Choline and carnitine acetyltransferases of heart

White, Helen L.; Wu, Jy S.

doi:10.1021/bi00729a009

Cited by 130 publications

(52 citation statements)

References 16 publications

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“…We used a concentration of NVP, 0.1 mM, that does not affect carnitine acetyltransferase but does inhibit CAT (32). Addition ofNVP to the assay incubation medium decreased measured activity by 87% and 85%'in control and NGF culture' groups, respectively, indicating that true CAT activity was, indeed, being measured.…”

Section: Resultsmentioning

confidence: 99%

Nerve growth factor promotes cholinergic development in brain striatal cultures.

Martínez¹,

Dreyfus²,

Jonakait³

et al. 1985

Proc. Natl. Acad. Sci. U.S.A.

175

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We have examined the effect of the trophic protein, nerve growth factor (NGF), on organotypic cultures of fetal rat striatum. Treatment of cultures with NGF for 10-11 days resulted in a 5-to 12-fold increase in the specific activity of the cholinergic enzyme chQline acetyltransferase (CAT; EC 2.3.1.6). in a dose-dependent fashion. This effect was not elicited by insulin, ferritin, or cytochrome c, proteins similar in structure or physicochemical properties to NGF. The effect of NGF on CAT activity Was specifically blocked by anti-NGF antiserum, whereas treatment with the antiserum alone did not have a significant effect on the enzyme. Immunocytochemical studies of the treated cultures, using a monoclonal antibody directed against CAT, revealed positively stained neurons exhibiting dendritic and axonal processes. NGF did not have an effect on total protein content ofthe striatal cultures, suggesting a highly specific effect. Moreover, levels of substance P, a peptide localized to other, noncholinergic neurons, were not altered by NGF. Substance P remained unchanged after treatment with NGF for 12 days, whereas CAT activity increased 12-fold in sister cultures. Although the mechanisms of action of NGF on striatal cholinergic interneurons remain to be determined, the marked, specific response of CAT suggests that this well-defined trophic protein may play a critical role in normal brain development.Although abundant evidence indicates that the protein nerve growth factor (NGF) is critical for normal survival and development of peripheral sympathetic and sensory neurons (for reviews, see refs. 1-3), little is known about the role of trophic agents in the brain. In the peripheral nervous system, NGF enhances neuronal survival (4), elicits neurite outgrowth (5), and may be active in the directional guidance of neurites (6). Moreover, NGF treatment increases the levels of catecholaminergic and peptidergic transmitters in receptive peripheral neurons (7-10).Despite these clearly delineated actions on the peripheral nervous system, actions of NGF on the central nervous system have resisted detection. Treatment with NGF or anti-NGF antiserum does not affect the pattern of locus coeruleus catecholamine histofluorescence (11). Further, NGF is not selectively transported by dopaminergic nigral neurons or by noradrenergic locus coeruleus neurons (12). Finally, NGF treatment does not increase tyrosine hydroxylase activity, the rate-limiting enzyme in catecholamine biosynthesis, in the above-mentioned brain nuclei in vivo (12) nor does it affect norepinephrine uptake in vitro (13).Nevertheless, more recent evidence has suggested that NGF may play a role in brain development and function. For example, NGF increases the activity of choline acetyltransferase (CAT; EC 2.3.1.6), the enzyme which synthesizes acetylcholine (AcCho) (HBSS). The brain was removed and was placed in a Petri dish for microscopic dissection. The anterior one-fourth of each cerebral hemisphere was removed by a coronal cut. The striata were exposed by...

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Section: Resultsmentioning

confidence: 99%

Nerve growth factor promotes cholinergic development in brain striatal cultures.

Martínez¹,

Dreyfus²,

Jonakait³

et al. 1985

Proc. Natl. Acad. Sci. U.S.A.

175

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“…Little is known about the mechanisms by which muscles can form ACh. However, it has been shown that enzymes able to acetylate choline are present in muscle (White & Wu, 1973;Roskoski, Mayer & Schmid, 1974;Tucek, Zelana, Ge & Vyscocil, 1978;Molenaar & Polak, 1980). Such enzymes could account for the small amounts of ACh formed in and released from denervated muscle.…”

Section: Discussionmentioning

confidence: 99%

Acetylcholine content and release in denervated or botulinum poisoned rat skeletal muscle

Polak

Sellin

Thesleff

1981

The Journal of Physiology

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3. Spontaneous release of ACh varied in normal innervated muscles between 40 and 100 fmol/min. In the presence of 25 mM-KCl the rate of release increased about fourfold. In BoTx poisoned muscles spontaneous release was reduced by up to 60 % of control and high potassium failed to accelerate the release at 2 d after poisoning and caused only a small increase at 8 d. Denervated muscles released ACh at a rate which was less than 20 % of control and it was not accelerated by high potassium.4. The results show that more than 90 % oftotal ACh in the innervated EDL muscle is present in the nerve and its terminals. The remaining ACh is apparently formed and stored in the muscle tissue. BoTx caused a larger reduction in ACh release than can be accounted for by assuming a selective blockade of quantal release of transmitter. It suggests that BoTx has an inhibitory effect also on non-quantal ACh release.

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“…Closely related enzymes may also form acetylcholine under in vivo conditions. For example, in mammals, acetylcholine can be synthesized by carnitine acetyltransferase which is expressed in mammalian heart and skeletal muscle (25,26). The following factors have been described to increase ChAT expression in neuronal tissue: activators of protein kinase A or cyclic AMP analogs, nerve growth factor, ciliary neurotrophic factor, leukemia inhibitory factor and retinoids; additionally, sex hormones and glucocorticoids can regulate ChAT gene expression and/ or ChAT enzyme activity (1,3,4,19,21).…”

Section: Expression Of Chat and Presence Of Acetylcholine In Non-neurmentioning

confidence: 99%

The Non-neuronal Cholinergic System

Wessler¹,

Kilbinger²,

Bittinger³

et al. 2001

Japanese Journal of Pharmacology

167

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ABSTRACT-Acetylcholine, one of the most exemplary neurotransmitters, has been detected in bacteria, algae, protozoa, tubellariae and primitive plants, suggesting an extremely early appearance in the evolutionary process and a wide expression in non-neuronal cells. In plants (Urtica dioica), acetylcholine is involved in the regulation of water resorption and photosynthesis. In humans, acetylcholine and/or the synthesizing enzyme, choline acetyltransferase, have been demonstrated in epithelial (airways, alimentary tract, urogenital tract, epidermis), mesothelial (pleura, pericardium), endothelial, muscle and immune cells (granulocytes, lymphocytes, macrophages, mast cells). The widespread expression of non-neuronal acetylcholine is accompanied by the ubiquitous expression of cholinesterase and acetylcholine sensitive receptors (nicotinic, muscarinic). Both receptor populations interact with more or less all cellular signalling pathways. Thus, non-neuronal acetylcholine can be involved in the regulation of basic cell functions like gene expression, proliferation, differentiation, cytoskeletal organization, cell-cell contact (tight and gap junctions, desmosomes), locomotion, migration, ciliary activity, electrical activity, secretion and absorption. Nonneuronal acetylcholine also plays a role in the control of unspecific and specific immune functions. Future experiments should be designed to analyze the cellular effects of acetylcholine in greater detail and to illuminate the involvement of the non-neuronal cholinergic system in the pathogenesis of diseases such as acute and chronic inflammation, local and systemic infection, dementia, atherosclerosis, and finally cancer.

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Choline and carnitine acetyltransferases of heart

Cited by 130 publications

References 16 publications

Nerve growth factor promotes cholinergic development in brain striatal cultures.

Nerve growth factor promotes cholinergic development in brain striatal cultures.

Acetylcholine content and release in denervated or botulinum poisoned rat skeletal muscle

The Non-neuronal Cholinergic System

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