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At least 955 records · Page 53Linked to original sources
PubMed2006

Neurite outgrowth in dorsal root ganglia induced by islet neogenesis-associated protein peptide involves protein kinase A activation.

Islet neogenesis-associated protein (INGAP) peptide is a candidate therapeutic for diabetes and corrects sensory dysfunction in experimental diabetes in mice. In this study, we investigated the mechanism of action by which INGAP peptide promotes neurite outgrowth in sensory neurons of the dorsal root ganglia. Treatment of dorsal root ganglia primary dispersed cultures with INGAP peptide led to the displacement of fluorescently labeled forskolin from adenylate cyclase, the cyclic AMP-generating enzyme that has been implicated in neuritogenesis. The addition of forskolin or dibutyryl cyclic AMP enhanced the effects of INGAP peptide on neurite outgrowth in dorsal root ganglia explant cultures. Furthermore, pharmacological inhibition of adenylate cyclase with SQ22,536 or of protein kinase A with H89 or KT5720 significantly reduced the neurite-promoting effects of INGAP peptide. These results suggest that INGAP peptide-induced neurite outgrowth in the dorsal root ganglia partially involves cyclic AMP-dependent activation of protein kinase A.

Adenylyl Cyclases↗
PubMed1979

Acute and latent infection of sensory ganglia with herpes simplex virus: immune control and virus reactivation.

The role of antiviral antibody in controlling the acute and latent phases of herpes simplex virus (HSV) infection in sensory ganglia of mice was studied in vitro and in vivo. Organ cultures of ganglia inoculated in vitro with HSV produced infectious virus for at least 3 weeks. In the presence of antiviral antibody, the titre of virus was markedly reduced, but the infection was not eliminated. Similarly, passive administration of antibody to HSV-infected immunodeficient (nude) mice reduced the virus titre but did not eliminate the acute phase of the ganglionic infection. Suppression of the cell-mediated immune response in latently infected immunocompetent mice by treatment with cyclophosphamide and/or X-irradiation resulted in reactivation of HSV in up to 70% of the animals. Reactivation was demonstrated by recovering infectious virus in cell-free homogenates of ganglia and eye globes and by finding virus antigens in ganglia by immunofluorescent staining. Reactivation occurred both in vitro and in vivo in the presence of high concentrations of neutralizing antibody. It is concluded that antibody alone is not sufficient to eliminate the acute phase of the ganglionic infection and that cytotoxic agents known to suppress the host's cellular immune response can reactivate virus in the presence of neutralizing antibody.

Animals↗
PubMed1989

Quantification of herpes simplex virus infection in cervical ganglia of mice.

Mice were inoculated with herpes simplex virus (HSV) type 1 in the skin of the neck. The extent of primary and latent infection in the second and third cervical ganglia was investigated. Immunoperoxidase staining of ganglia during primary infection demonstrated HSV antigens initially in a restricted area of the ganglion. By the 5th day after infection, antigen was more widespread. Such a change in the staining pattern is explicable in terms of the zosteriform spread of virus from neurons innervating the site of infection to others supplying other areas of the dermatome. A maximum of approximately 10% of neurons became infected. By the 7th day staining was limited to a few cells. During latent infection, enzymic disaggregation of ganglia followed by immunoperoxidase staining or infectious centre assay indicated that virus reactivation began within 30 h of removal of ganglia and occurred in approximately 1% of viable neurons.

Animals↗
PubMed2004

Increased expression of TRPV1 receptor in dorsal root ganglia by acid insult of the rat gastric mucosa.

It is still unknown which receptors of peripheral sensory pathways encode and integrate an acid-induced nociceptive event in the gastric mucosa. The transient receptor potential vanilloid receptor 1 (TRPV1) and the acid-sensing ion channel 3 (ASIC3) are two nociception-related receptors. Here we investigated (i) to what extent these receptors are distributed in stomach-innervating neurons of dorsal root and nodose ganglia, using immunohistochemistry and retrograde tracing, and (ii) whether their expression is altered in response to a noxious acid challenge of the stomach. We also explored the presence of TRPV1 in the gastric enteric nervous system because of its possible expression by intrinsic sensory neurons. Most stomach-innervating neurons in nodose ganglia were immunoreactive for TRPV1 (80%) and ASIC3 (75%), these results being similar in the dorsal root ganglia (71 and 82%). RT-PCR and Western blotting were performed up to 6 h after oral application of 0.5 m HCl to conscious rats. TRPV1 protein was increased in dorsal root but not in nodose ganglia whereas TRPV1 and ASIC3 mRNAs remained unchanged. TRPV1 mRNA was detected in longitudinal muscle-myenteric plexus preparations of control stomachs and was not altered by the acid challenge. Combined vagotomy and ganglionectomy abolished expression of TRPV1, indicating that it may derive from an extrinsic source. In summary, noxious acid challenge of the stomach increased TRPV1 protein in spinal but not vagal or intrinsic sensory afferents. The TRPV1 receptor may be a key molecule in the transduction of acid-induced nociception of the gastric mucosa and a mediator of visceral hypersensitivity.

Acid Sensing Ion Channels↗
PubMed2006

Functional redundancy of NSCL-1 and NeuroD during development of the petrosal and vestibulocochlear ganglia.

To study the role of different members of the bHLH gene family for sensory organ development we have generated NSCL-1 and NeuroD compound-mutant mice. Double homozygous animals were characterized by a more severe reduction of the petrosal and vestibulocochlear ganglia than NeuroD-knockout mice. The more severe reduction of the petrosal and vestibulocochlear ganglia in double-knockout mice indicates overlapping functions of the two genes during neuronal development. Interestingly, we also found that the two genes are jointly regulated by thyroid hormone during sensory hair cell development. We further present a detailed expression analysis of NSCL-1 and NSCL-2 during sensory neuron development. NSCL-1 expression was detected in all developing cranial ganglia including the petrosal and vestibulocochlear ganglion, in inner and outer hair cells of the organ of Corti and in hair cells of the vestibular system. Expression domains in other sensory structures include the retina, Merkel cells of the developing skin and sensory cells of the tongue. The expression of NSCL-2 was restricted to developing cranial ganglia, the retina and the vestibular nerve. Both NSCL-1 and NSCL-2 genes are active only in postmitotic neurons, indicating a role for neuronal cell migration and/or differentiation within the sensory system.

Animals↗
PubMed1998

Leukemia inhibitory factor induces sympathetic sprouting in intact dorsal root ganglia in the adult rat in vivo.

1. The role of the cytokine leukemia inhibitory factor (LIF) in axotomy-induced sprouting of postganglionic sympathetic fibres into the dorsal root ganglia was examined in the adult rat. 2. Immunocytochemistry was used to study the distribution and density of tyrosine hydroxylase-immunoreactive (TH-IR) fibres within the lumbar dorsal root ganglia and lumbar spinal nerves 14 days following continuous intrathecal infusion of LIF (0.33 mg ml-1), or 14 days following unilateral peripheral nerve axotomy. 3. In LIF-treated animals, numerous pericellular TH-IR basket-like structures were observed surrounding sensory neurones, which were absent from controls. 4. The number of TH-IR fibres within the L3, L4 and L5 spinal nerves was significantly higher in LIF-treated animals than in control or saline-treated animals (P < 0.01, Student's t test). 5. Unilateral ligation of the L4 spinal nerve or unilateral sciatic nerve ligation was also associated with the formation of TH-IR baskets around sensory neurons and a significant increase in the number of TH-IR fibres within the lumbar spinal nerves (P < 0.01, Student's t test). 6. The percentage of neurones surrounded by TH-IR baskets within the L3 and L4 dorsal root ganglia following sciatic axotomy was significantly reduced in animals treated continuously for 2 weeks with a monoclonal antibody against the LIF receptor motif, gp130 (0.833 mg ml-1) (P < 0.05, Mann-Whitney U test). Antibody treatment did not reduce the axotomy-induced increase in TH-IR fibres within lumbar spinal nerves. 7. These results demonstrate that exogenous application of the axotomy-associated cytokine LIF is associated with sprouting of uninjured postganglionic sympathetic neurones around sensory neurones within the dorsal root ganglion. It is likely that increased LIF expression following peripheral axotomy plays an important role in the novel sympathetic sprouting observed within sensory ganglia following peripheral nerve injury.

Adrenergic Fibers↗
PubMed1984

5-hydroxytryptamine measurements in molluscan ganglia and neurons using a modified radioenzymatic assay.

A radioenzymatic procedure for the determination of sub-picomole amounts of 5-hydroxytryptamine (5-HT) is described. It is a modification of the method originally described by Saavedra et al. (1973), in which 5-HT was measured as the radiolabelled product [3H]5-methoxy-N- acetyltryptamine , after incubation with [3H]S-adenosylmethionine, acetyl-CoA, and the enzymes hydroxyindole-O-methyltransferase (EC 2.1.1.4) and N-acetyltransferase (EC 2.3.1.5). Ganglia from various gastropod molluscs (Aplysia californica, Tritonia diomedia , Lymnaea stagnalis, and Helisoma trivolvis ), as well as individual neuronal somata isolated from these ganglia, were assayed for 5-HT. Among the homologous giant cerebral cells in these animals, the 5-HT concentrations were similar. Statistical analysis of the 5-HT values in paired 5-HT-containing neurons demonstrated that the variability was considerably greater in samples obtained from different animals than in those obtained from the same animal. This suggests that experiments aimed at manipulating amine levels in individual neurons may benefit by using a paired-cell paradigm. The effects of incubating Aplysia ganglia with 5-HT or with the 5-HT precursors tryptophan and 5-hydroxytryptophan (5-HTP) were studied. High concentrations of 5-HTP and 5-HT (100 microM) increased the levels of 5-HT in ganglia, but only incubation in high concentrations of 5-HTP resulted in an increase of 5-HT in the isolated somata of 5-HT-containing neurons C1 and P5.

5-Hydroxytryptophan↗
PubMed1971

Uptake of nicotine and extracellular space markers by isolated rat ganglia in relation to receptor activation.

1. Uptake of (3)H-nicotine by isolated rat superior cervical sympathetic (SCG) and nodose (NG) ganglia was measured in vitro. Depolarization of the ganglia by nicotine was measured electrically.2. Nicotine depolarized the SCG but not the NG. The mean ED50 for depolarization was 5.3 x 10(-6)M.3. Both ganglia accumulated nicotine when incubated in 3.1 x 10(-5)M(3)H-nicotine: after 30 min incubation the ratios of tissue to medium concentrations were (mean +/- S.E. of mean): SCG, 3.49 +/- 0.13; NG, 2.50 +/- 0.09.4. Total water contents, estimated by drying to constant weight, were: SCG, 83.8 +/- 0.12%; NG, 80.1 +/- 0.21%. Extracellular spaces, measured as (3)H-mannitol space, were: SCG, 38.8 +/- 1.3; NG, 40.3 +/- 0.8% wet weight. These values were not significantly altered by nicotine.5. Correction for tissue fluid spaces indicated that the ratio of the mean intracellular fluid concentration to the extracellular fluid concentration for (3)H-nicotine at 3.1 x 10(-5)M were: SCG, 7.4; NG, 5.6. The ratios were not altered in any consistent manner on varying the nicotine concentration between 3.1 x 10(-7) and 1.6 x 10(-4)M.6. When the nicotine concentration was sufficiently great (6.2 x 10(-6)M or more) to evoke large SCG depolarizations, hexamethonium (2.5 x 10(-3)M) reduced (3)H-nicotine uptake by the SCG by up to 19% without affecting uptake by the NG, and thereby reduced the uptake difference between the two ganglia. With nicotine concentrations <6.2 x 10(-6)M, hexamethonium did not modify uptake by either ganglion.7. It was concluded that nicotine may be concentrated within neurones, and that such intracellular accumulation may be augmented during depolarization induced by nicotine.

Animals↗
PubMed1982

Potassium activation of [3H]-choline accumulation by isolated sympathetic ganglia of the rat.

1 The effect of K-depolarization on the uptake of low and high concentrations of [3H]-choline by isolated superior sympathetic ganglia of the rat has been studied. 2 In unstimulated ganglia, the uptake of [3H]-choline (0.1 microM) ('high affinity uptake') was unaffected by denervation or by hemicholinium-3 (HC-3), suggesting uptake by structures other than cholinergic nerve terminals. 3 K-depolarization of the ganglia increased [3H]-choline accumulation by the high affinity uptake process but in contrast the 'low affinity' accumulation of [3H]-choline (100 microM) was decreased. 4 The K-activated, 'high affinity' component of choline uptake was highly sodium-dependent, inhibited by HC-3, and was abolished by denervation. 5 In incubation conditions designed to prevent transmitter release (Ca-free medium and high-Mg medium), the K-activated uptake of [3H]-choline was abolished. 6 It is concluded that in unstimulated ganglia, there is little choline uptake by nerve terminals. However, when the terminals are depolarized, choline uptake is increased by the activation of a sodium-dependent, HC-3-sensitive transport process. The activation of this uptake process is apparently associated with the release of acetylcholine from the terminals, or by changes in ionic fluxes, and not by the depolarization per se.

Animals↗
PubMed1982

Basal ganglia calcification on computer tomographic scan. A clinical and radiological correlation.

Computerised tomography of the brain was used to demonstrate basal ganglia calcification which may be of an insufficient degree to be seen on skull X-ray. Cases referred for CT scan from hospitals in Singapore for various reasons over a period of 12 months were studied for basal ganglia calcification. There was a startlingly high incidence of 1.5%, as 47 cases (all except 2 were Chinese) showed such calcification. In 42 cases there was no evidence of basal ganglia calcification on skull X-ray. 16 cases showed neurological affection, fits being the commonest manifestation. An unexpected finding was that no case had abnormality of calcium metabolism or evidence of hypoparathyroidism or pseudohypoparathyroidism. The CT scan is very sensitive in demonstrating minimal basal ganglia calcification and our impression is that such calcification is common.

Adolescent↗
PubMed1995

Basal ganglia and frontal lobe glucose metabolism. A reproducibility positron emission tomography study.

Positron emission tomography (PET) with 18F-fluoro-2-deoxy-D-glucose (FDG) is frequently used to study the metabolic correlates of movement and mental disorders. These studies generally focus on changes in the frontal cortex and the basal ganglia. The reproducibility of glucose metabolism estimates in these structures was tested in 13 normal subjects studied at rest using a standard and simple protocol. A reproducible dorsoventral metabolic gradient was demonstrated in the frontal cortex. Such a gradient was not present in the basal ganglia when the upper region of interest in the caudate nucleus, where the lower metabolic rate of glucose was probably attributable to partial volume effects, was not considered. Absolute values of glucose metabolic rates varied by 6.4 to 12.5% in the frontal cortex and by 6.8 to 14.7% in the basal ganglia. Variations in normalized values in the basal ganglia ranged from 4.0 to 8.6%. The number of subjects required to detect statistical differences in group comparison or in test-retest studies was calculated for different anticipated levels of change. With the variability detected in this experiment, less than 10 subjects were expected to be sufficient to detect a 15% change in most regions and in both types of studies.

Adult↗
PubMed1976

Synaptic transmission in parasympathetic ganglia in the urinary bladder of the cat.

1. Electrophysiological techniques were used to study the sacral para-sympathetic input to pelvic ganglia located on the surface of the urinary bladder of the cat. 2. Synaptic transmission in pelvic ganglia was mediated primarily via nicotinic receptors although muscarinic excitatory receptors were present. 3. The most prominent characteristic of transmission in pelvic ganglia was the marked recruitment elicited by increasing frequencies of preganglionic nerve stimulation. Post-ganglionic action potentials were of low amplitude at low frequencies of stimulation (0-1-0-5c/s), but commonly increased to five to twenty times control amplitudes during continuous stimulation at frequencies between 5 and 10c/s. Thus, it is proposed that vesical ganglia may act as "filters" in the micturition pathway; blocking the excitatory input to the bladder when intravesical pressure and parasympathetic firing is low and facilitating the neural input to the bladder during micturition when preganglionic activity is high. 4. Information was also obtained about the characteristics of the parasympathetic post-ganglionic neurones innervating the bladder. Stimulation of the preganglionic fibres in the pelvic nerve elicited a bimodal contraction consisting of an initial phasic response, which was atropine-resistant and a tonic response which was blocked by atropine. This suggests that two types of neurones, cholinergic and non-cholinergic, may mediate the sacral input to the vesical smooth muscle.

Action Potentials↗
PubMed1977

Discrimination between nicotinic receptors in vertebrate ganglia and skeletal muscle by alpha-bungarotoxin and cobra venoms.

1. We have used snake neurotoxins, alpha-bungarotoxin and venoms from Naja naja siamensis and Naja nivea, to distinguish the nicotinic receptors of ganglia from those of skeletal neuromuscular junctions. 2. These neurotoxins failed to block responses of isolated guinea-pig longitudinal muscle with adherent myenteric plexus to the nicotinic agonists, nicotine or dimethylphenylpiperazinium, to acetylcholine (ACh), or to electrical field stimulation. 3. The toxins failed to affect responses of the isolated guinea-pig stomach to pregnaglionic stimulation by way of the vagus nerves or of the vas deferens to preganglionic stimulation via the hypogastric nerves. 4. Snake neurotoxins did not block non-adrenergic inhibitory responses of the rabbit small intestine to nicotine or electrical field stimulation. 5. Neurotoxins were ineffective blockers against nicotinic agonists in new-born rabbit or embryonic chick intestine. 6. Attempts to increase the penetration of the toxins into tissues with dimethylsulphoxide, exposure to hypertonic solutions, or to ethylene-diaminetetracetic acid did not enable the toxins to act as nicotinic antagonists. 7. In contrast to diaphragmatic or oesophageal skeletal neuromuscular junctions no binding of rhodamine or tritium labelled toxins to structures in ganglia could be detected. 8. No potential permeability barriers were found by electron microscopy of the ganglia of the guinea-pig myenteric plexus. 9. The tracers, lanthanum ion and ruthenium red, readily penetrated into all regions of the myenteric plexus including synaptic gaps. 10. It is concluded that the failure of snake neurotoxins to act as nicotinic antagonists or to bind to ganglia is not due to their inability to reach ganglionic nicotinic receptors. Therefore, it is likely that ganglionic nicotinic receptors are different from those of the skeletal neuromuscular junction.

Action Potentials↗
PubMed1986

Eradication of herpes simplex virus persistence in rat trigeminal ganglia by retrograde axoplasmic transport.

Potential use of retrograde axoplasmic flow to eradicate virus persistence in ganglionic cells was studied in a new herpes simplex virus (HSV) persistence model in rat trigeminal ganglia. After injection of the F strain of HSV type 1 into the mental nerve, viral antigens were detectable in the ganglia by the immunofluorescence and peroxidase methods between postinoculation (p.i.) days 3 and 6 but not thereafter. None of 82 inoculated rats showed signs of acute illness, and some survived for more than 502 days without symptoms. By cocultivation of ganglion tissues with Vero cells, the virus was isolated from 42 of 49 ganglia (85.7%) between 15 and 386 days (p.i.). HSV DNA was solely localized in the nucleus of neurons by immunoperoxidase staining of paraffin sections with a biotinylated HSV DNA probe, and the presence of HSV DNA-positive cells was confirmed in four of four ganglia on p.i. day 6 and in five of six on p.i. day 502. The efficacy of axoplasmic flow in drug delivery to ganglionic cells was investigated by injection of doxorubicin (ADM) into the nerve once used for virus inoculation. As early as 19 h after injection, strong ADM-specific autofluorescence was seen in the nuclei of neurons parental to the mental nerve and in those of adjacent Schwann cells, and the death of ADM-positive cells subsequently ensued. A single injection of ADM reduced the virus isolation rate from 31/37 (84%) to 3/37 (8%).

Animals↗
PubMed2005

Latent infection with herpes simplex virus is associated with ongoing CD8+ T-cell stimulation by parenchymal cells within sensory ganglia.

CD8+ T-cell persistence can be seen in ganglia harboring latent herpes simplex virus (HSV) infection. While there is some evidence that these cells suppress virus reactivation, this view remains controversial. Given that maintenance of latency by CD8+ T cells would necessitate ongoing exposure to antigen within this site, we sought evidence for such chronic stimulation. Initial experiments showed infiltration by activated but not naïve CD8+ T cells into ganglia harboring latent HSV infection. While such infiltration was independent of T-cell specificity, once recruited, only virus-specific T cells expressed high levels of preformed granzyme B, a marker of ongoing activation. Moreover, bone marrow replacement chimeras showed that these elevated granzyme levels were totally dependent on presentation by parenchymal cells within the ganglia. Overall, this study argues that activated CD8+ T cells are nonspecifically recruited into latently infected ganglia, and in this site they are exposed to ongoing antigen stimulation, most likely by infected neuronal cells.

Animals↗
PubMed1999

Basal ganglia alterations and brain atrophy in Huntington's disease depicted by transcranial real time sonography.

OBJECTIVES AND METHODS: Transcranial real time sonography (TCS) was applied to 49 patients with Huntington's disease and 39 control subjects to visualise alterations in the echotexture of the basal ganglia. For comparison T1 weighted, T2 weighted, and fast spin echo MRI was performed in 12 patients with Huntington's disease with and in nine patients without alterations of the basal ganglia echotexture as detected by TCS and T1 weighted, T2 weighted, and fast spin echo MRI. Furthermore, the widths of the frontal horns, third ventricle, and the lateral ventricles were depicted in TCS examinations and correlations examined with corresponding CT slices. RESULTS: Eighteen out of 45 (40%) of the patients with Huntington's disease with adequate insonation conditions showed hyperechogenic lesions of at least one basal ganglia region. In 12 patients TCS depicted hyperechogenic lesions of the substantia nigra; in six patients the head of the caudate nucleus was affected. The lentiform nucleus (n=3) and the thalamus (n=0) were less often affected or spared. Hyperechogenic lesions were significantly more frequent in patients with Huntington's disease than in 39 control subjects, who had alterations of the echotexture in 12.8% (4/39) of the examinations. The number of CAG repeats and the clinical status correlated with the identification of hyperechogenic lesions of the substantia nigra (p<0.01). Hyperechogenic lesions of the caudate nucleus were associated with an increased signal intensity in T2 weighted MR images (p<0.05). All TCS parameters indicating brain atrophy correlated with CT findings (p<0.0001). CONCLUSIONS: TCS detects primarily abnormalities of the caudate nucleus and substantia nigra in Huntington's disease. These changes in the echotexture may represent degenerative changes in the basal ganglia matrix and are partially associated with CAG repeat expansion and the severity of clinical findings.

Adult↗
PubMed1993

Bilateral basal ganglia lesions: pediatric differential considerations.

Computed tomography (CT) and magnetic resonance (MR) imaging have dramatically improved the ability to visualize the deep gray structures of the basal ganglia (primarily, the caudate nucleus, putamen, and globus pallidus). Any process that alters cerebral metabolism can lead to basal ganglia damage. This article presents the spectrum of disease that may be seen with bilateral basal ganglia abnormalities in the pediatric population. A simplified approach to the differential diagnosis of these entities is based on acute versus chronic conditions and radiologic manifestations. Acute processes include hypoxia, hypoglycemia, carbon monoxide poisoning, hemolytic-uremic syndrome, osmotic myelinolysis, and encephalitis. Chronic conditions include inherited ("inborn errors of metabolism," Huntington disease, and dysmyelinating diseases) or acquired (sequelae of acute disorders) conditions that represent abnormal biochemical or structural processes within the basal ganglia. Elimination of acute causes gives little hope for improvement. Recognition of chronic disorders is important for counseling purposes, since most of these conditions have specific patterns of inheritance.

Acute Disease↗
PubMed1985

High-affinity substance P binding sites in rat sympathetic ganglia.

Substance P binding sites were characterized and quantitated in single rat sympathetic ganglia by incubation of tissue sections with 125I-Bolton-Hunter substance P, autoradiography, image analysis coupled with computer-assisted microdensitometry, and comparison with 125I standards. The prevertebral celiac-superior mesenteric sympathetic ganglia contained clusters of high-density, high-affinity substance P binding sites [maximum binding (Bmax) 7.12 +/- 0.20 pmol/mg protein; affinity constant (Ka) 2.08 +/- 0.02 X 10(9) M-1]. In the paravertebral superior cervical sympathetic ganglia, the number of high-affinity substance P binding sites was substantially lower (Bmax 1.38 +/- 0.04 pmol/mg protein; Ka 1.71 +/- 0.03 X 10(9) M-1). Future studies should address the issue of whether the substance P binding sites identified in prevertebral ganglia of the rat serve as receptors for the peptide presumed to be released by terminals of sensory neurons.

Animals↗