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PubMed1980

Evidence for an irreversible interaction of bromocryptine with central dopamine receptors.

The effects of the dopamine agonist bromocryptine on several measures dopaminergic function were assessed in the rat. Following inhibition of impulse flow with gamma-butyrolactone, and after dopa decarboxylase inhibition, dopa accumulation and its reversal by dopamine agonists is easily studied. In this model, bromocryptine (10 mg/kg, i.p.) caused a significant decrease in dopa accumulation in both the striatum and olfactory tubercle which was prevented, but not reversed, by the dopamine antagonist (+)-butaclamol (4 mg/mg, i.p.). The inactive isomer, (-)-butaclamol was without effect. Analysis of an vitro 3H-spiperone binding 2h after bromocryptine (10 mg/kg, i.p.) revealed a 30% decrease in the number of striatal dopamine receptors labelled (Bmax), with no change in receptor affinity for 3H-spiperone. No changes in binding were seen when animals were sacrificed 30 min or 48 h after bromocryptine. In extracellular single unit recording experiments, bromocryptine-induced depression of nigrostriatal dopamine cell firing was found to be largely reversible by the dopamine antagonist haloperidol when injected within 5 min of intravenous bromocryptine. However, when haloperidol was injected more than 20 min after bromocryptine, no reversal of bromocryptine-induced depression of cell firing was obtained. These results strongly suggest that bromocryptine interacts in an irreversible fashion with central dopaminergic receptors.

4-Butyrolactone↗
PubMed1999

Chronic supranigral infusion of BDNF in normal and MPTP-treated common marmosets.

BDNF or vehicle were administered by unilateral supranigral infusion in normal and chronically lesioned MPTP-treated common marmosets (Callithrix jacchus) for four weeks and locomotor activity, disability and response to apomorphine were assessed with nigral TH, GFAP and GAD immunoreactivity and striatal [3H]mazindol autoradiography. Selective contraversive orientation and ipsilateral neglect evolved in MPTP-treated marmosets receiving BDNF with no significant difference in disability or locomotor activity when compared to the vehicle-infused group. Apomorphine produced an ipsiversive rotational bias in BDNF-treated animals. In normal animals infused with BDNF contralateral neglect, ipsiversive turning, postural instability and ataxia rapidly evolved. In MPTP-treated marmosets BDNF caused increased ipsilateral striatal [3H]mazindol binding with increased somatic size and staining intensity in GAD-immunoreactive cells and a 10-20% loss of nigral TH-immunoreactive cells with increased GFAP staining. In normal common marmosets, both vehicle and BDNF infusion decreased nigral TH-immunoreactivity. Chronic supranigral infusion of BDNF alters motor behaviour and spatial attention in MPTP-treated marmosets which may reflect altered function in residual nigral dopaminergic neurons and brainstem GABAergic neurons and in normal animals produces behavioural and histological signs of nigrostriatal hypofunction.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1996

Melatonin increases the in situ activity of tyrosine hydroxylase in the mediobasal hypothalamus of male Syrian hamsters.

The effects of daily late afternoon injections of melatonin on the in situ activity of tyrosine hydroxylase (TH) were examined in the median eminence/arcuate region of the mediobasal hypothalamus (MBH) and the neurointermediate lobe (NIL) of the male Syrian hamster. TH activity was determined in tissue extracts by measuring the accumulation of L-DOPA following administration of the dopa decarboxylase inhibitor, NSD-1015. After 9 weeks of melatonin treatment, highly significant increases in the activity of MBH TH were demonstrated over a 24 hr period, compared to saline-treated controls. Melatonin-induced elevations in TH occurred concomitantly with decreases in tuberoinfundibular dopamine (TIDA) and tuberohypophyseal dopamine (THDA) concentrations. Similar findings were observed in castrated hamsters, indicating that the melatonin-induced increase in TH was not secondary to melatonin-induced changes in circulating levels of gonadal hormones. These data led to the interpretation that melatonin treatment elevated TIDA synthesis either through a direct action on the arcuate nuclei or on neurons impinging on these nuclei.

Animals↗
PubMed1989

Evidence that blood vessels in guinea-pig lung are supplied by both noradrenergic and dopaminergic axons.

Assay of catecholamines in guinea-pig lung showed that the amount of dopamine in this tissue is 3-4 times greater than that predicted to be associated only with noradrenergic nerves, and is depleted by animal treatment with 6-hydroxydopamine. Fluorescence microscopy after formaldehyde condensation did not reveal any non-neuronal stores of catecholamines within the lung. The pulmonary and bronchial arterial vessels are accompanied by numerous fine nerve fibres that exhibit immunoreactivity for tyrosine hydroxylase, and are therefore presumed to be catecholaminergic. A small proportion of these fibres are also immunoreactive for DOPA decarboxylase. The results are consistent with innervation of pulmonary and bronchial resistance vessels by dopaminergic as well as noradrenergic sympathetic axons.

Animals↗
PubMed2005

Immunomodulation with human recombinant autoantigens.

The loss of beta cells in type 1 diabetes is the consequence of a T cell-dependent autoimmune attack. Autoantibodies against GAD65 (Mr 65.000 isoform of glutamic acid decarboxylase), IA-2 (insulinoma-associated protein IA-2) or insulin, alone or in combination, predict disease. Preclinical studies in spontaneously diabetic rodents suggest that immunomodulation with autoantigens might alter the course of autoimmune diabetes. Oral insulin reduces the development of diabetes in risk subjects with high insulin autoantibody levels. Giving alum-formulated GAD65 to patients classified with latent autoimmune diabetes of the adult (LADA) is safe and suggests possible immunomodulating effects of GAD65. Future immunomodulation trials might better ascertain subjects based on HLA genetic risk factors, the level of insulin that is still produced or by combining autoantigens with, for example, anti-CD3 antibodies, to induce antigen-specific tolerance and thereby a long-lasting protection for beta cells.

Animals↗
PubMed1978

Ontogenetic development of kainate neurotoxicity: correlates with glutamatergic innervation.

Stereotaxic injection of kainic acid into the striatum of adult rats causes degeneration of neurons intrinsic to the striatum but spares axons of passage and of termination of extrinsic neurons. Neurochemical and histologic studies demonstrate that striatal neurons are almost insensitive to kainate at 7 days after birth and that their vulnerability increases with age; by 3 weeks after birth, striatal injection of kainate produces a lesion comparable to that of the adult. The intensity and duration of the acute behavioral response to kainate also increases with age. The maturational increase in striatal neuronal sensitivity to kainate correlates with the development of glutamatergic innervation to the striatum, as measured by [3H]glutamate uptake by synaptosomes, and with the development of a postsynaptic, high-affinity receptor site for kainate. These ontogenetic studies provide additional evidence that kainate's neurotoxicity is a receptor-mediated event related to glutamatergic innervation of vulnerable neurons.

Animals↗
PubMed2003

Diabetes Antibody Standardization Program: first assay proficiency evaluation.

The aims of the first proficiency evaluation of the Diabetes Antibody Standardization Program (DASP) were to assess general implementation of assay methods and to evaluate the new World Health Organization (WHO) reference reagent for autoantibodies to GAD and IA-2. Forty-six laboratories in 13 countries received coded sera from 50 patients with newly diagnosed type 1 diabetes and 50 blood donor control subjects, together with the WHO reference reagent and diluent serum. Results were analyzed using receiver operator characteristic (ROC) curves. Sensitivity was adjusted to 90% specificity in workshop controls. The median adjusted sensitivity for GADA (45 laboratories) was 84% (range 62-96%), for IA-2A (43 laboratories) was 58% (50-74%), and for insulin autoantibody (IAA; 23 laboratories) was 36% (13-66%). ROC curve analysis showed all GADA and IA-2A assays, and 18/23 IAA assays found significant differences between patients and control subjects. There was good concordance between laboratories in ranking of samples by GADA and IA-2A levels or if results were expressed in relation to the WHO reference reagent. Assays that achieved the highest sensitivity for IAA were also concordant in ranking samples, but overall concordance for IAA was poor. Differences in assay protocols between laboratories must be addressed so that all centers and kit manufacturers can perform to the same high standard.

Adolescent↗
PubMed2007

Role of autoantibodies in type 1 diabetes.

Type 1A, the immune mediated form of diabetes, is a relatively common disorder that develops in genetically susceptible individuals. The disease is associated with a series of anti-islet autoantibodies and the autoantibodies can be present for years prior to the onset of hyperglycemia. In general it is thought that type 1A diabetes is T cell mediated, but there is evidence from studies in the NOD mouse model that antibodies and B-lymphocytes contribute to pathogenesis. In man evidence is lacking that transplacental passage of anti-islet antibodies increases disease risk. Well characterized, high throughput autoantibody assays (tested in a series of international workshops) are now available, and are the mainstays of prediction of type 1A diabetes, diagnosis of the immune mediated form of diabetes, and are important for the design of trials for the prevention of type 1A diabetes. In addition to anti-islet autoantibodies, patients with type 1A diabetes develop a series of associated autoimmune disorders that are usually detected with screening for additional autoantibodies (e.g. anti-thyroid, anti-transglutaminase, anti-21 hydroxylase, anti-parietal cell). At present it is possible to predict the development of type 1A diabetes and prevent the disorder in animal models, but we lack proven therapies for disease prevention in man. The ability to detect specific anti-islet autoantibodies provides the foundation for developing and testing these preventive therapies.

Animals↗