Medial globus pallidus

The medial globus pallidus (or internal, GPi) is one of the output nuclei of the basal ganglia (the other being the substantia nigra pars reticulata). The GABA-containing neurons send their axons to specific nuclei of the dorsal thalamus (VA and VL), to the centromedian complex and to the pedunculopontine complex.

The efferent bundle is constituted first of the ansa and fasciculus lenticularis, then crosses the internal capsule as the Edinger's comb system then arrives at the laterosuperior corner of the subthalamic nucleus and constitutes the field H₂ of Forel, then H, and suddenly changes its direction to form field H₁ that goes to the inferior part of the thalamus. The distribution of axonal islands is widespread in the lateral region of the thalamus. The innervation of the central region is done by collaterals.

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GPI

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Glucose-6-phosphate isomerase

Glucose-6-phosphate isomerase (GPI), alternatively known as phosphoglucose isomerase (PGI) or phosphohexose isomerase (PHI), is an enzyme that in humans is encoded by the GPI gene on chromosome 19. This gene encodes a member of the glucose phosphate isomerase protein family. The encoded protein has been identified as a moonlighting protein based on its ability to perform mechanistically distinct functions. In the cytoplasm, the gene product functions as a glycolytic enzyme (glucose-6-phosphate isomerase) that interconverts glucose-6-phosphate (G6P) and fructose-6-phosphate (F6P). Extracellularly, the encoded protein (also referred to as neuroleukin) functions as a neurotrophic factor that promotes survival of skeletal motor neurons and sensory neurons, and as a lymphokine that induces immunoglobulin secretion. The encoded protein is also referred to as autocrine motility factor (AMF) based on an additional function as a tumor-secreted cytokine and angiogenic factor. Defects in this gene are the cause of nonspherocytic hemolytic anemia, and a severe enzyme deficiency can be associated with hydrops fetalis, immediate neonatal death and neurological impairment. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Jan 2014]