The Experts below are selected from a list of 228 Experts worldwide ranked by ideXlab platform
Glenda M. Halliday - One of the best experts on this subject based on the ideXlab platform.
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The midbrain Dopaminergic Cell Groups in the baboon Papio ursinus.
Brain research bulletin, 1998Co-Authors: D.a. Mcritchie, H. Cartwright, Susan M. Pond, C.j. Van Der Schyf, Neal Castagnoli, D. G. Van Der Nest, Glenda M. HallidayAbstract:Abstract The present study evaluates the cytoarchitecture of midbrain Dopaminergic regions in baboons using similar methodology to that recently applied to compare humans and rats. This information is relevant for the interpretation of nonhuman primate models of Parkinson’s disease (PD). The midbrains of four alpha male baboons were serially sectioned into 10 evenly spaced series of 50 μm sections. Series were stained with either cresyl violet or immunohistochemically reacted for tyrosine hydroxylase, substance P, calbindin-D 28k , or parvalbumin. The organization of Dopaminergic Cell Groups and the distribution of proteins within these Groups were found to be very similar to that previously described in humans [McRitchie et al ., J. Comp. Neurol. 364:121–150; 1996]. Dorsal and ventral tiers of the A9 substantia nigra (SN) pars compacta and all divisions of the A8 and A10 Cell Groups were identified revealing a high degree of homology in the arrangement of chemically distinct midbrain neurons between primates. The major difference between the organization of human and baboon midbrain Dopaminergic neurons is the anteroposterior extent of the dense Cell clusters within the SN pars compacta. In baboons the dorsomedial Cell cluster is absent at posterior levels. The ventral tier Cell clusters, which are targeted by PD in humans, are restricted to the posterior and ventral regions of the SN pars compacta of the baboon. In humans these Cell clusters are found throughout the rostrocaudal extent of the SN. These ventral Cell clusters have been previously shown to have reciprocal connections with sensorimotor regions of the putamen.
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Specific A10 Dopaminergic nuclei in the midbrain degenerate in Parkinson's disease.
Experimental neurology, 1997Co-Authors: D.a. Mcritchie, H. Cartwright, Glenda M. HallidayAbstract:Using unbiased quantitative techniques, we evaluated the effect of Parkinson's disease on the regional size and the number of tyrosine hydroxylase-producing neurons and all neurons in the midbrain A8 and A10 Dopaminergic Cell Groups located adjacent to the substantia nigra. Seven patients with Lewy body Parkinson's disease were evaluated and compared with five controls. Four of the patients with Parkinson's disease had additional neuropathology, and the effect of concomitant pathology on A10 populations was also determined. Degeneration was not observed in the A8 regions of any patient, and only certain A10 nuclei were affected by the disease. The parabrachial pigmented nucleus situated dorsal to the substantial nigra, and the parapeduncular nucleus located rostromedially were significantly reduced by 40-50% in patients with Parkinson's disease. Few differences were found between patients with or without additional pathology, suggesting a similar pathogenic mechanism to that observed in the substantia nigra of these patients. However, patients with additional pathology also had serotonergic Cell loss in the caudal linear nucleus. There was a reduction in tyrosine hydroxylase immunoreactivity but no overt neurodegeneration in other A10 regions, suggesting the disease may also influence the production of dopamine in some surviving neurons.
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Calbindin D28k-containing neurons are restricted to the medial substantia nigra in humans.
Neuroscience, 1995Co-Authors: D.a. Mcritchie, Glenda M. HallidayAbstract:Abstract A controversy exists in the literature as to whether neurons containing the calcium binding protein calbindin-D 28k are located within the human substantia nigra. The point of variance between reports, however, is not the anatomical distribution of these neurons, but rather the delineation of the dorsal border of the substantia nigra. It has been suggested that the dense substance P striatonigral innervation delimits the substantia nigra in the human. The aim of the present study is to re-examine the distribution of calbindin-D 28k -positive neurons throughout the substantia nigra using substance P to delimit its borders. Although a few calbindin-D 28k -positive neurons were found in the medial Cell group of the substantia nigra, the vast majority of positive neurons were located in the adjacent A8 and A10 Dopaminergic Cell Groups. This anatomical location of calbindin-D 28k -positive neurons is consistent with previous reports, though our results indicate that when the striatonigral projection is used to define the substantia nigra, calbindin-D 28k is not a notable feature of these neurons. This questions the neuroprotective role of this protein in Parkinson's disease.
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Cytoarchitecture and Chemistry of Midbrain Dopaminergic Cell Groups
Advances in Behavioral Biology, 1995Co-Authors: D.a. Mcritchie, Glenda M. HallidayAbstract:The ventral midbrain contains three Dopaminergic Cell Groups in the rat which have been designated A8, A9, and A10, on their rostrocaudal position and relations with surrounding structures (Dahlstrom and Fuxe, 1964). Each of these Groups has extensive cortical and subcortical projections. These Cell Groups are closely homologous with those identified in humans, where the A8 Cell group is present in the lateral and caudolateral midbrain, the A9 Cell group in the substantia nigra, and the heterogeneous A10 Cell group, dorsal and medial to the A9 group (Bogerts, 1981; Saper and Petito, 1982; Halliday and Tork, 1986; Pearson et al., 1990).
E. C. Hirsch - One of the best experts on this subject based on the ideXlab platform.
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Nitric oxide synthase and neuronal vulnerability in parkinson's disease
Neuroscience, 1996Co-Authors: Stéphane Hunot, A. Mouatt-prigent, Yves Agid, Baptiste Faucheux, Florence Boissière, Bernard Brugg, E. C. HirschAbstract:Parkinson's disease is characterized by a loss of Dopaminergic neurons in the mesencephalon. Although the mechanism of this neuronal loss is still unknown, oxidative stress is very likely involved in the cascade of events leading to nerve Cell death. Since nitric oxide could be involved in the production of free radicals, we analysed, using immunohistochemistry and histochemistry, the production systems of nitric oxide in the mesencephalon of four patients with idiopathic Parkinson's disease and three matched control subjects. Using specific antibodies directed against the inducible isoform of nitric oxide synthase (the enzyme involved in the synthesis of nitric oxide), we found evidence to suggest that this isoform was present solely in glial Cells displaying the morphological characteristics of activated macrophages. Immunohistochemical analysis performed with antibodies against the neuronal isoform of nitric oxide synthase, however, revealed perikarya and processes of neurons but no glial Cell staining. The number of nitric oxide synthase-containing Cells was investigated by histoenzymology, using the NADPH-diaphorase activity of nitric oxide synthase. Histochemistry revealed (i) a significant increase in NADPH-diaphorase-positive glial Cell density in the Dopaminergic Cell Groups characterized by neuronal loss in Parkinson's disease and (ii) a neuronal loss in Parkinson's disease that was two-fold greater for pigmented NADPH-diaphorase-negative neurons than for pigmented NADPH-diaphorase-positive neurons. These data suggest a potentially deleterious role of glial Cells producing excessive levels of nitric oxide in Parkinson's disease, which may be neurotoxic for a subpopulation of Dopaminergic neurons, especially those not expressing NADPH-diaphorase activity. However, it cannot be excluded that the presence of glial Cells expressing nitric oxide synthase in the substantia nigra of patients with Parkinson's disease represents a consequence of Dopaminergic neuronal loss.
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Biochemistry of Parkinson's disease with special reference to the Dopaminergic systems
Molecular Neurobiology, 1994Co-Authors: E. C. HirschAbstract:The cardinal neurochemical abnormality in Parkinson's disease is the decreased dopamine content in the striatum, resulting from the loss of Dopaminergic neurons in the mesencephalon. Precise analysis of the Dopaminergic neurons in the midbrain demonstrates, however, that this Cell loss is not uniform. Some Dopaminergic Cell Groups are more vulnerable than others. The degree of Cell loss is severe in the substantia nigra pars compacta, intermediate in the ventral tegmental area and Cell group A8, but nonexistent in the central gray substance. This heterogeneity provides a good paradigm for analyzing the factors implicated in this differential vulnerability. So far, the neurons that degenerate have been shown to contain neuromelanin, high amounts of iron, and no calbinding_28K, and to be poorly protected against oxidative stress. By contrast, the neurons that survive in Parkinson's disease are free of neuromelanin, calbindin_D28-positive, contain low amounts of iron, and are better protected against oxidative stress. The analysis of the pattern of Cell loss in Parkinson's disease may thus bring new clues as to the mechanism of nerve Cell death in Parkinson's disease.
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Distribution of 125I-Ferrotransferrin Binding Sites in the Mesencephalon of Control Subjects and Patients with Parkinson's Disease
Journal of neurochemistry, 1993Co-Authors: Baptiste Faucheux, A. Mouatt-prigent, E. C. Hirsch, F. Javoy-agid, J. Villares, F. Selimi, Jean-jacques Hauw, Yves AgidAbstract:Iron is abnormally accumulated in the substantia nigra pars compacta of patients with Parkinson's disease (PD). Because neuronal and glial iron uptake seems to be mediated by the binding of ferrotransferrin to a specific high-affinity receptor on the Cell surface, the number of transferrin receptors could be altered in this disease. The regional distribution of specific binding sites for human 125I-diferric transferrin has been studied in the mesencephalon, on cryostat-cut sections from autopsy brains of control subjects and parkinsonian patients by in vitro autoradiography. Densities of binding sites were highest in the central gray substance (approximately 10 fmol/mg of tissue equivalent), intermediate in the catecholaminergic Cell group A8, superior colliculus, and ventral tegmental area, and almost nonexistent in the substantia nigra. The density of 125I-transferrin binding sites was not significantly different between parkinsonian and control brains in any region analyzed. These results show that in the mesencephalon the regional density of transferrin binding sites is lowest in the Dopaminergic Cell Groups, which are the most vulnerable to PD, and suggest that iron does not accumulate through an increased density of transferrin receptors at the level of the substantia nigra.
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Glutathione peroxidase, glial Cells and Parkinson's disease
Neuroscience, 1993Co-Authors: P. Damier, Yves Agid, E. C. Hirsch, P. Zhang, F. Javoy-agidAbstract:Abstract Hyperoxidation phenomena are suspected to be involved in Dopaminergic Cell death in Parkinson's disease, which affects preferentially the neuromelanin-containing Dopaminergic neurons of the substantia nigra. Glutathione peroxidase is the major protective enzyme against hydrogen peroxide toxicity. The distribution of glutathione peroxidase-containing Cells was investigated by immunohistochemistry in the midbrain of four control subjects and four patients with Parkinson's disease. (1) Glutathione peroxidase-like immunoreactivity was detected exclusively in glial Cells. (2) In control brains, the density of glutathione peroxidase-positive Cells was higher in the vicinity of the Dopaminergic Cell Groups known to be resistant to the pathological process of Parkinson's disease. (3) In Parkinson's disease, an increased density of glutathione peroxidase-immunostained Cells was observed, surrounding the surviving Dopaminergic neurons. The increase in glutathione peroxidase-containing Cells was correlated with the severity in Dopaminergic Cell loss in the respective Cell Groups. The data suggest that in control brains, a low density of glutathione peroxidase-positive Cells surround the Dopaminergic neurons the most vulnerable to Parkinson's disease, and that in parkinsonian brains, the increased number of glutathione peroxidase-positive Cells may contribute to protect neurons against pathological death. Thus, the amount of glutathione peroxidase protein-containing Cells may be critical for a protective effect against oxidative stress, although it cannot be excluded that the level of the enzyme activity remains the crucial factor.
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Immunocytochemical Quantification of Tyrosine Hydroxylase at a Cellular Level in the Mesencephalon of Control Subjects and Patients with Parkinson's and Alzheimer's Disease
Journal of neurochemistry, 1993Co-Authors: A. Kastner, E. C. Hirsch, F. Javoy-agid, Maria Trinidad Herrero, Yves AgidAbstract:Parkinson's disease is characterized by massive degeneration of the melanized Dopaminergic neurons in the substantia nigra. The functional capacity of the surviving nigral neurons is affected, as indicated by the subnormal levels of tyrosine hydroxylase (TH) mRNA in these neurons and the presence in the parkinsonian mesencephalon of melanized neurons lacking TH immunoreactivity. This is apparently in contraction with the known overactivity of dopamine synthesis and release that occurs in the remaining Dopaminergic terminals. To test the ability of the surviving neurons to express TH protein, a semiquantitative immunocytochemical method was developed. The relative amounts of TH were estimated with a computer-assisted image analysis system in the Dopaminergic neurons of representative mesencephalic sections of control and parkinsonian brains and for comparison in brains from patients with Alzheimer's disease. In control brains, the mean TH content per neuron differed from one subject to another and between the different Dopaminergic Cell Groups of the mesencephalon in the same subject. Within a given Dopaminergic region, the level of TH was variable among neurons. In patients with Parkinson's disease, the ratio of TH protein content per neuron in the substantia nigra by reference to that of the central gray substance was reduced. In patients with Alzheimer's disease, the amount of TH was selectively reduced in the remaining Dopaminergic neurons of the ventral tegmental area, a region characterized by a loss in Dopaminergic neurons. The decrease in Cellular TH content might therefore be related to the presence of the neurodegenerative process in the area considered. In patients with Parkinson's disease, the incapacity of the surviving neurons to express normal TH levels may reduce the efficiency of the hyperactivity mechanisms that develop in the remaining striatal Dopaminergic terminals.
Yves Agid - One of the best experts on this subject based on the ideXlab platform.
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Nitric oxide synthase and neuronal vulnerability in parkinson's disease
Neuroscience, 1996Co-Authors: Stéphane Hunot, A. Mouatt-prigent, Yves Agid, Baptiste Faucheux, Florence Boissière, Bernard Brugg, E. C. HirschAbstract:Parkinson's disease is characterized by a loss of Dopaminergic neurons in the mesencephalon. Although the mechanism of this neuronal loss is still unknown, oxidative stress is very likely involved in the cascade of events leading to nerve Cell death. Since nitric oxide could be involved in the production of free radicals, we analysed, using immunohistochemistry and histochemistry, the production systems of nitric oxide in the mesencephalon of four patients with idiopathic Parkinson's disease and three matched control subjects. Using specific antibodies directed against the inducible isoform of nitric oxide synthase (the enzyme involved in the synthesis of nitric oxide), we found evidence to suggest that this isoform was present solely in glial Cells displaying the morphological characteristics of activated macrophages. Immunohistochemical analysis performed with antibodies against the neuronal isoform of nitric oxide synthase, however, revealed perikarya and processes of neurons but no glial Cell staining. The number of nitric oxide synthase-containing Cells was investigated by histoenzymology, using the NADPH-diaphorase activity of nitric oxide synthase. Histochemistry revealed (i) a significant increase in NADPH-diaphorase-positive glial Cell density in the Dopaminergic Cell Groups characterized by neuronal loss in Parkinson's disease and (ii) a neuronal loss in Parkinson's disease that was two-fold greater for pigmented NADPH-diaphorase-negative neurons than for pigmented NADPH-diaphorase-positive neurons. These data suggest a potentially deleterious role of glial Cells producing excessive levels of nitric oxide in Parkinson's disease, which may be neurotoxic for a subpopulation of Dopaminergic neurons, especially those not expressing NADPH-diaphorase activity. However, it cannot be excluded that the presence of glial Cells expressing nitric oxide synthase in the substantia nigra of patients with Parkinson's disease represents a consequence of Dopaminergic neuronal loss.
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Does the calcium binding protein calretinin protect Dopaminergic neurons against degeneration in Parkinson's disease?
Brain Research, 1994Co-Authors: A. Mouatt-prigent, Yves Agid, Etienne C. HirschAbstract:Parkinson's disease (PD) is characterized by a heterogeneous loss of Dopaminergic neurons in the human mesencephalon affecting mainly the substantia nigra pars compacta (SNpc) and to a lesser extent the other Dopaminergic Cell Groups. A rise in intraCellular calcium concentrations represents one of the final events leading to nerve Cell death. Calbindin D28k, a protein capable of buffering intraCellular calcium concentrations is present in the Dopaminergic neurons that are selectively preserved in PD but not in those that degenerate. To determine whether other calcium-binding proteins also represent putative protective factors of Dopaminergic neurons in PD, we analyzed immunohistochemically the distribution of calretinin-containing (CR+) neurons, in the human mesencephalon of three control subjects and four patients with PD. No significant differences were observed between the number of CR+ neurons in the two subject Groups. Sequential double immunostaining for calretinin and tyrosine hydroxylase showed a variable proportion of CR+ neurons among Dopaminergic neurons: moderate co-localization was found in catecholaminergic Cell group A8 and in the dorsal part of the ventral tegmental area (VTA) and low co-localization in the SNpc, the ventral part of the VTA and the central gray substance. This indicates that calretinin may only protect some Dopaminergic neurons against degeneration in PD. Yet, in the SNpc a selective preservation of CR+ Dopaminergic neurons was observed, suggesting a neuroprotective role in some Dopaminergic Cell Groups only.
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Distribution of 125I-Ferrotransferrin Binding Sites in the Mesencephalon of Control Subjects and Patients with Parkinson's Disease
Journal of neurochemistry, 1993Co-Authors: Baptiste Faucheux, A. Mouatt-prigent, E. C. Hirsch, F. Javoy-agid, J. Villares, F. Selimi, Jean-jacques Hauw, Yves AgidAbstract:Iron is abnormally accumulated in the substantia nigra pars compacta of patients with Parkinson's disease (PD). Because neuronal and glial iron uptake seems to be mediated by the binding of ferrotransferrin to a specific high-affinity receptor on the Cell surface, the number of transferrin receptors could be altered in this disease. The regional distribution of specific binding sites for human 125I-diferric transferrin has been studied in the mesencephalon, on cryostat-cut sections from autopsy brains of control subjects and parkinsonian patients by in vitro autoradiography. Densities of binding sites were highest in the central gray substance (approximately 10 fmol/mg of tissue equivalent), intermediate in the catecholaminergic Cell group A8, superior colliculus, and ventral tegmental area, and almost nonexistent in the substantia nigra. The density of 125I-transferrin binding sites was not significantly different between parkinsonian and control brains in any region analyzed. These results show that in the mesencephalon the regional density of transferrin binding sites is lowest in the Dopaminergic Cell Groups, which are the most vulnerable to PD, and suggest that iron does not accumulate through an increased density of transferrin receptors at the level of the substantia nigra.
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Glutathione peroxidase, glial Cells and Parkinson's disease
Neuroscience, 1993Co-Authors: P. Damier, Yves Agid, E. C. Hirsch, P. Zhang, F. Javoy-agidAbstract:Abstract Hyperoxidation phenomena are suspected to be involved in Dopaminergic Cell death in Parkinson's disease, which affects preferentially the neuromelanin-containing Dopaminergic neurons of the substantia nigra. Glutathione peroxidase is the major protective enzyme against hydrogen peroxide toxicity. The distribution of glutathione peroxidase-containing Cells was investigated by immunohistochemistry in the midbrain of four control subjects and four patients with Parkinson's disease. (1) Glutathione peroxidase-like immunoreactivity was detected exclusively in glial Cells. (2) In control brains, the density of glutathione peroxidase-positive Cells was higher in the vicinity of the Dopaminergic Cell Groups known to be resistant to the pathological process of Parkinson's disease. (3) In Parkinson's disease, an increased density of glutathione peroxidase-immunostained Cells was observed, surrounding the surviving Dopaminergic neurons. The increase in glutathione peroxidase-containing Cells was correlated with the severity in Dopaminergic Cell loss in the respective Cell Groups. The data suggest that in control brains, a low density of glutathione peroxidase-positive Cells surround the Dopaminergic neurons the most vulnerable to Parkinson's disease, and that in parkinsonian brains, the increased number of glutathione peroxidase-positive Cells may contribute to protect neurons against pathological death. Thus, the amount of glutathione peroxidase protein-containing Cells may be critical for a protective effect against oxidative stress, although it cannot be excluded that the level of the enzyme activity remains the crucial factor.
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Immunocytochemical Quantification of Tyrosine Hydroxylase at a Cellular Level in the Mesencephalon of Control Subjects and Patients with Parkinson's and Alzheimer's Disease
Journal of neurochemistry, 1993Co-Authors: A. Kastner, E. C. Hirsch, F. Javoy-agid, Maria Trinidad Herrero, Yves AgidAbstract:Parkinson's disease is characterized by massive degeneration of the melanized Dopaminergic neurons in the substantia nigra. The functional capacity of the surviving nigral neurons is affected, as indicated by the subnormal levels of tyrosine hydroxylase (TH) mRNA in these neurons and the presence in the parkinsonian mesencephalon of melanized neurons lacking TH immunoreactivity. This is apparently in contraction with the known overactivity of dopamine synthesis and release that occurs in the remaining Dopaminergic terminals. To test the ability of the surviving neurons to express TH protein, a semiquantitative immunocytochemical method was developed. The relative amounts of TH were estimated with a computer-assisted image analysis system in the Dopaminergic neurons of representative mesencephalic sections of control and parkinsonian brains and for comparison in brains from patients with Alzheimer's disease. In control brains, the mean TH content per neuron differed from one subject to another and between the different Dopaminergic Cell Groups of the mesencephalon in the same subject. Within a given Dopaminergic region, the level of TH was variable among neurons. In patients with Parkinson's disease, the ratio of TH protein content per neuron in the substantia nigra by reference to that of the central gray substance was reduced. In patients with Alzheimer's disease, the amount of TH was selectively reduced in the remaining Dopaminergic neurons of the ventral tegmental area, a region characterized by a loss in Dopaminergic neurons. The decrease in Cellular TH content might therefore be related to the presence of the neurodegenerative process in the area considered. In patients with Parkinson's disease, the incapacity of the surviving neurons to express normal TH levels may reduce the efficiency of the hyperactivity mechanisms that develop in the remaining striatal Dopaminergic terminals.
Gregory F. Ball - One of the best experts on this subject based on the ideXlab platform.
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Fos expression in monoaminergic Cell Groups in response to sociosexual interactions in male and female Japanese quail.
Behavioral Neuroscience, 2014Co-Authors: Onur Iyilikci, Samantha Baxter, Jacques Balthazart, Gregory F. BallAbstract:Monoaminergic neurotransmitters regulate different components of sexual behaviors, but how the different monoaminergic Cell Groups selectively regulate these behaviors is not well understood. We examined the potential contribution of these different Cell Groups in the control of different aspects of sexual behaviors in male and female quail. We used double-label immunohistochemistry, labeling the protein product of the immediate early gene, Fos, along with tyrosine hydroxylase (TH) or tryptophan hydroxylase (TPH), markers for catecholaminergic or indolaminergic Cells, respectively. Rhythmic Cloacal Sphincter Movements (RCSM) were recorded as a measure of male appetitive sexual behavior. Consummatory sexual behaviors were evaluated based on the species-typical copulation sequence. Enhanced Fos expression in the medial preoptic nucleus and bed nucleus of the stria terminalis was observed in association with both physical and visual contact to the opposite sex for males, but not for females. Fos induction associated with physical contact was observed in the ventral tegmental area and anterior periaqueductal gray in both sexes. In males only, the number of Fos-immunoreactive (ir) Cells increased in the visual contact condition in these two Dopaminergic Cell Groups, however no significant effect was observed for double-labeled TH-Fos-ir Cells. In addition, consummatory but not appetitive sexual behavior increased Fos expression in TPH-ir Cells in the raphe pallidus of males. This increase following physical but not visual contact agrees with the notion that activation of the serotoninergic system is implicated in the development of sexual satiation but not activated by simply viewing a female, in contrast to the Dopaminergic system.
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differential effects of global versus local testosterone on singing behavior and its underlying neural substrate
Proceedings of the National Academy of Sciences of the United States of America, 2013Co-Authors: Beau A Alward, Jacques Balthazart, Gregory F. BallAbstract:Steroid hormones regulate multiple but distinct aspects of social behaviors. Testosterone (T) has multiple effects on learned courtship song in that it regulates both the motivation to sing in a particular social context as well as the quality of song produced. The neural substrate(s) where T acts to regulate the motivation to sing as opposed to other aspects of song has not been definitively characterized. We show here that T implants in the medial preoptic nucleus (POM) of castrated male canaries (Serinus canaria) increase song rate but do not enhance acoustic features such as song stereotypy compared with birds receiving peripheral T that can act globally throughout the brain. Strikingly, T action in the POM increased song control nuclei volume, consistent with the hypothesis that singing activity induces neuroplasticity in the song control system independent of T acting in these nuclei. When presented with a female canary, POM-T birds copulated at a rate comparable to birds receiving systemic T but produced fewer calls and songs in her presence. Thus, POM is a key site where T acts to activate copulation and increase song rate, an appetitive sexual behavior in songbirds, but T action in other areas of the brain or periphery (e.g., HVC, Dopaminergic Cell Groups, or the syrinx) is required to enhance the quality of song (i.e., stereotypy) as well as regulate context-specific vocalizations. These results have broad implications for research concerning how steroids act at multiple brain loci to regulate distinct sociosexual behaviors and the associated neuroplasticity.
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The activation of birdsong by testosterone: multiple sites of action and role of ascending catecholamine projections.
Annals of the New York Academy of Sciences, 2003Co-Authors: Gregory F. Ball, Christina B. Castelino, Donna L. Maney, Didier Appeltants, Jacques BalthazartAbstract:Birdsong is a species-typical stereotypic vocalization produced in the context of reproduction and aggression. Among temperate-zone songbirds, it is produced primarily by males, and its frequency and quality are enhanced by the presence of the gonadal steroid hormone testosterone in the plasma. In the brain, the effects of testosterone on song behavior involve both estrogenic and androgenic metabolites of testosterone that are locally produced and act via their cognate receptors. Androgen, and in some cases estrogen, receptors are present in many specialized forebrain song control nuclei. Testosterone can regulate catecholamine steady-state levels and turnover in these song control regions. Tracing studies combined with immunocytochemistry for tyrosine hydroxylase (a marker of catecholamine synthesis) reveal several catecholamine Cell Groups that project to forebrain song control nuclei. These brain areas also express the mRNA for either androgen receptors or estrogen receptor alpha, and androgens enhance the expression of tyrosine hydroxylase. Dopaminergic Cell Groups that project to song nuclei express the protein product of the immediate early gene fos in association with the production of territorial song. Thus, testosterone may be acting on song behavior via these ascending catecholamine Cell Groups. Chemical lesioning studies suggest that noradrenergic projections to the song system are involved in the latency to produce song and the ability to discriminate conspecific from heterospecific song. The song control circuit may thus be modulated in significant ways via the androgen regulation of forebrain catecholamine systems.
D.a. Mcritchie - One of the best experts on this subject based on the ideXlab platform.
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The midbrain Dopaminergic Cell Groups in the baboon Papio ursinus.
Brain research bulletin, 1998Co-Authors: D.a. Mcritchie, H. Cartwright, Susan M. Pond, C.j. Van Der Schyf, Neal Castagnoli, D. G. Van Der Nest, Glenda M. HallidayAbstract:Abstract The present study evaluates the cytoarchitecture of midbrain Dopaminergic regions in baboons using similar methodology to that recently applied to compare humans and rats. This information is relevant for the interpretation of nonhuman primate models of Parkinson’s disease (PD). The midbrains of four alpha male baboons were serially sectioned into 10 evenly spaced series of 50 μm sections. Series were stained with either cresyl violet or immunohistochemically reacted for tyrosine hydroxylase, substance P, calbindin-D 28k , or parvalbumin. The organization of Dopaminergic Cell Groups and the distribution of proteins within these Groups were found to be very similar to that previously described in humans [McRitchie et al ., J. Comp. Neurol. 364:121–150; 1996]. Dorsal and ventral tiers of the A9 substantia nigra (SN) pars compacta and all divisions of the A8 and A10 Cell Groups were identified revealing a high degree of homology in the arrangement of chemically distinct midbrain neurons between primates. The major difference between the organization of human and baboon midbrain Dopaminergic neurons is the anteroposterior extent of the dense Cell clusters within the SN pars compacta. In baboons the dorsomedial Cell cluster is absent at posterior levels. The ventral tier Cell clusters, which are targeted by PD in humans, are restricted to the posterior and ventral regions of the SN pars compacta of the baboon. In humans these Cell clusters are found throughout the rostrocaudal extent of the SN. These ventral Cell clusters have been previously shown to have reciprocal connections with sensorimotor regions of the putamen.
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Specific A10 Dopaminergic nuclei in the midbrain degenerate in Parkinson's disease.
Experimental neurology, 1997Co-Authors: D.a. Mcritchie, H. Cartwright, Glenda M. HallidayAbstract:Using unbiased quantitative techniques, we evaluated the effect of Parkinson's disease on the regional size and the number of tyrosine hydroxylase-producing neurons and all neurons in the midbrain A8 and A10 Dopaminergic Cell Groups located adjacent to the substantia nigra. Seven patients with Lewy body Parkinson's disease were evaluated and compared with five controls. Four of the patients with Parkinson's disease had additional neuropathology, and the effect of concomitant pathology on A10 populations was also determined. Degeneration was not observed in the A8 regions of any patient, and only certain A10 nuclei were affected by the disease. The parabrachial pigmented nucleus situated dorsal to the substantial nigra, and the parapeduncular nucleus located rostromedially were significantly reduced by 40-50% in patients with Parkinson's disease. Few differences were found between patients with or without additional pathology, suggesting a similar pathogenic mechanism to that observed in the substantia nigra of these patients. However, patients with additional pathology also had serotonergic Cell loss in the caudal linear nucleus. There was a reduction in tyrosine hydroxylase immunoreactivity but no overt neurodegeneration in other A10 regions, suggesting the disease may also influence the production of dopamine in some surviving neurons.
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Calbindin D28k-containing neurons are restricted to the medial substantia nigra in humans.
Neuroscience, 1995Co-Authors: D.a. Mcritchie, Glenda M. HallidayAbstract:Abstract A controversy exists in the literature as to whether neurons containing the calcium binding protein calbindin-D 28k are located within the human substantia nigra. The point of variance between reports, however, is not the anatomical distribution of these neurons, but rather the delineation of the dorsal border of the substantia nigra. It has been suggested that the dense substance P striatonigral innervation delimits the substantia nigra in the human. The aim of the present study is to re-examine the distribution of calbindin-D 28k -positive neurons throughout the substantia nigra using substance P to delimit its borders. Although a few calbindin-D 28k -positive neurons were found in the medial Cell group of the substantia nigra, the vast majority of positive neurons were located in the adjacent A8 and A10 Dopaminergic Cell Groups. This anatomical location of calbindin-D 28k -positive neurons is consistent with previous reports, though our results indicate that when the striatonigral projection is used to define the substantia nigra, calbindin-D 28k is not a notable feature of these neurons. This questions the neuroprotective role of this protein in Parkinson's disease.
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Cytoarchitecture and Chemistry of Midbrain Dopaminergic Cell Groups
Advances in Behavioral Biology, 1995Co-Authors: D.a. Mcritchie, Glenda M. HallidayAbstract:The ventral midbrain contains three Dopaminergic Cell Groups in the rat which have been designated A8, A9, and A10, on their rostrocaudal position and relations with surrounding structures (Dahlstrom and Fuxe, 1964). Each of these Groups has extensive cortical and subcortical projections. These Cell Groups are closely homologous with those identified in humans, where the A8 Cell group is present in the lateral and caudolateral midbrain, the A9 Cell group in the substantia nigra, and the heterogeneous A10 Cell group, dorsal and medial to the A9 group (Bogerts, 1981; Saper and Petito, 1982; Halliday and Tork, 1986; Pearson et al., 1990).