Neuron acetylcholine-secreting

Adrenaline (epinephrine)-producing (adrenergic) and acetylcholine secreting (cholinergic) neurones of the autonomic nervous system have direct and complimentary effects on the tone of blood vessels. 

Important in the study of neurotransmitters is the identification of specific agonists, which mimic the action of a transmitter, and of antagonists, which block the action of the transmitter. Two groups of compounds influence acetylcholine-secreting neurons, leading... 

The direct slowing of sinoatrial rate and atrioventricular conduction that is produced by muscarinic agonists is often opposed by reflex sympathetic discharge, elicited by the decrease in blood pressure (see Figure 6-7). The resultant sympathetic-parasympathetic interaction is complex because muscarinic modulation of sympathetic influences occurs by inhibition of norepinephrine release and by postjunctional cellular effects. Muscarinic receptors that are present on postganglionic parasympathetic nerve terminals allow neurally released acetylcholine to inhibit its own secretion. The neuronal muscarinic receptors need not be the same subtype as found on effector cells. Therefore, the net effect on heart rate depends on local concentrations of the agonist in the heart and in the vessels and on the level of reflex responsiveness. 

Acetylcholine is the neurotransmitter found in many areas of the brain as well as in the periphery (skeletal neuromuscular junction, some autonomic synapses). In the brain, acetylcholine is abundant in the cerebral cortex, and seems to play a critical role in cognition and memory.22 32 Neurons originating in the large pyramidal cells of the motor cortex and many neurons originating in the basal ganglia also secrete acetylcholine from their terminal axons. In general, acetylcholine synapses in the CNS are excitatory in nature. 

Verhage M, Maia AS, Plomp JJ, Brussaard AB, Heeroma JH, et al. (2000) Synaptic assembly of the brain in the absence of neurotransmitter secretion. Science 287 864—9 Wonnacott S (1997) Presynaptic nicotinic ACh receptors. Trends Neurosd 20 92-8 Weber T, Zemelman BV, McNew JA, Westermann B, Gmachl M, Parlati F, Sollner TH, Rothman JE (1998) SNAREpins minimal machinery for membrane fusion. Cell 92 759-72 Whittaker VP, Sheridan MN (1965) The morphology and acetylcholine content of isolated cerebral cortical synaptic vesicles. J Neurochem 12 363-72 Xu J, Mashimo T, Siidhof TC (2007) Synaptotagmin-1, -2, and -9 Ca2+ sensors for fast release that spedfy distinct presynaptic properties in subsets of neurons. Neuron 54 567-81 Zucker RS, Regehr WG (2002) Short-term synaptic plasticity. Annu Rev Physiol 64 355 405... 

In neurons, the Ca2+-independent secretion is restricted to small synaptic vesicles, as demonstrated by synaptosomal and NMJ experiments, where glutamate, GABA, and acetylcholine are released in the absence of Ca2+, while catecholamines or peptides are not (Matteoli et al. 1988 Davletov et al. 1998 Khvotchev et al. 2000). Ca2+-independent release does not normally occur in endocrine cells (Grasso et al. 1980 Michelena et al. 1997 Silva et al. 2005), although in some cultured cells it does (Meldolesi et al. 1983 Lang et al. 1998 Tse and Tse 1999). 

LC consists mostly of NE neurons. However, y-aminobutyric acid (GABA)-secreting neurons are also found in the peripheries of the LC (Iijima and Ohtomo 1988). The NE neurons of LC have local and distant afferent and efferent connections. The local bilateral connections of LC arrive from and project to the GABA cells of periaqueductal gray (PAG) and acetylcholine (ACH) neurons of pontomesencephalic tegmentum (PMT) (Jones, 1991). 

Muscarinic stimulation leads to activation of K+ channels in sympathetic [128] and parasympathetic ganglia [129,130], as well as in central neurons [131,132]. Similarly, in atrial heart cells, acetylcholine combines with muscarinic receptors and opens a K+ channel [133,134]. Increased K+ causes the cells to hyperpolarize and become less excitable. Secretion is attenuated in neuronal cells and chronotropy is inhibited in atrial cells (for review see Ref. 135). 

Results of pharmacological studies employing antagonists to various neurotransmitters reveal that neurons that transmit signals with endogenous kappa and/or mu opioids, serotonin, histamine and acetylcholine are involved to some extent with stress-induced inhibition of TIDA neurons and the consequent secretion of prolactin (Demarest et al., 1985b,c Freeman et al., 2001). 

Neurotransmitters are chemical agents secreted at the end of axons of nerve cells that diffuse across the synaptic gap and transmit information to adjoining cells such as neurons, muscle cells, and glands, by altering their electrical state or activity. There are many neurotransmitters with a variety of structures and functions two of the principle ones are acetylcholine and norepinephrine. Since the neurotransmitters convey information, anything that affects their behavior affects the function of the organism. 

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