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At least 433 records · Page 24Linked to original sources
PubMed1997

Longitudinal change in basal ganglia volume in patients with Huntington's disease.

Cross-sectional MRI studies demonstrating an association between caudate atrophy and symptom severity and duration of symptoms in patients with Huntington's disease (HD) have been assumed to reflect longitudinal changes in basal ganglia, but such neuropathologic progression has never been directly demonstrated. Subjects in the current study were 23 HD patients at various stages of the disorder who had two MRI images at least 10 months apart (mean interimage interval = 20.8 months). We measured volumes of caudate, putamen, and globus pallidus blind to the order of the images. For each structure, we calculated a change score by subtracting the volume obtained on the follow-up imaging from that obtained on the initial imaging. Results indicated significant decreases over time in caudate, putamen, and total basal ganglia volume. Age at onset and length of trinucleotide repeat correlated significantly with amount of volume change in caudate and total basal ganglia, even after controlling for length of interimage interval, duration of disease, and measures of symptom severity. Amount of change in basal ganglia structures was not significantly correlated with neurologic symptom severity at the time of the initial imaging or duration of symptoms. This is the first longitudinal MRI study to document progressive basal ganglia atrophy in HD, and suggests that quantitative neuroimaging with serial MRI may be useful in monitoring effectiveness of potential treatments. In addition, demonstration of greater rate of basal ganglia atrophy in patients with earlier symptom onset suggests that treatment effects may be more quickly observed in this subgroup of patients than in the general HD population.

Adult↗
PubMed2000

Cerebrovascular changes in the basal ganglia with HIV dementia.

BACKGROUND: HIV dementia is a form of subcortical dementia. Clinical, radiologic, pathologic, and biochemical studies suggest a major contribution of basal ganglia dysfunction to the pathogenesis of this disorder. Many investigators have proposed a contribution of a disrupted blood-brain barrier (BBB) to the pathogenesis of HIV dementia. OBJECTIVE: To identify microvascular abnormalities in vivo in basal ganglia or white matter of persons with HIV dementia. METHODS: Time course of MRI postcontrast enhancement was determined in basal ganglia and white matter of HIV-infected persons without dementia (Memorial Sloan Kettering [MSK] score of 0; n = 4); HIV-infected persons with mild dementia (MSK score of 0.5; n = 2); and HIV-infected persons with moderate-to-severe dementia (MSK > or = 1.0; n = 6). RESULTS: Increased basal ganglia enhancement was observed in individuals with moderate-to-severe dementia relative to nondemented individuals, both immediately and 30 minutes after contrast administration. Decline of basal ganglia enhancement was slower in the moderately to severely demented patients and, when normalized to intravascular enhancement of sagittal sinus, suggested leakage of contrast agent, consistent with increased permeability of BBB. A significant correlation between the postcontrast fractional enhancement at 30 minutes (FE30) and the MSK score was noted. White matter showed no significant differences in postcontrast enhancement among the three groups. CONCLUSION: Increased early enhancement in basal ganglia of the HIV dementia group is consistent with increased regional cerebral blood volume (rCBV). Increased late enhancement is strongly suggestive of BBB disruption. Similar abnormalities were absent in the white matter adjacent to the caudate nucleus.

AIDS Dementia Complex↗
PubMed2006

Eph/ephrins and N-cadherin coordinate to control the pattern of sympathetic ganglia.

Previous studies have suggested that the segmental pattern of neural-crest-derived sympathetic ganglia arises as a direct result of signals that restrict neural crest cell migratory streams through rostral somite halves. We recently showed that the spatiotemporal pattern of chick sympathetic ganglia formation is a two-phase process. Neural crest cells migrate laterally to the dorsal aorta, then surprisingly spread out in the longitudinal direction, before sorting into discrete ganglia. Here, we investigate the function of two families of molecules that are thought to regulate cell sorting and aggregation. By blocking Eph/ephrins or N-cadherin function, we measure changes in neural crest cell migratory behaviors that lead to alterations in sympathetic ganglia formation using a recently developed sagittal slice explant culture and 3D confocal time-lapse imaging. Our results demonstrate that local inhibitory interactions within inter-ganglionic regions, mediated by Eph/ephrins, and adhesive cell-cell contacts at ganglia sites, mediated by N-cadherin, coordinate to sculpt discrete sympathetic ganglia.

Animals↗
PubMed2000

Excitatory and inhibitory roles of central ganglia in initiation of the insect ecdysis behavioural sequence.

Insects shed their old cuticle by performing the ecdysis behavioural sequence. To activate each subunit of this set of programmed behaviours in Manduca sexta, specific central ganglia are targeted by pre-ecdysis-triggering (PETH) and ecdysis-triggering (ETH) hormones secreted from Inka cells. PETH and ETH act on each abdominal ganglion to initiate, within a few minutes, pre-ecdysis I and II, respectively. Shortly thereafter, ETH targets the tritocerebrum and suboesophageal ganglion to activate the ecdysis neural network in abdominal ganglia through the elevation of cyclic GMP (cGMP) levels. However, the onset of ecdysis behaviour is delayed by inhibitory factor(s) from the cephalic and thoracic ganglia. The switch from pre-ecdysis to ecdysis is controlled by an independent clock in each abdominal ganglion and is considerably accelerated after removal of the head and thorax. Eclosion hormone (EH) appears to be one of the central signals inducing elevation of cGMP levels and ecdysis, but these actions are quite variable and usually restricted to anterior ganglia. EH treatment of desheathed ganglia also elicits strong production of cGMP in intact ganglia, suggesting that this induction occurs via the release of additional downstream factors. Our data suggest that the initiation of pre-ecdysis and the transition to ecdysis are regulated by stimulatory and inhibitory factors released within the central nervous system after the initial actions of PETH and ETH.

Animals↗
PubMed1989

Autonomic neurons and paraneurons (SIF cells) in the sympathetic ganglia regulating guinea pig proximal colon: immunohistochemical studies.

Additional evidence for the existence of subclasses of SIF cells is described. Type II SIF cells in the inferior mesenteric ganglia contain enkephalin, vasoactive intestinal polypeptide (VIP), somatostatine (SOM), neuropeptide tyrosine (NPY), or dynorphin (DYN) in variable combinations in addition to noradrenalin. These transmitters or modulators can affect the autoreceptors of the SIF cell themselves or modify the synatpic transmission and the activity of sympathetic ganglionic neurons through portal blood vessels. Tyrosine hydroxylase/NPY immunoreactive nerve terminals from sympathetic ganglia innervate blood vessels and both submucous and myenteric ganglia. DYN/VIP/cholecystokinin neurons in the nerve plexus send axon collaterals to the inferior mesenteric ganglia and form a feedback loop. Substance P (SP) and calcitonin gene related peptide may exist in sensory nerve terminals. SP neurons in the myenteric ganglia innervate smooth muscles. SOM neurons inhibitory interneurons in the ganglia. SIF cells act as secretory paraneurons, the effect being long-lasting and nonspecific, while sympathetic neurons innervate both nerve plexus and intestinal tissues, and the effects in this case are specific, fast and of short duration.

Animals↗
PubMed2001

Target specific organization and neuron types of the dog pelvic ganglia: a retrograde-tracing and immunohistochemical study.

The major pelvic ganglion in both the rat and guinea pig has been extensively studied because of its anatomical simplicity. To clarify the target specific neural pathway in the diffusely distributed pelvic ganglia of larger animals, the pelvic plexus of the female dog was investigated by retrograde tracing and immunohistochemistry. The whole mount staining of the pelvic plexus with acetylcholinesterase histochemistry revealed 70-100 ganglia of varying sizes. Neurons retrogradely labeled from the rectum were mainly found in ganglia located in the dorso-caudal part of the plexus. The majority of these were non-catecholaminergic, immunoreactive for either calbindin (Calb) or neuropeptide Y (NPY), and characteristically associated with baskets of enkephalin (ENK)-immunoreactive varicose fibers. Neurons projecting to the utero-vaginal walls were distributed in ganglia located in the ventro-caudal part of the plexus. These mainly consisted of two major neuron groups: catecholaminergic Calb-immunoreactive neurons, and non-catecholaminergic neurons containing nitric oxide synthase (NOS) and/or vasoactive intestinal peptide (VIP), which were preferentially associated with a network of ENK-immunoreactive varicose fibers. Neurons retrogradely labeled from the urinary bladder mainly occurred in ganglia located around the junction between the ureter and the bladder. These consisted of catecholaminergic Calb neurons and noncatecholaminergic neurons containing Calb or NOS. Only a few ENK-immunoreactive fibers were found within the clusters of catecholaminergic neurons. These results indicate that organ specific neurons are located in separate ganglia and have both a distinctive composition of neuron types as well as different innervation by preganglionic fibers.

Animals↗
PubMed2002

Modulation of the basal ganglia by metabotropic glutamate receptors: potential for novel therapeutics.

The basal ganglia are implicated in a number of disorders including neurodegenerative motor diseases such as Huntington's and Parkinson's disease, as well as psychiatric disorders such as schizophrenia and obsessive compulsive disorder. In recent years, a great deal of effort has been focused on determining the basal ganglia circuitry that underlies normal behavior, as well as many of these syndromes. This has led to a detailed understanding of both the normal and pathophysiological flow of information through the basal ganglia, and has provided the opportunity to begin developing novel pharmacological methods of intervention by targeting neuromodulatory receptors with in the basal ganglia circuit. One group of receptors that holds much promise for several basal ganglia disorders is the metabotropic glutamate receptors. Data from behavioral, neurochemical, neuroanatomical and electrophysiological studies has begun to reveal the functional roles that the metabotropic glutamate receptors play in modulating the basal ganglia circuit, and suggests that compounds selectively targeting these receptors may provide novel therapies for a variety of disorders including Parkinson's disease, addiction, and epilepsy.

Animals↗
PubMed1995

Morphometric analysis of neurons in ganglia: geniculate, submandibular, cervical spinal and superior cervical.

The geniculate ganglia (GG), the submandibular ganglion (SG), the cervical spinal ganglion (CSG) and the superior cervical ganglion (SCG) are clinically important. But details of these ganglia have not been included in textbook descriptions. We conducted research to bring precise figures to light. We prepared serial sections of these ganglia in five Japanese adults after precise dissections to count the numbers, measure the perimeters and the areas, and calculate the circularity ratios (CRs) of the ganglion cells. The numbers of neurons were in the following order: SCG > CSG > SG > GG, and the average neuronal areas in the following order: CSG > GG > SG > SCG. Average neuronal CRs were around 0.90 in all ganglia. In other words, the morphometric evaluation showed that neurons in such ganglia are practically circular in shape. Our morphometry thus reveals that the neurons in these ganglia are sensory neurons in the broad definition of the word from a quantitative point of view.

Adult↗
PubMed1999

Neurokinin-1 receptor localisation in guinea pig autonomic ganglia.

We have used multiple-labelling immunohistochemistry and confocal microscopy to determine the distribution of immunoreactivity to the tachykinin neurokinin-1 (NK(1)) receptors in guinea pig sympathetic ganglia. Although nerve fibres containing immunoreactivity to substance P were common in all ganglia except the superior cervical ganglia, most neurons expressing NK(1) receptor immunoreactivity were not closely surrounded by pericellular baskets of substance P-immunoreactive boutons. Conversely, many neurons surrounded by baskets of substance P-immunoreactive boutons lacked NK(1) immunoreactivity. In the coeliac and inferior mesenteric ganglia, NK(1) receptor expression was restricted almost entirely to noradrenergic neurons that contained somatostatin immunoreactivity and projected to the enteric plexuses. In the lumbar chain and paracervical ganglia, NK(1) immunoreactivity was expressed by nonnoradrenergic vasodilator neurons containing immunoreactivity to vasoactive intestinal peptide. Taken together, our results show that sympathetic neurons in different functional pathways express NK(1) receptor immunoreactivity. However, the neurons that could respond to endogenously released substance P through NK(1) receptors may be distant from presynaptic release sites. These observations suggest that, in sympathetic ganglia, substance P may modulate ganglionic transmission through heterosynaptic actions on NK(1) receptors.

Animals↗
PubMed2002

Seizures and the basal ganglia: a review of the clinical data.

This article attempts an overview of the clinical and electrophysiological evidence supporting the involvement of the basal ganglia in epileptic seizures. In contrast to animal data, evidence for a role of these structures in human epilepsies is lacking. However, from the theoretical point of view, it remains conceivable that, given their strong interconnectivity, basal ganglia could be functionally linked to the cerebral cortex during an epileptic seizure. Several clinical ictal aspects have been suggested to be compatible with the involvement of basal ganglia, namely, ictal dystonic posturing during temporal lobe seizures, rotatory seizures and paroxysmal dyskinesia-like seizures. On the other hand, basal ganglia dysfunction may also influence some aspects of epilepsy, as suggested by pure basal ganglia pathology such as Parkinson's disease, or the described effect of an acute basal ganglia lesion in epileptic patients. The data discussed in this review may stimulate further research to link basic scientific data to human epilepsies, and lead to the development of novel therapeutical solutions.

Animals↗
PubMed2003

Does asymmetric basal ganglia or thalamic activation aid in seizure foci lateralization on ictal SPECT studies?

UNLABELLED: Basal ganglia or thalamic activation has been reported in ictal SPECT studies of patients with intractable epilepsy. We hypothesized that lateralization of activation of these subcortical structures may aid in the lateralization of seizure foci in patients in whom the cortical focus is subtle or equivocal. METHODS: This was a retrospective analysis of 72 ictal (99m)Tc-ethylcysteinate dimer SPECT studies in 43 patients with intractable epilepsy in whom seizure laterality could be eventually determined. All patients underwent video-electroencephalography (EEG) monitoring, MRI, and one or more ictal SPECT scans as well as an interictal SPECT scan. Intracranial electrode EEG monitoring and surgery were performed as clinically indicated. Ictal and interictal studies were coregistered with patients' MRI scans using automated software, and ictal minus interictal subtraction images were obtained. The presence of asymmetric basal ganglia or thalamic activation was determined by 2 experienced observers who were unaware of clinical information. The final seizure focus was determined by surgical cure in 37 patients. In patients in whom surgery was not indicated or initial surgery was performed at another institution (n = 6), a consistent focus detected by intracranial electrode monitoring or repeated stereotypical seizures all originating from the same site on video-surface EEG monitoring was considered to indicate the final seizure focus. RESULTS: Thirty-five patients had neocortical seizures and 8 had mesial temporal lobe seizures. Asymmetric basal ganglia activation was seen in 22 (30.6%) studies. This activation was ipsilateral to the final determined seizure focus in 17 of 22 of these studies (77.3%) and contralateral in 5 of 22 (21.7%). Asymmetric thalamic activation was seen in 15 studies (20.8%), of which 12 of 15 (80%) were ipsilateral to the final seizure focus, whereas 3 of 15 (20%) were contralateral. In 3 of 5 studies with contralateral basal ganglia activation and 1 of 3 studies with contralateral thalamic activation, the SPECT study as a whole was found to be falsely localizing. In another 2 cases of contralateral subcortical activation, the SPECT study as a whole was considered nonlocalizing. Worse outcome was not observed in patients with false ictal SPECT subcortical lateralization; however, the presence of asymmetric subcortical uptake, regardless of relationship to seizure focus, was associated with decreased incidence of seizures at 1 y after surgery. CONCLUSION: Although asymmetric basal ganglia or thalamic activation is common, it is rarely the sole indicator of seizure localization. However, it may be a useful confirmatory sign in subtle cases of cortical localization. In cases of false ictal SPECT subcortical lateralization, the basal ganglia appear to follow cortical activation pattern. Furthermore, there appears to be a correlation between lateralizing uptake in subcortical structures on ictal SPECT and postsurgical outcome in intractable epilepsy patients.

Adult↗
PubMed2004

Morphometric study of age-related changes in the human intracardiac ganglia.

The present study was performed in order to determine morphological age-related changes of the human intracardiac ganglia. Paraffin sections of 40 ganglia from infants, adult and aged human hearts were stained with Picro-Mallory method. The ganglia area, nerve cell (with clearly visible nucleolus) area, neuron soma long axis length, perimeter, area of neuronal nuclei and neuron soma form factor were measured with the aid of computer images analyzing program "Sigma Scan Pro 5.0". Also, the neuronal density and the area occupied by nerve cells per ganglion section were calculated. The relative frequency of satellite cells, in close contact with nerve cell soma, was estimated. Based on the data of this study, we concluded that the area of ganglia, neurons and their nuclei increased with age. Neuronal packing density significantly decreased, but the area occupied by nerve cells within the ganglia decreased non-significantly. Satellite cells were more numerous nearby ganglion neurons from infant hearts. Shape factor of neurons was stable between the groups. In conclusion, the present study confirms significant differences in the morphology of the intrinsic cardiac ganglia with age.

Adult↗
PubMed2004

Reticuline exposure to invertebrate ganglia increases endogenous morphine levels.

OBJECTIVES: Given the presence of morphine, its metabolites and precursors in mammalian and invertebrate tissues, it became important to determine if exposing tissues to an opiate alkaloid precursor, reticuline, would result in increasing endogenous morphine levels. METHOD: Endogenous morphine levels were determined by high pressure liquid chromatography coupled to electrochemical detection and radioimmunoassay following incubation of Mytilus edulis pedal ganglia with reticuline. Nitric oxide (NO) release was determined in real-time via an amperometric probe. Mu opiate receptor affinity for opiate alkaloid precursors was determined by a receptor displacement assay. RESULTS: Morphine is present in the pedal ganglia of Mytilus edulis (1.43 +/- 0.41 ng/mg +/- SEM ganglionic wet weight). Ganglia incubated with 50 ng of reticuline, a morphine precursor in plants, for 1 hour exhibited a statistical increase in their endogenous morphine levels (6.7 +/- 0.7 ng/mg tissue wet weight; P<0.01). This phenomenon is concentration dependent. The increase in ganglionic morphine levels occurs gradually over the 60 min incubation period, beginning 10 minutes post reticuline addition. We show that reticuline (10(-6) M) does not stimulate ganglionic NO release in a manner resembling that of morphine (10(-6) M), which releases NO seconds after its exposure to the ganglia and lasts for 5 minutes. With reticuline, there is a 3 minute delay, which is followed by an extended release period. Furthermore, in binding displacement experiments both reticuline and salutaridine (another morphine precursor) exhibit no binding affinity for the pedal ganglia mu opiate receptor subtype. This finding is further substantiated using the positive control of human monocytes where the mu3 opiate receptor subtype has been cloned. CONCLUSION: Taken together, we surmise that the morphine's precursors are being converted to morphine. The experiments strongly indicate that pedal ganglia can synthesize morphine from reticuline.

Alkaloids↗
PubMed1985

[Cyclic AMP content of autonomic ganglia as affected by catecholamines].

The relative content of cAMP was measured in the rat ganglion nodosum, lumbar ganglia of the sympathetic trunk, the main pelvic ganglion and intramural ganglia of the heart. It was observed that the basal level of cAMP in the cardiac ganglia was lower than in other ganglia. The process of stimulation of the cAMP content by noradrenaline was most pronounced in the main pelvic and lumbar ganglia, that by dopamine in the cardiac ganglia. The catecholamines failed to alter the cAMP content in the ganglion nodosum.

Animals↗
PubMed1986

Parasympathetic ganglia in the airways.

Catecholamines seem to inhibit transmission through airway parasympathetic ganglia by two mechanisms: Beta-2-adrenoceptor stimulation induces a ganglionic inhibition characterised by: slow onset, effect mainly on neural signals of high frequency, localisation to the presynaptic nerve terminal in the ganglion (inhibition of transmittor release). In vivo this mechanism could be operated upon by circulating adrenaline, which is active on beta-2-adrenoceptors. Alpha-adrenoceptor stimulation induces a ganglionic inhibition characterised by: rapid onset, localisation to the presynaptic level (inhibition of transmittor release). This mechanism could be operated upon by noradrenaline released by sympathetic nerves supplying airway ganglia. In bronchial hyperreactivity the effect of catecholamines on transmission through airway ganglia could serve as a negative feed back mechanism reducing bronchoconstriction induced by neural reflexes. Tentatively, fascilitation of transmission through airway ganglia could contribute to bronchial hyperreactivity. However, such fascilitation has not yet been demonstrated for airway ganglia, although it has been found in sympathetic ganglia.

Animals↗
PubMed1987

Neuropeptide Y-like immunoreactivity in bullfrog sympathetic ganglia is restricted to C cells.

Staining the entire chain of paravertebral sympathetic ganglia in the bullfrog with an antiserum against porcine neuropeptide Y (NPY) revealed that, in each ganglion, a subpopulation of neurons expresses NPY-like immunoreactivity. Chromaffin cells in the sympathetic ganglia and in the adrenal gland were not stained by the anti-NPY serum. Since neurons in ganglia 9 and 10 of the sympathetic chain can be classified into 3 distinct groups on the basis of established electrophysiological criteria, we sought to identify the neurons in these ganglia that contain the NPY-like immunoreactivity. Accordingly, a series of cells was impaled with intracellular recording electrodes, identified as either fast B-, slow B-, or C-type neurons, filled with Lucifer yellow, and then processed with the anti-NPY serum for indirect immunofluorescence. These double-label experiments revealed that NPY-like immunoreactivity is expressed selectively by C-type sympathetic neurons. Counts of immunoreactive cells indicate that 55% of the neurons in ganglia 9 and 10 are C cells. A major target of the C cells appears to be the vasculature. In 3 different tissues innervated by sympathetic neurons, namely, the adrenal gland, the sartorius muscle, and the skin of the hindlimb, axons containing NPY-like immunoreactivity were found primarily within or near blood vessels. Within 14-60 d after extirpation of sympathetic ganglia 9 and 10, most immunoreactive axons in the sartorius muscle and nearby skin disappeared. In conjunction with other evidence, the possibility arises that sympathetic C cells function as vasomotor neurons that use an NPY-like substance and epinephrine as cotransmitters.

Animals↗
PubMed1975

A study of the distribution of chromaffin-positive (CH+) and small intensely fluorescent (SIF) cells in sympathetic ganglia of the rat at various ages.

Small intensely fluorescent (SIF) and chromaffin-positive (CH+) cells were independently investigated by formol-induced fluorescence and by chromaffin techniques in the superior cervical, thoracic and coeliac-mesenteric ganglia of neonatal (2--10 days), adolescent (2--4 months) and adult (6--15 months) rats. Identification of CH+ cells was facilitated by glutaraldehyde fixation prior to chromatin. Intraganglionic blood vessels were displaced by antemortem injection of either India ink or the fluorescent dye Thioflavine-S. SIF and CH+ cells were randomly distributed through the ganglia, either singly or in pairs related to principal neurons, or in variably-sized, highly vascularized groups. In chromaffin preparations these groups either consisted entirely of CH+ cells or else they contained a mixture of CH+ and CH- cells. CH+ cells were present in some adolescent and adult ganglia of all types, and in the neonatal coeliac-mesenteric ganglion at 10 days. In neonatal material generally, SIF cells were mostly green fluorescent, occurring separately or in homogeneous or mixed groups, but both yellow and green cells occurred in coeliac-mesenteric ganglia at 10 days. All ganglia in adolescent and older animals contained both yellow and green cells. There were more green than yellow cells, and more SIF than CH+ cells in all ganglia studied.

Age Factors↗
PubMed1980

Inhibition and facilitation in parasympathetic ganglia of the urinary bladder.

Neurons in vesical parasympathetic ganglia receive excitatory and inhibitory inputs from both divisions of the autonomic nervous system. Sacral parasympathetic pathways (cholinergic) provide the major excitatory input to these ganglia via activation of nicotinic receptors. Parasympathetic pathways also activate muscarinic inhibitory and excitatory receptors, which may exert a modulatory influence on transmission. Cholinergic transmission is relatively inefficient when preganglionic nerves are stimulated at low frequencies (< 1 Hz). However, excitatory postsynaptic potentials (EPSPs) and postganglionic firing markedly increase during repetitive stimulation at frequencies of 1-10 Hz. It is concluded that enhanced transmitter release accounts for the temporal facilitation and that vesical ganglia function as "high pass filters" that amplify the parasympathetic excitatory input to the detrusor muscle during micturition. Transmission in vesical ganglia is also sensitive to adrenergic inhibitory and facilitatory synaptic mechanisms elicited by efferent pathways in the hypogastric nerves. The effects of exogenous norepinephrine indicate that adrenergic inhibition is mediated by alpha receptors and reflects primarily a presynaptic depression of transmitter release although postsynaptic adrenergic hyperpolarizing and depolarizing effects have also been noted. Adrenergic facilitation is mediated by beta receptors as well as unidentified receptors. Norepinephrine also can inhibit or excite spontaneously active neurons in vesical ganglia. The existence of inhibitory and facilitatory synaptic mechanisms in vesical ganglia provides the basis for a complex ganglionic modulation of the central autonomic outflow to the bladder.

Animals↗