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At least 811 records · Page 45Linked to original sources
PubMed1981

High resolution analysis of [3H]2-deoxyglucose incorporation into neurons and glial cells in invertebrate ganglia: histological processing of nervous tissue for selective marking of glycogen.

The 2-deoxyglucose (2-DG) autoradiographic technique, in conjunction with 3H-labelled 2-DG and glutaraldehyde fixation, was applied to the isolated ganglia of the leech and the snail in order to analyse its potential use for the understanding of energy utilization in these simple nervous systems. Approximately 50% of the label is retained in these tissues after histological processing, and the method can be satisfactorily applied at the subcellular level. In both species most neurons progressively accumulate radioactivity over 15 min-1 h, although to different extents. In the leech the glial cells showed greater uptake than the neurons. Paired homologous neurons in contralateral buccal ganglia of the snail were equally labelled. In all structures studied by electron-microscope autoradiography the label was positively associated with glycogen. Freshly extracted glycogen from ganglia previously exposed to 2-DG was significantly labelled (2-10% of total radioactivity in the ganglia); thus the glutaraldehyde fixation did not appear responsible for artifactual binding of the label. The significance of the glycogen labelling and the potential of the technique for metabolic mapping in these nervous systems are discussed.

Animals↗
PubMed1996

beta 2-adrenoreceptor immunoreactivity in cardiac ganglia of the guinea pig.

Previous pharmacological studies in co-culture systems have indicated the presence of beta-adrenoreceptors on intrinsic cardiac neurons of the guinea pig (Horackova et al., 1993) but radioligand binding studies on tissue sections failed to provide a definite answer as to the presence of such receptors on cardiac neurons in situ, due to the iodine-binding properties of cardiac nerve bundles and ganglia (Molenaar et al., 1992). We therefore addressed this question by immunohistochemistry, using antisera raised against synthetic peptides of the beta 2-adrenoreceptor. For comparison, cholinergic and catecholaminergic neurons were identified immunohistochemically by means of antibodies against the enzymes involved in the synthesis of acetylcholine (choline acetyltransferase), and of catecholamines (tyrosine hydroxylase). Virtually all intrinsic cardiac neurons contained both beta 2-adrenoreceptor- and choline acetyltransferase-immunoreactivities. In addition, some nerve fibre bundles exhibited beta 2-adrenoreceptor-immunoreactivity. Several ganglia were innervated by tyrosine hydroxylase-immunoreactive axons, but the majority of ganglia did not receive tyrosine hydroxylase-immunoreactive nerve terminals, and additional intraganglionic sources of catecholamine synthesis could not be identified. Thus, the results are in favour of beta-adrenergic modulation of guinea pig cardiac ganglia by humorally and, partially, by locally released catecholamines.

Animals↗
PubMed1996

Reinnervation of frog sympathetic ganglia after selective denervation of B or C neurons.

Selective transection of the B or C preganglionic nerve fibres respectively innervating the B and C sympathetic neurons was carried out on the last two ganglia of the sympathetic chain of the frog Rana esculenta. At different times thereafter, the cross-reinnervation of one type of denervated neuron by nerve endings sprouting within the ganglia from intact fibres innervating the other type was investigated by both the quantitative morphology of the synaptic contacts and related structures and electrophysiological recordings of ganglionic transmission. As there are no fine ultrastructural criteria for distinguishing B from C neurons, the overall density of synapse, simple contact, and 'vacated' postsynaptic differentiation profiles was measured in the two cases of selective section and compared with the values for normal ganglia, therefore permitting the progress of cross-reinnervation with time for each type of neuron to be followed. At ten days after section of the C preganglionic fibres, immunocytochemistry showed that there were no anti-LH-RH-like peptide containing fibres within the ganglia. The B myelinated preganglionic fibres were able to reinnervate the denervated C neurons, with return to normal values of synaptic density and fully efficient transmission at two months in all tested C neurons. However, the latency of orthodromic action potentials was close to that of normally innervated B neurons. In contrast, the C non-myelinated preganglionic fibres reinnervated the denervated B neurons with limited efficiency, the synaptic density being two-thirds the normal value after five months, while subthreshold excitatory postsynaptic potentials or action potentials were only recorded in 44% of the tested B neurons. The latency of these orthodromic responses was close to that of normally innervated C neurons. It is postulated that the poor cross-reinnervation of B neurons could be due to insufficient sprouting of C fibres and/or lack of 'affinity' between C fibres and B neurons. In addition, these experiments demonstrated that the subsynaptic apparatus, fairly characteristic of frog ganglionic synapses, is present in both types of sympathetic neurons, although predominantly in B neurons.

Animals↗
PubMedDate not supplied

Effects of GM1-ganglioside and alpha-sialyl cholesterol on amino acid uptake, protein synthesis, and Na+,K(+)-ATPase activity in superior cervical and nodose ganglia excised from adult rats.

We examined the effect of GM1-ganglioside in combination with cholera toxin B, and synthetic alpha-sialyl cholesterol (alpha-SC) on neutral amino acid (tritiated alpha-aminoisobutyric acid, [3H]AIB) uptake, protein synthesis [( 3H]leucine incorporation), and Na+,K(+)-ATPase activity in isolated superior cervical ganglia (SCG) and nodose ganglia (NG) from adult rats after aerobic incubation, usually for 2 h at 37 degrees C in vitro. Cholera toxin B, that specifically masks the oligosaccharide chain of GM1-ganglioside, antagonized the GM1-induced changes in [3H]AIB uptake, [3H]leucine incorporation, and Na+,K(+)-ATPase activity almost completely in SCG, but partially in NG. Although cholesterol itself had little effect on either [3H]AIB uptake and Na+,K(+)-ATPase activity both in SCG and NG, alpha-SC caused considerable reduction of both amino acid uptake and the transport enzyme activity in each ganglia. However, cholesterol was more effective than alpha-SC in decreasing [3H]leucine incorporation in either ganglia. Whereas addition of EGTA markedly reduced either GM1-induced or alpha-SC-induced change in [3H]leucine incorporation into acid-insoluble fraction in both SCG and NG, application of Ca2+ ionophore produced considerable recovery of the protein synthesis from the inhibited level by Ca2(+)-deprivation. ATP and creatine phosphate contents in SCG were elevated by the presence of GM1 or alpha-SC, whereas [3H]AIB uptake and Na+,K(+)-ATPase activity were inhibited, suggesting that utilization for membrane transport was diminished as a result of GM1- or alpha-SC-induced decrease of ATPase activity.

Amino Acids↗
PubMed2001

A computational model of action selection in the basal ganglia. I. A new functional anatomy.

We present a biologically plausible model of processing intrinsic to the basal ganglia based on the computational premise that action selection is a primary role of these central brain structures. By encoding the propensity for selecting a given action in a scalar value (the salience), it is shown that action selection may be recast in terms of signal selection. The generic properties of signal selection are defined and neural networks for this type of computation examined. A comparison between these networks and basal ganglia anatomy leads to a novel functional decomposition of the basal ganglia architecture into 'selection' and 'control' pathways. The former pathway performs the selection per se via a feedforward off-centre on-surround network. The control pathway regulates the action of the selection pathway to ensure its effective operation, and synergistically complements its dopaminergic modulation. The model contrasts with the prevailing functional segregation of basal ganglia into 'direct' and 'indirect' pathways.

Animals↗
PubMed2004

123I-beta-CIT SPECT demonstrates increased presynaptic dopamine transporter binding sites in basal ganglia in vivo in schizophrenia.

RATIONALE: The dopamine hypothesis for schizophrenia postulates overactivity of dopamine transmission in the basal ganglia. Most effective antipsychotic drugs block postsynaptic dopamine receptors, but in-vivo imaging studies have not been able to show changes in these receptors in drug-naive schizophrenics. OBJECTIVES: The presynaptic dopamine transporter (DAT) is thought to be an important regulator of synaptic dopamine concentration. We have used SPECT with (123)I-beta-CIT, which has a high affinity for DAT, in order to further examine the dopamine hypothesis for schizophrenia. METHODS: Six patients with chronic schizophrenia treated with classic dopamine D(2)-receptor blocking neuroleptics were investigated. The number of DAT binding sites in the basal ganglia was calculated and compared with five healthy volunteers and ten parkinsonian patients. RESULTS: The schizophrenic patients showed a 36-63% increase in DAT binding sites compared with the volunteers, whereas the parkinsonian patients showed a 57-96% decrease. The differences between the groups were highly significant (even after correction for different age composition within the groups). CONCLUSIONS: There was an increased number of DAT binding sites in the schizophrenic patients treated with dopamine D(2)-receptor blocking neuroleptics. This fits well with several recent reports that have shown increased volumes of basal ganglia in this patient category. It thus appears that there is an increased number of presynaptic dopamine releasing nerve terminals in the basal ganglia, possibly as a biological adaptation to counteract the postsynaptic dopamine D(2)-receptor blockade.

Adult↗
PubMed2006

Predictive and reactive control of grasping forces: on the role of the basal ganglia and sensory feedback.

We comparatively investigated predictive and reactive grip force behaviour in 12 subjects with basal ganglia dysfunction (six subjects with Parkinson's disease, six subjects with writer's cramp), two subjects chronically lacking all tactile and proprioceptive sensory feedback and 16 sex- and age-matched control subjects. Subjects held an instrumented receptacle between the index finger and thumb. A weight was dropped into the receptacle either unexpectedly from the experimenter's hand with the subject being blindfolded or expectedly from the subject's opposite hand. This paradigm allowed us to study predictive and reactive modes of grip force control. All patients generated an overshoot in grip force, irrespective of whether the weight was dropped expectedly or unexpectedly. When the weight was dropped from the experimenter's hand, a reactive grip force response lagged behind the load perturbation at impact in patients with basal ganglia dysfunction and healthy controls. When the weight was dropped expectedly from the subject's opposite hand, patients with basal ganglia dysfunction and healthy subjects started to increase grip force prior to the release of the weight, indicating a predictive mode of control. We interpret these data to support the notion that the motor dysfunction in basal ganglia disorders is associated with deficits of sensorimotor integration. Both deafferented subjects did not show a reactive mode of force control when the weight was dropped unexpectedly, underlining the importance of sensory feedback to initiate reactive force responses. Also in the predictive mode, grip force processing was severely impaired in deafferented subjects. Thus, at least intermittent sensory information is necessary to establish and update predictive modes of grasping force control.

Adult↗
PubMed2006

Depth perception in cerebellar and basal ganglia disease.

There is increasing evidence that the cerebellum and the basal ganglia serve not only a role in motor control but also in visual perception. Patients with Parkinson's disease (PD) as well as patients with cerebellar lesions exhibit impairments of vision that are not fully explained by ocular motor deficits. It is less clear to which extent these visual deficits contribute to an impaired control of visually guided movements. This study examined whether a dysfunction of the cerebellum or the basal ganglia induces impairments in depth perception, which affect action. We employed an illusionary display, the Ames trapezoidal window, to determine the ability of PD patients (n=10) and patients with spinocerebellar ataxia (SCA) (n=6) to process depth cues when estimating object slant. Participants either pointed to the edges of the window (motor judgement) or verbally indicated the perceived orientation of the display (verbal judgement). To control for ocular and limb motor deficits, participants judged the slant of a non-illusionary display in a second task. Slant estimation of the non-illusionary window was not impaired in either patient group when compared to control subjects (all P>0.2). In contrast, SCA as well as PD patients exhibited significantly greater slant estimation errors than controls when pointing to the illusionary window (P=0.005). In addition, both patient groups made larger errors than controls in their verbal judgements during binocular viewing of the illusion (P=0.005), but not during monocular viewing (P>0.2). In sum, the present findings point towards a role for both the basal ganglia and cerebellum for the processing of visual information about depth. Since the deficits were seen both in the context of action and perception and were only partially reconciled by the availability of binocular depth cues, we conclude that basal ganglia as well as cerebellar disease may affect the visual perception of depth.

Adult↗
PubMed2000

A putative hyperglycemic factor from the cerebral ganglia of Otala lactea (Mollusca: Pulmonata).

Mantle tissue pieces from adult Otala lactea continuously synthesized glycogen over a 72-h incubation period. Acid-saline extract of the cerebral ganglia inhibited glycogen synthesis by mantle tissue in vitro. This effect was dose-dependent. The glycogen reduction factor from the cerebral ganglia was heat stable, protease sensitive, and relatively hydrophobic. The cerebral ganglia extract also stimulated mantle glycogen phosphorylase in vitro in a dose-dependent manner. The results suggest the presence of a hyperglycemic factor in the cerebral ganglia of Otala. The molecular weight of this factor, estimated by size-exclusion chromatography, was approximately 10,000. Mammalian glucagon had no significant effect on glycogen synthesis by the mantle pieces.

Animals↗
PubMed2006

Post-stroke affective or apathetic depression and lesion location: left frontal lobe and bilateral basal ganglia.

This study was designed to examine the correlation between damage to the basal ganglia or frontal lobe and depression status (both affective and apathetic dimensions) in 243 stroke patients. We assessed the affective dimension in post-stroke depression (PSD) using the Zung Self-rating Depression Scale (SDS) and the apathetic dimension in PSD using the apathy scale (AS). We classified basal ganglia or frontal lobe damage into four groups: no damage, damage to the left side only, damage to the right side only, and damage to both sides. Affective and/or apathetic PSD was found in 126 patients (51.9%). The severity of affective depression (SDS score) was associated with left frontal lobe (but not basal ganglia) damage, and that of apathetic depression (AS score) was related to damage to the bilateral basal ganglia (but not to the frontal lobe). The anatomical correlates of PSD differ depending on the PSD dimension (affective or apathetic) and may explain interstudy differences regarding the association between lesion location and type of PSD.

Aged↗
PubMed1997

Cytochrome b558 and hydrogen peroxide production in small intensely fluorescent cells of sympathetic ganglia.

Small intensely fluorescent (SIF) cells are paraganglionic cells derived from sympathicoblasts which may serve as interneurons, endo-/paracrine cells or arterial chemoreceptors within sympathetic ganglia. Like paraganglionic cells of other locations, e.g., carotid body glomus cells, they are responsive to hypoxia. Recent studies on glomus cells and other hypoxia-sensing cells suggested the involvement of a b558-type cytochrome and intracellular generation of H2O2 in the process of oxygen sensing. In the present study, we demonstrate the occurrence of the small subunit of cytochrome b558, p22phox, in SIF cells of guinea-pig sympathetic ganglia by immunohistochemistry using two different antisera. H2O2 production was monitored in explanted intact superior cervical ganglia of 2-day-old rats by confocal laser scanning analysis of rhodamine 123 fluorescence generated due to oxidation of dihydrorhodamine 123 by H2O2. Using this technique, SIF cell clusters appeared as sites of highest H2O2 production within the ganglia. Thus, SIF cells exhibit two key features of an oxidase system generating reactive oxygen species. This may be involved in the proposed chain of events in oxygen sensing, but alternative cellular functions of this system have also to be considered.

Animals↗
PubMed2006

Sensory collaterals, intramural ganglia and motor nerves in the guinea-pig bladder: evidence for intramural neural circuits.

The afferent output from the bladder is important for triggering micturition. This study identifies different types of afferent nerve and explores the connections of their collateral fibres on intramural ganglia and potential ganglionic targets. The experiments were performed on tissues from male guinea-pigs (n=16). Fibres positive for choline acetyl transferase (ChAT(+)) were found to originate close to the urothelium, to transit the sub-urothelial interstitial cell layer and to pass into the lamina propria. A different population of fibres, immunopositive for calcitonin gene-related peptide (CGRP), capsaicin receptors or neurofilament protein (NF), were seen to intertwine with the ChAT(+) fibres in the lamina propria. The ChAT(+) fibres did not express NF. Ganglia with ChAT(+) and NF(+) neurones were found in the lamina propria and muscle. ChAT(+) fibres, with pronounced terminal varicosities, were present on the nerve cell bodies. Two types were noted: NF(+) terminals and those with little or no NF (NF(-)) suggesting that their origins were the ChAT(+) afferent collaterals and the adjacent ganglia. Fibres containing CGRP or substance P were seen on the ganglionic cells. alpha1B adrenergic receptors were also found on the neurones indicative of adrenergic synapses. Thus, the ganglia had multiple inputs. Different types of ChAT(+) nerves were seen in the muscle: NF(+) and NF(-). The ChAT(+)/NF(+) nerves may represent a ganglionic output to the muscle. This complex neuronal network may therefore represent the elements generating and modulating bladder sensations. The role of such a scheme in bladder pathology and the therapeutic sites of action of anticholinergic and sympathomimetic drugs are discussed.

Animals↗
PubMed1998

Neuronal subpopulations in autonomic ganglia associated with the chicken ureter: an immunohistochemical study.

The neurochemical coding of neurones located in ganglia of the nerve trunk accompanying the chicken ureter was analysed and quantified using NADPH-diaphorase reactivity and immunohistochemistry against tyrosine hydroxylase (TH), nitric oxide synthase (NOS), calbindin (CAL), vasoactive intestinal polypeptide (VIP), neuropeptide Y (NPY), somatostatin (SOM), substance P (SP) and calcitonin gene-related peptide (CGRP) in untreated or colchicine-treated preparation. Almost all neurones were either positive for TH (38%) or for SOM (60%). Only 4% of the neurones were both TH- and SOM-positive and 3% of the neurones exhibited neither TH nor SOM immunoreactivity. The relative numbers of NPY-, NOS-, CAL- and VIP-positive neurones were 57%, 28%, 14% and 7%, respectively. No SP- or CGRP-positive neurones were observed. All NADPH-diaphorase-positive neurones expressed NOS immunoreactivity. Only in some TH-positive neurones was NPY and/or NOS found. Four major subpopulations were found in the ureteric ganglia. The SOM-positive neurones were subdivided into SOM/NPY/NOS- (28% of all neurones), SOM/NPY- (18%) and SOM/CAL/NPY-positive neurones (14%). A subpopulation of these peptid- ergic neurones also contained VIP. About 35% of the neurones contained TH only. Neurones of all subpopulations (72% of the neurones), except most of the CAL-positive neurones, were encircled by dense plexus of varicose SP/CGRP-positive, presumably sensory nerve fibres. Dense plexus of VIP-positive fibres were observed around 89% of the neurones. The chemical coding of the neuronal subpopulations identified in the ganglia accompanying the chicken ureter resembled that observed in the ganglia of Remak's nerve but was remarkably different from that of the autonomic neurones described in mammalian species.

Animals↗
PubMed1987

Atrial natriuretic peptide receptors in sympathetic ganglia: biochemical response and alterations in genetically hypertensive rats.

High concentration of atrial natriuretic peptide (99-126) (ANP) receptors were localized by quantitative autoradiography in superior cervical and stellate ganglia from young and adult Wistar Kyoto (WKY) rats. ANP increased cyclic GMP formation in stellate ganglia from adult rats. Both young and adult spontaneously hypertensive rats (SHR) had a much lower number of ANP receptors in the sympathetic ganglia. In spite of low receptor concentration, the cyclic GMP response to ANP in SHR was unchanged. These results suggest the existence of physiologically active ANP receptors in the rat sympathetic ganglia. These receptors may also be involved in the pathophysiology of spontaneous hypertension.

Animals↗
PubMed1989

Brain natriuretic peptide receptors in the rat peripheral sympathetic ganglia.

High affinity binding sites for brain natriuretic peptide were characterized in the rat superior cervical ganglia by quantitative autoradiography. In addition, the peptide increased the formation of cyclic GMP in the ganglia in vitro. Brain natriuretic peptide displaced atrial natriuretic peptide from its binding sites. Our results suggest that brain natriuretic peptide and atrial natriuretic peptide may share physiologically active receptors in sympathetic ganglia. Brain natriuretic peptide may modulate the synaptic transmission in sympathetic ganglia, in addition or in conjunction with atrial natriuretic peptide.

Animals↗
PubMed1990

No difference in basal ganglia mineralization between schizophrenic and nonschizophrenic patients: a quantitative computerized tomographic study.

The role of iron in schizophrenia (SC) has aroused attention because of its modulatory effect on the dopamine receptor and its role as a cofactor for tyrosine hydroxylase. In addition, several postmortem studies suggest that increased mineralization (especially iron) of the basal ganglia is a possible clinicopathological correlate of schizophrenia. In order to quantitate the in vivo mineral content in the basal ganglia of patients with SC, a protocol was developed to analyze CT scans films with a LOATS computer analysis system. A total of 725 consecutive CT scans (275 SC, 450 nonSC) from a psychiatric population were reviewed. Eighteen scans (2.3%) revealed basal ganglia mineralization of which 7 cases carried a diagnosis of SC and 11 had other psychiatric disorders. All subjects had received neuroleptics, and 8 of the 11 patients in the nonschizophrenic group were demented. Both the SC and nonSC patients exhibited a prevalence (2.5%) of basal ganglia mineralization similar to that found in a postmortem series of the general population.

Adult↗
PubMed1977

Selective induction of tyrosine hydroxylase and dopamine beta-hydroxylase by nerve growth factor: comparison between adrenal medulla and sympathetic ganglia of adult and newborn rats.

Administration of NGF to newborn and adult rats elicits a selective increase in TH and DBH both in sympathetic ganglia and adrenal medulla. This effect does not depend on intact preganglionic cholinergic fibers. The augmented enzyme activity results from enhanced enzyme synthesis since it can be abolished by cycloheximide and NGF has been shown to enhance the incorporation of [3H]leucine into DBH molecules. The responsiveness of the adrenal medulla to NGF is also supported by light and electron microscopic autoradiograms which show that intravenously injected 125I-NGF is accumulated with high selectivity in adrenal chromaffin as compared to adjacent adrenal cortical cells. In spite of the many similarities between the response of the adrenergic neurons and adrenal chromaffin cells to NGF, there are also two distinct differences. (a) In newborn rats the ratio between the TH increase effected by a single and 10 subsequent daily injections of NGF is 1:2 in the adrenal medulla and 1:7 in the superior cervical ganglia. (b) If adrenal medullae are transferred to organ culture after intravenous injection of NGF, maximal TH response is initiated 60-90 min after NGF administration. In superior cervical ganglia only a half-maximal response is initiated at that time. After a stationary phase a second increase starts after about 6 h to reach the maximum after 12 h. The biphasic time course of the initiation of TH induction by NGF in sympathetic ganglia is in agreement with the time course of 125I-NGF accumulation after intravenous injection27 reflecting the moiety of NGF reaching the cell bodies of the adrenergic neurons directly by the blood stream (initial accumulation) and by retrograde axonal transport (second phase).

Adrenal Medulla↗
PubMed1981

The effects of alpha- and beta-neurotoxins from the venoms of various snakes on transmission in autonomic ganglia.

We have previously shown that certain commercially available lots of alpha-bungarotoxin block transmission in ciliary and choroid neurons of both pigeon and chicken ciliary ganglia at a concentration of 10 microgram/ml (1.2 microM). The blockade is antagonized by pre-incubation with 100 microM tubocurarine. Further evidence that this blockade is produced by a postsynaptic action, as one would expect of an alpha-neurotoxin, are our findings that: (a) exposure to the toxin prevents the depolarization of ganglion cells normally seen in response to the cholinergic agonist, carbachol; and (b) the blocking activity of the toxin is removed by treatment with membranes purified from Torpedo electric organ containing an excess of alpha-neurotoxin binding sites. A high affinity binding site for [125I]alpha-bungarotoxin was characterized in the chicken ciliary ganglion. However, since it is labelled equally well by lots of alpha-bungarotoxin which block transmission and those that do not, this site does not appear to be involved in the blockade of transmission. alpha-Cobratoxin (from Naja naja siamensis), the alpha-neurotoxin L.s. III (from Laticauda semifasciata) and certain lots of alpha-bungarotoxin produce a partial blockade of transmission in ciliary neurons of the pigeon ciliary ganglion at a concentration of 10 microgram/ml (1.2 microM), but have no effect on transmission in choroid neurons. Two other alpha-neurotoxins from Laticauda semifasciata, erabutoxin a and erabutoxin b, have no effect on transmission in either cell population at this concentration. None of the alpha-neurotoxins tested had any effect on transmission in either the rat superior cervical ganglion or the rat pelvic ganglion at concentrations up to 100 microgram/ml (12 microM). Collagenase treatment of these ganglia, in an attempt to increase access of the toxins to ganglion cells, did not alter these negative results. beta-Bungarotoxin (0.5 microgram/ml, 0.02 microM) produces a complex blockade of transmission in both avian ciliary ganglia and rat superior cervical ganglia. Unlike the action of alpha-bungarotoxin, the blockade of ciliary ganglion transmission by beta-bungarotoxin is irreversible and is not prevented by pretreatment with tubocurarine.

Animals↗