Biomedical subjects

A O Ige

Publications and source records attributed to A O Ige.

4 recordsLinked to original sources

PubMed2001

Advances in the molecular understanding of GABA(B) receptors.

The molecular nature of the metabotropic GABA(B) receptor was for some time a mystery, however it was recently discovered that two related G-protein-coupled receptors have to heterodimerize to form the functional GABA(B) receptor at the cell surface. This review discusses the most recent findings in the rapidly expanding field of GABA(B) receptor research, and includes a summary of all splice variants of both receptor subunits identified to date. It also evaluates emerging evidence that certain splice variants might play a role in determining pharmacologically distinguishable receptors, and reviews receptor localization at the sub-cellular level and involvement in neuronal development.

Alternative Splicing↗

PubMed2000

Cellular and sub-cellular localisation of GABA(B1) and GABA(B2) receptor proteins in the rat cerebellum.

Following the recent discovery that GABA(B) receptors expressed in cell lines are only functional when both GABA(B1) and GABA(B2) are expressed, the present study reports on the development of polyclonal antisera specific for carboxyl-terminal portions of the two related GABA(B) receptor components respectively. Western blotting indicated the specificity of affinity-purified antibodies for native or recombinant expressed GABA(BR1) and GABA(BR2), with no cross-reactivity, both antisera detecting the heterodimer in rat cerebellar membranes. Immunohistochemistry revealed a distinct distribution of both receptor proteins in rat cerebellum. GABA(B1) immunoreactivity was primarily located in the granule cell layer and Purkinje cells, with discrete immuno-positive cell bodies being present in the molecular layer. GABA(B2) staining revealed intense immunoreactivity in the molecular layer, with weaker staining in the granule cell layer. Purkinje cell bodies were less intensely immuno-positive for GABA(B2). Co-localisation of both receptor proteins was observed using double immunofluorescence techniques, consistent with the notion that both proteins are required for the formation of functional GABA(B) receptors in vivo. Immunofluorescence also indicated that GABA(B) receptors did not co-localise with glial fibrillary acid protein, confirming a neuronal localisation for GABA(B) receptors. Electron microscopic analysis of the molecular layer revealed that the distribution of immunolabelling for both GABA(B1) and GABA(B2) was mainly located on the membrane of Purkinje cell dendrites and spines and in parallel fibre terminals.

Animals↗

PubMed2000

GABA(B) receptor heterodimer-component localisation in human brain.

In recombinant cell lines, functional GABA(B) receptors are only formed by the heterodimerisation between two related G-protein coupled receptor proteins GABA(B)R1 (GBR1) and GABA(B)R2 (GBR2), whilst the individual GBR1 or GBR2 do not produce fully functional receptors. To determine whether the heterodimerisation occurs in vivo, novel polyclonal antibodies targeting the C termini of GBR1 and GBR2, were raised in different species, characterised, and used to determine the relative localisation of the reported heterodimer components in human brain tissue, using immunohistochemistry. The use of different species for the raising of the antisera allowed double immunofluorescent labelling of the receptors as an indication of GBR1/GBR2 receptor co-localisation in human brain. The presence of both proteins is reported in cerebellum, hippocampus, cortex, thalamus and basal ganglia. Regions of the brainstem including pons and medulla, also express GBR1 and GBR2 protein. The double immunofluorescence demonstrated that GBR1 and GBR2 are co-localised in the human cerebellar cortex. Together these results suggest the widespread distribution of GABA(B) receptors in human brain, and that GABA(B) receptors GBR1 and GBR2 can exist in the same cell, and therefore may function as a heterodimer in the human brain.

Aged↗

PubMed1992

African histoplasmosis (Duboisii) of the skull with neurological complication--a case report and review of literature.

A case of African histoplasmosis of the skull associated with neurological deficit has been reported. There was complete recovery of neurological features after excision of the lesion followed by a course of co-trimoxazole. A review of the available literature indicates the rarity of this particular mode of presentation. The reversibility of the neurological complications makes it important that clinicians increase their awareness of this treatable condition.

Abducens Nerve↗