Acetylcholine and Norepinephrine

Consequently, all preganglionic neurons and parasympathetic postganglionic neurons are said to be cholinergic in nature because of the presence of acetylcholine at their respective synapses. Most sympathetic 

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Neurotransmitters include molecules such as glutamate, GABA, dopamine, serotonin, acetylcholine, and norepinephrine as well as a family of peptides. 

D. Acetylcholine and norepinephrine are important neurotransmitters in the peripheral autonomic nervous system but are not nearly as prominent in the CNS. Glycine is a major inhibitory neurotrans-... 

Modulation of long-term synaptic depression in visual cortex by acetylcholine and norepinephrine./ Neurosci 19 1599-1609. 

Acetylcholine and norepinephrine are the transmitters Separate transmitters are necessary for the contraction and relaxation of smooth muscles, which are slow Smooth muscle shows autoregulation Both stimulants and depressants of smooth muscles are used for clinical purposes... 

In aged animal models, chronic administration of ginkgo for 3-4 weeks led to modifications in central nervous system receptors and neurotransmitters. Receptor densities increased for muscarinic, 2, and 5-HTla receptors and decreased for B-adrenoceptors. Increased serum levels of acetylcholine and norepinephrine and enhanced synaptosomal reuptake of serotonin have also been reported. Additional mechanisms that may be involved include reversible inhibition of MAO-A and MAO-B, reduced corticosterone synthesis, inhibition of amyloid-beta fibril formation, and enhanced GABA levels. 

Effects of Chronic Poisoning by an Organophosphorus Cholinesterase Inhibitor on Acetylcholine and Norepinephrine Content of the Brain... 

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. 

Black Widow spider venom contains several different protein fractions. The most significant component of the venom is the neurotoxin, a-latrotoxin. This neurotoxin acts at the presynaptic membrane of the neuronal and the neuromuscular junctions. The binding of the a-latrotoxin results in the opening of nonspecific cation channels, a massive influx of calcium, release of acetylcholine and norepinephrine and decreased uptake of the neurotransmitter. The neurotransmitter release is most likely responsible for hypertension, muscle fasciculations, and spasms frequently experienced by victims of a bite. Later, generalized muscle weakness and labored breathing may develop in severe cases. While the venom of the black widow spider has been characterized as being more potent than that of many poisonous snakes, the small amount of venom injected limits the degree of toxicity. 

Diagrammatic representation of insulin secretion from pancreatic fi cells. The sequence of events of insulin secretion coupled to glucose entry into fi cells consists of glucokinase action, ATP production, inhibition of the ATP-sensitive K+ channel, membrane depolarization, Ca + influx, and insulin release. Neurotransmitters acetylcholine and norepinephrine stimulate and inhibit insulin secretion via trimeric G-proteins Gq and Gj, respectively. Glucagon-like peptide (GLP) promotes insulin release via the G-protein G. Sulfonamides and diazoxide have direct effects on sulfonylurea receptors (SURs) the former promotes insulin release and the latter inhibits insulin release. +, Stimulation —, inhibition. Other abbreviations are given in the text. 

The fact that many available drugs used in the treatment of the depressed patient are given in dosages that produce either potent anticholinergic side effects (mydriasis, dry mouth, or constipation) or a rise in brain norepinephrine levels would implicate both acetylcholine and norepinephrine as two mutually antagonistic neurohormones in the control of brain function. Hence, the first question must be answered in the affirmative at this time. Our own structure-activity studies have failed to uncover a piperidyl or pyrrolidyl ester in the above series with weak anticholinergic and potent CNS properties, although the reverse has been found to be true in many instances. 

SSRIs have less sedative, anticholinergic, and cardiovascular effects than do the tricyclic antidepressants, due to dramatically decreased binding to receptors of histamine, acetylcholine, and norepinephrine. 

Name examples of inhibitors of acetylcholine and norepinephrine synthesis, storage, and release. Predict the effects of these inhibitors on the function of the major organ systems. 

Thousands of neuronal signals race through our brains each moment, controlling our breathing, movements, thoughts and emotions with admirable precision. Neuronal circuits provide the basic "road map" for brain signals, and chemical neurotransmitters carry information from one neuron to another. Neurotransmission in the brain parallels that in the autonomic nervous system (Chapter 2), but utilizes several chemicals and peptides in addition to acetylcholine and norepinephrine. Neurotransmitters that have been most carefully studied are introduced below. 

Receptor interactions clonidine acts at postsyn-aptic alpha-2-adrenoreceptors in the CNS, mimicking the effects of norepinephrine to produce analgesia in animals and humans. Clonidine also stimulates release of the inhibitory neurotransmitters acetylcholine and norepinephrine in the dorsal horn. Stimulation of postsynaptic alpha-2-adrenoceptors in the brainstem and sympathetic preganglionic neurons in the spinal cord decreases sympathetic outflow, causing hypotension and bradycardia depending on the extent of spread. Alpha-2-adrenergic activity in the... 

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