Disease relevance of GAP43

• Because of this we sought to characterize the expression of GAP 43 after retinal detachment (RD) [1].
• Although GAP 43 is downregulated at the time of synapse formation, it can be re-expressed following injury such as axotomy or ischemia [1].

Psychiatry related information on GAP43

• Under our experimental conditions, sensory deprivation did not significantly alter GAP-43 levels in the visual cortex [2].
• However, the slow decline in membrane-associated GAP-43 levels after 40 d of age may be an index of relative plasticity remaining after the peak of the critical period [3].

High impact information on GAP43

• We have examined the regulation of expression of the genes for the neuronal growth-associated protein GAP43, the type II calcium/calmodulin-dependent protein kinase, and glutamic acid decarboxylase in the kitten visual cortex during normal postnatal development and after a period of visual deprivation [4].
• We asked two questions: Following axotomy, where in the entire neuron does the immunoreactivity for MAP2a/b and GAP-43 change and do these changes reflect a transformation of dendrite to axon or growth from terminal dendrites [5]?
• Substance P-, calcitonin gene-related peptide, growth-associated protein-43, and neurotrophin receptor-like immunoreactivity associated with unmyelinated axons in feline ventral roots and pia mater [6].
• One, 3, 5 and 7 weeks after induction of the lesion, the neuropil levels of synapsin and GAP-43 in the dorsal lateral geniculate nucleus (dLGN) and area 17 were determined by immunocytochemistry [2].
• The demonstration of GAP-43 and neurotrophin receptor-immunoreactivities associated with unmyelinated fibers in ventral roots and the pia mater is discussed in relation to previous reports on postnatal plasticity in these axonal populations [6].

Biological context of GAP43

• QPCR shows the upregulation of GAP 43 message by 6hr of detachment [1].
• Protein kinase C (PKC) and substrate proteins such as F1/GAP-43 have been previously implicated in the synaptic plasticity of long-term potentiation (LTP) [7].
• According to the proposed functions of B-50 (GAP-43), its persistence in mature spinal axon terminals may indicate a latent capability of functional and structural remodeling, as well as an involvement in long-term enhancement in synaptic transmission [8].
• Developmental and environmental changes in GAP-43 gene expression in cat visual cortex [9].
• Protein kinase C activity and substrate (F1/GAP-43) phosphorylation in developing cat visual cortex [7].

Anatomical context of GAP43

• The results of the present study imply that the ventral root afferents comprise several different types of sensory axons, which all contain SP-, CGRP-, GAP-43-, and p75NGFr-like immunoreactivities [6].
• B-50 (GAP-43) in the spinal cord caudal to hemisection: indication for lack of intraspinal sprouting in dorsal root axons [10].
• Double-labeling experiments demonstrated that 50-70% of primary pulpal GAP-43-positive nerve fibers showed CGRP-like immunoreactivity [11].
• GAP 43 became upregulated in a subset of retinal ganglion cells following at least 7 days of RD [1].
• After axotomy by an incision in the ventral funiculus or a transection of ventral roots or peripheral nerves, GAP-43 mRNA was clearly upregulated in axotomized motoneurons, including both alpha and gamma motoneurons [12].

Associations of GAP43 with chemical compounds

• At 3 and 6 months, neuropeptide immunoreactivity reappeared but far fewer number of pulpal nerve fibers were SP-, NKA- and CGRP-immunoreactive than under normal conditions, as demonstrated by double-labeling experiments with GAP-43- or LANR-antiserum [13].
• After 1, 2, and 5 weeks postlesion (wPL), we addressed whether functional reorganization correlated in time with changes in the expression of MAP-2, GAP-43, GFAP, GABA(A) receptor subunit alpha1 (GABA(A)alpha1), subunit 1 of the NMDA receptor (NMDAR1), and in neurotransmitter levels at the border of the lesion [14].

Analytical, diagnostic and therapeutic context of GAP43

• Alterations to neuronal polarity following permanent axotomy: a quantitative analysis of changes to MAP2a/b and GAP-43 distributions in axotomized motoneurons in the adult cat [5].
• Using intracellular labeling and immunocytochemistry, changes in MAP2a/b and GAP-43 immunoreactivity were also found in processes with a morphology typical of terminal branches of intact motoneurons (called simple distal processes [SDPs]), as well as UDPs [5].
• Immunoblot, immunocytochemical and quantitative polymerase chain reaction (QPCR) techniques were used to assess the level of GAP 43 expression after experimental RD [1].
• Cat dental pulp after denervation and subsequent re-innervation: changes in blood-flow regulation and distribution of neuropeptide-, GAP-43- and low-affinity neurotrophin receptor-like immunoreactivity [13].
• In situ hybridization histochemistry was used to detect cell bodies expressing mRNA encoding for the phosphoprotein GAP-43 in the lumbosacral spinal cord of the adult rat, cat and monkey under normal conditions and, in the cat and rat, also after different types of lesions [12].

References