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Results for “Choline O-Acetyltransferase”

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At least 19 recordsLinked to original sources
PubMed1977

Aging and extrapyramidal function.

Measurements on human brain samples of some enzymes concerned with neurotransmitter synthesis suggest serious losses with age. The most severe loss found was that in striatal tyrosine hydroxylase activity, the rate-controlling enzyme in the synthesis of dopamine. Cell counts in the substantia nigra where this dopaminergic tract originates suggest that the decrease in enzyme activity is partly due to cell loss, but must largely reflect decreased activity of residual cells. It is possible that this loss may account for some of the difficulties in movement seen in aged individuals and that it might be less if pigment formation in these cells could be inhibited.

Adolescent↗
PubMed1976

Choline acetyltransferase, glutamate decarboxylase and tyrosine hydroxylase in the cochlea and cochlear nucleus of the guinea pig.

Activities of choline acetyltransferase (ChAC), glutamate decarboxylase (GAD) and tyrosine hydroxylase (TH), enzymes catalyzing the synthesis of acetylcholine (ACh), gamma-aminobutyric acid (GABA) and catecholamines, respectively, were measured in the cochlea and cochlear nucleus of the guinea pig. ChAc activity in the organ of Corti, third turn, was 1270 pmole ACh formed/min/mg protein (ChAc, 1270) and was higher than in turn 4 (ChAc, 543). ChAc activity was higher when the preparation included the inner hair cell region than when not. GAD activity in samples of turn 3 and 4 combined was low, 0.17 nmole GABA formed/min/mg protein (GAD, 0.17). All 3 enzymes were low in auditory nerve: ChAc, 1.7, GAD, 0.10 and TH, 1.0 pmole DOPA formed/min/mg protein. In the cochlear nucleus, the values were: ChAc, 129, GAD, 1.70 and TH, 2.7. The findings on the distribution of ChAc activity in the organ of Corti fit the hypothesis that the olivocochlear nerve fibers are cholinergic. Because of low GAD in the cochlea, GABA is unlikely to be transmitter in the organ of Corti. Similarly, it is unlikely that ACh, GABA or a catecholamine is a transmitter between the auditory nerve and the cochlear nucleus.

Acetyltransferases↗
PubMed1976

Effects of axotomy on the trans-synaptic regulation of enzyme activity in adult rat superior cervical ganglia.

The effects of surgical transection of the postganglionic nerve trunk of the superior cervical ganglion on the total protein content and levels of the enzymes tyrosine hydroxylase, DOPA decarboxylase and choline acetyltransferase have been studied in the adult rat. There is a minor decrease in the total activities of these 3 enzymes accompanied by a large increase in the total protein content of the ganglion. The trans-synaptic induction of the enzyme tyrosine hydroxylase by reserpine is not affected by postganglionic axotomy. Increased activity mediated by reserpine caused no change in the total activities of either DOPA decarboxylase or choline acetyltransferase. Previously observed effects of postganglionic axotomy on preventing transmission through the ganglion are compared with these results and the possible mechanisms by which trans-synaptic induction may occur are discussed.

Animals↗
PubMed1976

A quantitative comparison of the formation of synapses in the rat superior cervical sympathetic ganglion by its own and by foreign nerve fibres.

The rat superior cervical sympathetic ganglion (SCG) has about 36,000 neurones in a volume of about 1 cu.mm. There are about 8.8 X 10(6) synapses, and 6000-9000 preganglionic axons. Section of the preganglionic chain causes a loss of 93% of the synapses. In the denervated SCG there are 0.6 X 10(6) remaining ('intrinsic') synapses, and a proportion of the synaptic sites are identifiable as vacated synaptic thickenings (3 X 10(6) per SCG, as compared with 0.5 X 10(6) in the normal intact SCG). After deducting the intrinsic synapses, this indicates that each preganglionic axon forms about 1100 (900-1400) synapses. After freezing the preganglionic chain, subsequent axonal regeneration restores synapse numbers to 85% of normal (7.5 X 10(6) synapses per SCG). After anastomotic repair by suture of the cut ends of the preganglionic chain (a necessary control for the foreign nerve anastomoses), the SCG contains only 60% of the normal complement of synapses (5.2 X 10(6) synapses per SCG). The results of this anastomosis are very variable. However, in individual ganglia the numbers of synapses are directly correlated with the numbers of axons which reach the SCG. After deducting the intrinsic synapses it can be calculated that each axon forms about 700 synapses. This is probably an underestimation of the numbers which would be achieved at longer survival times. After anastomosis of the vagal nerve into the denervated SCG there are about 4.4 X 10(6) synapses per SCG. Morphologically the majority have axon terminals with large dense cored vesicles, and it is likely that these belong to the axons of the parasympathetic preganglionic neurones in the dorsal motor nucleus of the vagus. A smaller population of axon terminals are devoid of large dense cored vesicles; their origin is unknown. The dorsal motor nucleus of the vagus has between 1000 and 2000 neurones. After deducting the intrinsic synapses, this indicates that each axon may form up to 1900-3800 synapses. To the extent that other, unidentified vagal fibres also contribute to the synapses found after this anastomosis, this figure is an overestimate. After anastomosis of the hypoglossal nerve into the denervated SCG, there are 1.5 X 10(6) synapses per SCG. A morphologically distinctive type of axon terminal is found, and it is argued that this may belong to a special category of skeletomotor neurones located in the caudoventral part of the hypoglossal nucleus and distinguished by pseudocholinesterase staining. There are about 600 of these neurones, which would indicate that they form about 1500 synapses per axon (after deducting the numbers of intrinsic synapses). The majority of the hypoglossal neurones do not form intraganglionic synapses; this suggests that although the possession of a cholinergic mechanism may be necessary for axons to be able to form ganglionic synapses, it is not in itself sufficient. For each of the types of anastomosis, the numbers of vacated thickenings are inversely proportional to the numbers of synapses...

Acetyltransferases↗
PubMed1976

Biochemical differentiation of mechanically dissociated mammalian brain in aggregating cell culture.

Mouse and rat brain cells were dissociated by a simple mechanical sieving technique and studied in culture for the formation of aggregates and the activities of choline acetyltransferase, acetylcholinesterase, glutamic acid decarboxylase, tyrosine 3-monooxygenase, aromatic L-amino acid decarboxylase, catechol methyltransferase, and monoamine oxidase. Cells from fetal and neonatal tissue formed aggregates but not cells from tissue older than two days after birth. The pattern of development of enzyme activities in these aggregates varied with the age of starting tissue. The highest levels of specific activity for the neuron-specific enzymes were found after 3-4 weeks in culture for aggregates of cells derived from relatively undeveloped brains.

Acetylcholinesterase↗
PubMed1976

Effect of surgical isolation of the hypothalamus on its neurotransmitter content.

The concentrations of norepinephrine, dopamine-beta-hydroxylase, dopamine, tyrosine hydroxylase, phenylethanolamine-N-methyltransferase, serotonin, tryptophan hydroxylase, histamine, glutamic acid decarboxylase, and choline acetyltransferase were determined in selected hypothalamic nuclei and in the median eminence after deafferentation of the medial basal hypothalamus. Norepinephrine and dopamine-beta-hydroxylase fell markedly while dopamine and tyrosine hydroxylase did not. Serotonin also decreased in all regions studied; histamine decreased in none. Choline acetyltransferase, phenylethanolamine-N-methyltransferase, and glutamic acid decarboxylase declined in some areas, but not in others.

Animals↗
PubMed1977

The effect of a single dose of reserpine administered prior to incubation on the development of tyrosine hydroxylase activity in chick sympathetic ganglia.

A single dose of reserpine administered into the yolk sac of chicken eggs prior to incubation produces two distinct periods of significant increase in tyrosine hydroxylase (TH) activity over controls. The first period is 21 days of incubation (55%) and the second is between day 14 and 30 after hatching (a.h.) (69%). Cholineacetyltransferase (ChAc) and dopadecarboxylase (DDC) are not modified in the two periods of increased TH activity. Reserpine had no effect on cholinergic parasympathetic synapses and neurons in the ciliary ganglion, as judged by ChAc activity. When reserpine was acutely administered in three different posthatching periods only the injection at the latest period (days 26 and 27) caused a significant (38%) increase in TH activity at day 30. Postsynaptic nicotinic receptors were blocked selectively by injecting chlorisondamine in the chick starting at hatching for one week. The administration of chlorisondamine almost completely abolished the reserpine induced increase of TH activity at day 15 a.h. The present results support the view that the development of enzyme activities specifically related to neurotransmitter biosynthesis in chick autonomic ganglia is regulated not only by transsynaptic influences but also by regulatory inputs originating in the periphery.

Animals↗
PubMed1977

Target organ regulation of sympathetic neuron development.

The role of target organs in the morphological and biochemical development of sympathetic neurons was examined in the neonatal rat. The superior cervical ganglion (SCG) and its end organs, the salivary glands and iris were employed as a model system. Unilateral sialectomy and iridectomy prevented the normal developmental increase in ipsilateral ganglion tyrosine hydroxylase (T-OH) activity, a marker for adrenergic maturation. Enzyme activity remained depressed by approximately 30% for at least 6 months, the longest time tested. Ganglion morphometry was performed to investigate the basis of the abnormal biochemical ontogeny. Target organ removal significantly decreased the number of adrenergic neurons in the Scg by approximately 30%. Total ganglion volume was reduced in a parallel fashion. Thus, end organ extirpation may prevent the biochemical maturation of the SCG by decreasing adrenergic neuron survival. Sialectomy without iridectomy prevented the normal postnatal increase in ganglion T-OH activity, but did not alter iris activity. These observations suggest that target removal prevents the development of only those neurons destined to innervate that organ. In addition to preventing normal adrenergic neuron ontogeny, target extirpation also prevented the normal development of presynaptic choline acetyltransferase activity. Presynaptic ganglion terminal may have failed to mature normally secondary to adrenergic destruction, or may have responded in some other manner to target organ extirpation.

Animals↗
PubMed2024

Tuft cell acetylcholine is released into the gut lumen to promote anti-helminth immunity.

Upon parasitic helminth infection, activated intestinal tuft cells secrete interleukin-25 (IL-25), which initiates a type 2 immune response during which lamina propria type 2 innate lymphoid cells (ILC2s) produce IL-13. This causes epithelial remodeling, including tuft cell hyperplasia, the function of which is unknown. We identified a cholinergic effector function of tuft cells, which are the only epithelial cells that expressed choline acetyltransferase (ChAT). During parasite infection, mice with epithelial-specific deletion of ChAT had increased worm burden, fitness, and fecal egg counts, even though type 2 immune responses were comparable. Mechanistically, IL-13-amplified tuft cells release acetylcholine (ACh) into the gut lumen. Finally, we demonstrated a direct effect of ACh on worms, which reduced their fecundity via helminth-expressed muscarinic ACh receptors. Thus, tuft cells are sentinels in naive mice, and their amplification upon helminth infection provides an additional type 2 immune response effector function.

Animals↗