Evaluation of pelvis postural systems in spinal cord injury patients: Outcome research.

Objectives: Compare three commercially available postural systems to determine the best for treatment of patients suffering from spinal cord injury lesion below the cervical spine.

Design: Outcome Research.

Setting: Ambulatory.

Adenosine A(2A) antagonism increases striatal glutamate outflow in the quinolinic acid rat model of Huntington's disease.

In the quinolinic acid (QA)-rat model of Huntington's disease (HD), 15 days after QA injection, striatal glutamate, measured by in vivo microdialysis, was unchanged while a significant decrease in adenosine occurred. The decrease in adenosine may depend on QA-induced striatal cell loss. Probe perfusion of the adenosine A(2A) receptor antagonist SCH 58261 significantly increased striatal glutamate outflow, suggesting a potential detrimental effect of A(2A) antagonism at later stages of the neurodegenerative process induced by QA.

Adenosine A2A receptor antagonism increases striatal glutamate outflow in dopamine-denervated rats.

The objective of the work was to study, by in vivo microdialysis, the effect of the adenosine A(2A) receptor antagonist 7-(2-phenylethyl)-5-amino-2-(2-furyl)-pyrazolo-[4,3-e]-1,2,4-triazolo[1,5-c]pyrimidine (SCH 58261) on glutamate outflow in the striata of unilateral 6-hydroxydopamine-infused rats. Two vertical microdialysis probes were implanted bilaterally in both the denervated striatum and in the intact striatum. Glutamate concentrations in the dialysate were determined by high-performance liquid chromatography (HPLC).

An autocrine role for pituitary GABA: activation of GABA-B receptors and regulation of growth hormone levels.

There is increasing evidence suggesting that the neurotransmitter gamma-aminobutyric acid (GABA) is a local factor involved in the regulation of endocrine organs. Examples of such functions are documented in the pancreas, but recent results suggest that GABA may act in a similar way in the pituitary, in which GABA receptors are expressed and pituitary growth hormone (GH) cells provide a source of GABA. We hypothesised that GABA secreted in somatotropes may act as an autoregulatory signaling molecule.

Modification of adenosine extracellular levels and adenosine A(2A) receptor mRNA by dopamine denervation.

Adenosine A(2A) receptor antagonists have been proposed as an effective therapy in the treatment of Parkinson's disease. To explore the possibility that dopamine denervation may produce modifications in adenosine A(2A) transmission, we measured the extracellular concentration of adenosine and adenosine A(2A) receptor mRNA in the striatum of rats infused unilaterally with 6-hydroxydopamine in the medial forebrain bundle. Fifteen days after 6-hydroxydopamine infusion, extracellular adenosine levels, measured by in vivo microdialysis, were significantly lower (-35%) in the dopamine-denervated striatum.