Disease relevance of CHAT

• Choline acetyltransferase, choline kinase, and acetylcholinesterase activities during the development of the chick ciliary ganglion [1].

Psychiatry related information on CHAT

• Administration of limb muscle extract at either embryonic days 1-3 or 4-7 produced a significant increase in choline acetyltransferase activity in the brain, indicating that the critical period of limb muscle extract in the brain to be between embryonic days E1 and E7, a period of neuronal proliferation and differentiation in the brain [2].

High impact information on CHAT

• The expression of the alpha 2 nAChR gene is thus developmentally regulated and appears concomitant with the entry of cholinergic fibers into the SpL, as demonstrated by choline acetyltransferase immunohistochemistry [3].
• Myoblasts, aligned myoblasts and young myotubes expressed the synthetic enzyme Choline acetyltransferase and stained positively with antibodies against acetylcholine [4].
• The membranes capable of increasing ChAT and those which are ineffective all contain NCAM, however their relative levels of NCAM polysialic acid differ [5].
• E10 chick sympathetic ganglion cells display a cell contact-dependent rise in choline acetyltransferase (ChAT) specific activity over the first several days in culture [5].
• Neural cell adhesion molecule regulates cell contact-mediated changes in choline acetyltransferase activity of embryonic chick sympathetic neurons [5].

Chemical compound and disease context of CHAT

• The numbers of synapses and of synaptic vesicles per ganglion increase roughly in concert with biochemical markers of presynaptic development (activity of choline acetyltransferase and levels of acetylcholine) as well as postsynaptic development (tyrosine hydroxylase; based on biochemical data reported elsewhere) [6].
• Chiappinelli et al. have reported that choline acetyltransferase (ChAT) is reduced in chick iris and ciliary ganglion after chronic treatment with chlorisondamine (on days 5, 8, 10 and 13 of incubation) [7].
• No change was observed in either ChAT or GAD activity in OL in response to ALCAR administration during the critical period (E1-E3) at doses ranging from 10 to 500 micrograms/day [8].

Biological context of CHAT

• When neurones were grown on hydrated collagen gels, considerable cell survival and ChAT activity were obtained even in the absence of tissue extract [9].
• CONCLUSIONS: The localization of ChAT in the differentiating fibers of the lens indicates that acetylcholine is synthesized during differentiation and modulates morphogenesis and elongation of mAChR-positive progenitor cells in the equatorial zone [10].
• The data showing onset of ChAT expression prior to the onset of FGFR expression argue against a role of FGFR in the determination of the cholinergic transmitter phenotype [11].
• Choline acetyltransferase (CAT) activity of chick latissimus dorsii muscles was studied during embryonic development and at post-hatching states [12].
• The data demonstrate an intracellular signal transduction pathway from the developmentally-activated insulin receptor through c-jun to ChAT and cholinergic differentiation [13].

Anatomical context of CHAT

• Whereas membranes with high polysialic acid NCAM are ineffective, selective enzymatic removal of polysialic acid renders them capable of producing an increase in ChAT [5].
• Significant 125I-NGF binding is observed in this period of development before the appearance of neurochemical markers (choline acetyltransferase, dopamine-beta-hydroxylase, and 125I-alpha-bungarotoxin binding) which are associated with synaptosomes [14].
• A+ cells proliferated in the presence of 15% fetal bovine serum (FBS) and high concentrations (10-15%) of chick embryo extract, but did not differentiate, although they retained basal levels of choline acetyltransferase (ChAT) activity [15].
• Development of choline acetyltransferase activity in chick cranial neural crest cells in culture [16].
• Cell survival characteristics and choline acetyltransferase activity in motor neurone-enriched cultures from chick embryo spinal cord [9].

Associations of CHAT with chemical compounds

• Different time course of development for high-affinity choline uptake and choline acetyltransferase in the chick retina [17].
• Within 2 hours after injection there is a significant decrement in the specific activities of tyrosine hydroxylase, choline acetyltransferase, and glutamic acid decarboxylase; by 48 hours after injection there is nearly a complete loss in the presynaptic neurochemical markers for the cholinergic and GABAergic neurons [18].
• Cholinergic and GABAergic phenotypic expression were both significantly reduced following ethanol exposure as assessed by the activities of choline acetyltransferase and glutamate decarboxylase, respectively [19].
• We found that 81.2 +/- 2.8% of the cells present in the culture were stained immunocytochemically with an antibody against choline acetyltransferase, and 38.5 +/- 4.8% of the cells were stained with an antibody against GABA [20].
• NMDA and QA destroyed many amacrine cells, including those immunoreactive for vasoactive intestinal polypeptide, Met-enkephalin, and choline acetyltransferase, but they had little effect upon tyrosine hydroxylase-immunoreactive cells [21].

Regulatory relationships of CHAT

• VIP induces a 10- to 15-fold increase in the activity of choline acetyltransferase and an approximately twofold increase in the activity of tyrosine hydroxylase [22].

Other interactions of CHAT

• Bundles of nerve fibers showing somatostatin and choline acetyltransferase immunoreactivity were found in the choroid layers of the eye [23].
• The developmental expression of choline acetyltransferase (ChAT) and the neuropeptide VIP in chick sympathetic neurons: evidence for different regulatory events in cholinergic differentiation [24].
• Distribution of R-cognin and choline acetyltransferase in the ganglion cell layer of developing chick neural retina [25].

Analytical, diagnostic and therapeutic context of CHAT

• Double labeling with ChAT and synapsin antibodies showed that the two markers colocalized in all nerve terminals that were identified in BP whole-mounts and frozen sections [26].
• A search for a second such agent, a putative cholinergic neuronotrophic factor (CNTF), has been undertaken using as indicators neuronal survival, neurite outgrowth and choline acetyltransferase (CAT) activity in monolayer cell cultures [27].
• Neuron-enriched cultures derived from 6-day-old chick embryo cerebral hemispheres were treated with morphine or methadone, 10(-5) M or 10(-6) M, on days 4-6 or 6-8 in culture and were evaluated morphologically and biochemically at day 9 using phase contrast microscopy and choline acetyltransferase activity (ChAT) as a cholinergic marker [28].
• Whole-mount preparations of basilar papillae were labeled with phalloidin to label the actin cytoskeleton and antibodies to neurofilaments, choline acetyltransferase, and synapsin to label neurons; and examined by confocal laser scanning microscopy [29].

References