread innervations of the primate neocortex and spinal cord has been experimentally reported (Bjorklund & Lindvall, 1984; Bjorklund & Skagerberg, 1979; Blessing & Chalmers, 1979; Heise & Kayalioglu, 2008; Shirouzou et al., 1990; Weil-Fugazza & Godefroy, 1993; Williams & Goldman-Rakic, 1998) and recently reviewed by the Cutsuridis and Perantonis (2006) computational study. Briefly, the sources of the dopaminergic fibers in neocortex are the neurons of the substantia nigra (SN), the ventral tegmental area (VTA), and retrorubral area (RRA) (Williams & Goldman-Rakic, 1995).
In studies of electromyographic (EMG) patterns during movements in Parkinson’s disease, often a repetitive and sometimes co-contractive pattern of antagonist muscle activation is observed. It has been suggested that the origin of such patterns of muscle activation is a central one arising from impairments in the basal ganglia structures and/or the cortex, although afferent inputs can also modulate the voluntary activity. A neural network model of Parkinson’s disease, bradykinesia and rigidity, is extended to quantitatively study the conditions under which such a repetitive and co-contractive pattern of muscle activation appears. Computer simulations show that an oscillatory disrupted globus pallidus internal segment (GPi) response signal comprising at least two excitation–inhibition sequences as an input to a normally functioning cortico-spinal model of movement generation results in a repetitive, but not co-contractive agonist–antagonist pattern of muscle activation. A repetitive and co-contractive pattern of muscle activation results when also dopamine is depleted in the cortex. Finally, additional dopamine depletion in the spinal cord sites results in a reduction of the size, duration and rate of change of the repetitive and co-contractive EMG bursts. These results have important consequences in the development of Parkinson’s Disease therapies such as dopamine replacement in cortex and spinal cord, which can alleviate some of the impairments of Parkinson’s Disease such as slowness of movement (bradykinesia) and rigidity.
A neural network model of Parkinson's disease bradykinesia
2006, Neural Networks
Citation Excerpt :
The lowest density is in area 17, where the DA afferents are mostly restricted to layer I (Berger et al., 1988). In addition to the dopaminergic innervation of the neocortex, the presence of dopaminergic fibers in the spinal cord has been observed by several groups (Bjorklund & Skagerberg, 1979; Blessing & Chalmers, 1979; Takada, Li, & Hattori, 1988). These dopaminergic fibers are predominately localized in the superficial layers, the laminae III–V of the dorsal horn, and in lamina X.
Parkinson's disease (PD) is caused by dopamine (DA) depletion consequent to cell degeneration in the substantia nigra pars compacta (SNc) and the ventral tegmental area (VTA). Although computational analyses of PD have focused on DA depletion in DA-recipient parts of the basal ganglia, there is also extensive DAergic innervation of the frontal and parietal cortex as well as the spinal cord. To understand PD bradykinesia, a comprehensive network model is needed to study how patterns of DA depletion at key cellular sites in the basal ganglia, cortex and spinal cord contribute to disordered neuronal and spinal cord activity and other PD symptoms. We extend a basal ganglia-cortico-spinal circuit for control of voluntary arm movements by incorporating DAergic innervation of cells in the cortical and spinal components of the circuit. The resultant model simulates successfully several of the main reported effects of DA depletion on neuronal, electromyographic (EMG), and movement parameters of PD bradykinesia.
Pain in Parkinson's disease
2005, Revue Neurologique
Dans la maladie de Parkinson, des syndromes douloureux sont rapportés aussi bien à la phase présymptomatique qu’au stade des fluctuations motrices. La diversité et la pathophysiologie de ces syndromes restent peu connues.
Caractériser du point de vue clinique les différents syndromes douloureux de la maladie de Parkinson, leurs relations avec le décours de la maladie et leurs rapports avec les fluctuations motrices et le traitement.
Nous avons revu les syndromes douloureux de 388 patients consécutifs du Registre Lausannois des Mouvements Anormaux, collectés prospectivement par un questionnaire qui caractérise la douleur selon sa description, sa topographie, la date de début et sa relation aux fluctuations motrices éventuelles.
Sur cet ensemble de patients présentant une maladie de Parkinson dopa-sensible diagnostiquée cliniquement, 269 soit 67 p. 100 ont présenté des syndromes douloureux. Parmi ceux-ci, 94 p. 100 avaient des douleurs musculaires : raideurs (86 p. 100), crampes, pseudo-crampes ou spasmes (43 p. 100) ou myalgies diverses (7 p. 100) ; 51 p. 100 avaient présenté des douleurs ostéo-ligamentaires (rhumatologiques), articulaires (23 p. 100), périarticulaires (3 p. 100) ou rachidiennes (31 p. 100). Les douleurs neurogènes étaient moins fréquents (16 p. 100) : paresthésies (6 p. 100), sensations non désagréables non définissables (6 p. 100), dysesthésies (< 1 p. 100), brûlures (2 p. 100), lourdeur (< 1 p. 100), démangeaisons (< 1 p. 100), distribuées de façon segmentaire (86 p. 100), axiale (54 p. 100), radiculaire ou pseudoradiculaire (14 p. 100) ou distale (4 p. 100). Enfin, un syndrome des jambes sans repos ou une akathisie étaient parfois représentés (10 p. 100). Moins de 1 p. 100 reportaient des algies faciales ou des céphalées. Nous n’avons pas rencontré de douleurs fantômes. Près du quart des douleurs étaient présentes au début de la maladie, seulement 3 p. 100 d’entre elles ont disparu en phase d’évolution. Un tiers des douleurs était clairement en relation avec les fluctuations motrices, la majorité (90 p. 100) apparaissait en phase off, dont l’intensité maximale était toujours ipsilatérale au côté le plus atteint. Nous n’avons pas trouvé de corrélation significative des douleurs avec l’âge, le sexe, le stade, la durée de la maladie, un état dépressif, des troubles du sommeils ou végétatifs ou la dose moyenne équivalente de L-dopa.
Des syndromes douloureux sont rencontrés chez un tiers des patients avec une maladie de Parkinson. La plupart sont d’origine musculaire, suivi par les douleurs ostéoarticulaires et les douleurs neurogènes, un quart sont présentes au stade précoce de la maladie, un tiers ont des relations temporelles avec les fluctuations motrices.
Pain may be a presenting symptom of Parkinson's disease or may occcur during the motor fluctuation stages of the disease. The complexity and pathophysiology of pain in Parkinson's disease still remains poorly understood.
To characterize clinically the different painful presentations of Parkinson's disease, their relationship to the stage of the disease and their connections with motor fluctuations and treatment.
We reviewed painful syndromes in 388 consecutive parkinsonian patients of the Lausanne Movement Disorders Registry, based on an itemized questionnaire used prospectively to characterize the pain by its description, topography, date of appearance and possible relationship with motor fluctuations. Among these patients with clinically-diagnosed dopa-responsive Parkinson's disease, 269, i.e. 67 percent presented sensory or painful syndromes. Among them, 94 percent had muscular pain: stiffness (85 percent), cramps, pseudo-cramps, spasms (3 percent) or various myalgias (7 percent); 51 percent presented osteo-ligamentar “rheumatologic” pain, articular (23 percent), periarticular (3 percent) or spinal (31 percent), but less defined and localized neurogenic painful syndromes were less frequent (8 percent), such as paresthesia (6 percent), dysesthesia (<1 percent), burning sensation (2 percent), itching (<1 percent), ill defined discomfort (6 percent) or a feeling of heaviness (1 percent), with segmental (86 percent), axial (54 percent), radicular or pseudoradicular (14 percent), acral distal (4 percent) or less frequently anorectal or visceral distribution. Restless legs or akathiasia were occasional (10 percent). Headaches and facial pain were less frequent (1 percent), we did not encounter phantom pain. More than one quarter were present at the beginning of the disease, only (3 percent) of them resolved during the development of the disease. About one-third were clearly linked with motor fluctuations, the majority occurring in off phase (34 percent). We did not find any correlation with age, gender, duration or stage of disease, L dopa equivalent dose, depression, insomnia or autonomic dysfunction.
Painful syndromes are found in two thirds of patients with Parkinson's disease, with mainly pain of muscular origin, followed by osteoarticular and neurgenic painful syndromes, a quarter of the patients experience pain in early phases of the disease and a third in relation with motor fluctuations.
Interconnections between the neuroendocrine hypothalamus and the central autonomic system
1999, Frontiers in Neuroendocrinology
Tract-tracing techniques in combination with immunohistochemistry and in situ hybridization were used in intact and operated rats (hypothalamic lesions, transections of neuronal pathways) to localize and characterize neuronal connections between the hypothalamus and autonomic centers. Viscerosensory and somatosensory signals which relay in the spinal cord and the medulla oblongata reach the hypothalamus through various catecholaminergic and noncatecholaminergic neuronal pathways. Vice versa, the hypothalamus influences autonomic activities through humoral and neurohumoral pathways. Descending hypothalamic efferents carry feedback signals to viscerosensory and brainstem catecholaminergic neurons and regulatory inputs to parasympathetic (dorsal vagal nucleus) and sympathetic (thoracolumbar intermediolateral cell column) preganglionic neurons. These fibers arise mainly from neurons of the paraventricular, arcuate, perifornical, and dorsomedial nuclei and the lateral hypothalamus. The major neuroanatomical observations are the following: (1) pathways between the hypothalamus and autonomic centers are bidirectional: the ascending and descending fibers may use the same avenues; (2) the descending axons are mainly peptidergic (CRF, vasopressin, oxytocin, somatostatin, enkephalin, POMC, and cANP), while the ascending fibers are both peptidergic (enkephalin, NPY, neurotensin, dynorphins) and catecholaminergic; (3) descending hypothalamic axons terminate directly on the sensory, preganglionic, and catecholaminergic neurons in the medulla and the spinal cord; (4) hypothalamic projections to the autonomic centers are always bilateral; (5) while medullary autonomic and catecholaminergic fibers innervate hypothalamic neurons directly, spinohypothalamic axons are relayed on neurons in the lateral hypothalamus.
Inhibitory and indirect excitatory effects of dopamine on sympathetic preganglionic neurones in the neonatal rat spinal cord in vitro
1999, Brain Research
Regions of the thoraco-lumbar spinal cord containing sympathetic preganglionic neurones are rich in dopamine terminals. To determine the influence of this innervation intracellular recordings were made from antidromically identified sympathetic preganglionic neurones in (400 μm) transverse neonatal rat spinal cord slices. Dopamine applied by superfusion caused a slow monophasic hyperpolarisation in 46% of sympathetic preganglionic neurones, a slow monophasic depolarisation in 28% of sympathetic preganglionic neurones and a biphasic effect consisting of a slow depolarisation followed by a slow hyperpolarisation or vice-versa in 23% of sympathetic preganglionic neurones. Three percent of sympathetic preganglionic neurones did not respond to the application of dopamine. Low Ca²⁺/high Mg²⁺ Krebs solution or TTX did not change the resting membrane potential but abolished the slow depolarisation elicited by dopamine, indicating this was synaptic and did not prevent the dopamine induced hyperpolarisation. The dopamine induced slow hyperpolarisation was mimicked by the selective D₁ agonists SKF 38393 or SKF 81297-C and blocked by superfusion with the D₁ antagonist SCH 23390. It was not prevented by superfusion of the slices with alpha₁ or alpha₂ or beta-adrenoceptor antagonists, whereas the inhibitory or excitatory actions of adrenaline were prevented by alpha₁ or alpha₂ antagonists, respectively. The dopamine induced slow depolarisation occurring in a sub-population of sympathetic preganglionic neurones was mimicked by quinpirole, a D₂ agonist, and blocked by haloperidol, a D₂ antagonist. Haloperidol did not block the dopamine induced hyperpolarisations. Dopamine also induced fast synaptic activity which was mimicked by a D₂ agonist and blocked by haloperidol. D₁ agonists did not elicit fast synaptic activity.
Direct evidence for the link between monoaminergic descending pathways and motor activity. I. A study with microdialysis probes implanted in the ventral funiculus of the spinal cord
1995, Brain Research
Monoaminergic projections to the spinal cord are involved in the modulation of motor, autonomic, and sensory functions. More specifically, the increase of electrical activity of serotonergic neurons in raphe obscurus has been correlated with locomotion in t treadmill-trained cats [Jacobs,B.L. and Fornal, C.,Trends Neurosci., 9 (1993) 346–352]. In order to test the direct correlation between locomotion and the release of monoamines, microdialysis probes were permanently implanted for 45 days into the ventral funiculus of the spinal cord (white matter) of adult rats. Eight days after implantation, these rats were subjected to an endurant exercise on a treadmill, and dialysis sessions were organized in such a way that microdialysate samples of 15 min duration were collected during pre-, per- and post-exercise periods. Measurements of serotonin, 5-hydroxyindoleacetic acid, dopamine and 3-methoxy-4-hydroxyphenylethylglycol concentration in the extracellular space showed significant increases during locomotion when compared with both pre- and post-exercise values. Histological analysis shows that serotonergic axons were present close to the dialysis probe. These results demonstrate that the implantation of a microdialysis probe in the ventral funiculus, close to a potential target of monoaminergic projections, is a suitable technique for the collection of neuromediators released during spontaneous running.

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^∗: Research Fellow of the Life Insurance Medical Research Fund of Australia and New Zealand.

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Direct projection of catecholamine (presumably dopamine)-containing neurons from hypothalamus to spinal cord

Abstract

Brain Res.

Neurosci. Lett.

Neurosci. Lett.

Neurosci. Lett.

Neurosci. Lett.

Brain Res.

Brain Res.

Brain Res.

Distribution of catecholamine-containing cell bodies in the rabbit central nervous system

J. comp. Neurol.

Catecholamine-containing cell groups projecting to the rabbit spinal cord

Spinal projections from the midbrain in monkey

J. comp. Neurol.

Catecholamine distribution in feline hypothalamus

J. comp. Neurol.

Evidence for the existence of monoamine-containing neurons in the central nervous system. I. Demonstration of monoamines in the cell bodies of brain stem neurons

Acta physiol. scand.