Acetylcholine glutamate and

The effect of allethrin (a Type I pyrethroid), cyhalothrin, and deltamethrin (Type II pyrethroids) on neurotransmitter release from the hippocampus (acetylcholine, glutamate, and GABA release) and striatum (dopamine release) has recently been investigated using ex vivo microdialysis in freely moving rats exhibiting the symptoms of pyrethroid poisoning [94-97]. Deltamethrin increased the release... 

At present, in addition to acetylcholine, glutamate, and y-aminobutyrate (GABA), glycine, noradrenaline (norepinephrine), and dopamine and 5-hydroxytryptamine (serotonin) are regarded as established transmitters. Other probable (putative) or possible candidate transmitters are also known. Aspartate, taurine, and a large number of peptides (Tables 30-1,30-4) are under consideration. 

Excitatory ion-channel synapses have neuroreceptors that are sodium channels. When the channels open, sodium ions flow in, causing a local depolarisation and making an action potential more likely. Typical excitatory neurotransmitters are acetylcholine, glutamate and aspartate. 

In some mammalian cells, enzymes comprising partial spans of biosynthetic pathways are inside and some outside the mitochondrial matrix space. Therefore, in the liver, six mitochondrial membrane transport proteins are required for urea synthesis, three for gluconeogenesis [7,8], and three others participate in ammonia-genesis [9] in the kidney. The synthesis of neurotransmitter substances such as acetylcholine, glutamate and y-amino butyric acid requires the participation of metabolite transporters in mitochondrial membranes of nervous tissue [9,10]. 

Vyas S, Bradford HE (1987) Co-release of acetylcholine, glutamate and taurine from synaptosomes of Torpedo electric organ. Neurosci Lett S2 58-64. 

Spencer,., Gribkoff, V. K., and Lynch, G. S., 1978, Distribution of acetylcholine, glutamate, and aspartate sensitivity over dendritic fields of hippocampal CAl neurones, in Iontophoresis and Transmitter Mechanism of the Mammalian Central Nervous System (R. W. Ryall and J. S. Kelly, eds.), Elsevier/North-Holland, Amsterdam. 

The major neurotransmitters are listed in Table I. Typical excitatory neurotransmitters are acetylcholine, glutamate, and serotonin. They bind to receptors that are named in the same way, for instance, the acetylcholine receptor, glutamate receptor, etc. These receptors on binding their specific neurotransmitter form transmembrane channels specific for the inorganic sodium and potassium cations. They are called excitatory receptors because they shift the transmembrane potential of the cell membrane to more positive values. A change in Vm of about - -20 mV is required for the electrical signal to be transmitted to the nerve terminal where the release of a neurotransmitter is elicited. Typical inhibitory neurotransmitters are glycine... 

The AMPA receptors for glutamate, the nicotinic acetylcholine receptor and the 5-HT3-receptor for serotonin are cation channels (Table 1). When they open, the major consequence is a sudden entry of Na+, depolarization and an excitatory postsynaptic potential (EPSP Fig. 1). 

The exocytotic release of neurotransmitters from synaptic vesicles underlies most information processing by the brain. Since classical neurotransmitters including monoamines, acetylcholine, GABA, and glutamate are synthesized in the cytoplasm, a mechanism is required for their accumulation in synaptic vesicles. Vesicular transporters are multitransmembrane domain proteins that mediate this process by coupling the movement of neurotransmitters to the proton electrochemical gradient across the vesicle membrane. 

After an overview of neurotransmitter systems and function and a consideration of which substances can be classified as neurotransmitters, section A deals with their release, effects on neuronal excitability and receptor interaction. The synaptic physiology and pharmacology and possible brain function of each neurotransmitter is then covered in some detail (section B). Special attention is given to acetylcholine, glutamate, GABA, noradrenaline, dopamine, 5-hydroxytryptamine and the peptides but the purines, histamine, steroids and nitric oxide are not forgotten and there is a brief overview of appropriate basic pharmacology. 

To achieve their different effects NTs are not only released from different neurons to act on different receptors but their biochemistry is different. While the mechanism of their release may be similar (Chapter 4) their turnover varies. Most NTs are synthesised from precursors in the axon terminals, stored in vesicles and released by arriving action potentials. Some are subsequently broken down extracellularly, e.g. acetylcholine by cholinesterase, but many, like the amino acids, are taken back into the nerve where they are incorporated into biochemical pathways that may modify their structure initially but ultimately ensure a maintained NT level. Such processes are ideally suited to the fast transmission effected by the amino acids and acetylcholine in some cases (nicotinic), and complements the anatomical features of their neurons and the recepter mechanisms they activate. Further, to ensure the maintenance of function in vital pathways, glutamate and GABA are stored in very high concentrations (10 pmol/mg) just as ACh is at the neuromuscular junction. 

Galantamine is a ChE inhibitor, which elevates acetylcholine in the cerebral cortex by slowing the degradation of acetylcholine.37 It also modulates the nicotinic acetylcholine receptors to increase acetylcholine from surviving presynaptic nerve terminals. In addition, it may increase glutamate and serotonin levels. The clinical benefit of action of these additional neurotransmitters is unknown. 

Alterations in neurotransmitter uptake and metabolism in glial cells / Modification in the ratio and function of inhibitory circuits / Local neurotransmitter imbalances (e.g., glutamate, y-aminobutyric acid [GABA]), acetylcholine, norepinephrine, and serotonin)... 

Giovannini M, Rakovska A, Benton R, Pazzagli M, Bianchi L, et al. 2001. Effects of novelty and habituation on acetylcholine, GABA, and glutamate release from the frontal cortex and hippocampus of freely moving rats. Neuroscience 106(1) 43-53. 

Moor E, Schirm E, Jacso J, Westerink BH. 1998. Involvement of medial septal glutamate and GABAA receptors in behaviour-induced acetylcholine release in the hippocampus a dual probe microdialysis study. Brain Res 789(1) 1-8. 

Balfour DJ (2002) Neuroplasticity within the mesoaccumbens dopamine system and its role in tobacco Dependence, Curr Drug Targets CNS Neurol Disord 1 413-21 Balfour DJ (2004) The neurobiology of tobacco dependence a preclinical perspective on the role of the dopamine projections to the nucleus accumbens. Nicotine Tob Res 6 899-912 Barik J, Wonnacott S (2006) Indirect modulation by alpha7 nicotinic acetylcholine receptors of noradrenaline release in rat hippocampal slices interaction with glutamate and GABA systems and effect of nicotine withdrawal. Mol Pharmacol 69 618-628... 

There are more than 10 billion neurons that make up the human nervous system, and they interact with one another through neurotransmitters. Acetylcholine, a number of biogenic amines (norepinephrine, dopamine, serotonin, and in all likelihood, histamine and norepinephrine), certain amino acids and peptides, and adenosine are neurotransmitters in the central nervous system. Amino acid neurotransmitters are glutamic and aspartic acids that excite postsynaptic membrane receptors of several neurons as well as y-aminobutyric acid (GABA) and glycine, which are inhibitory neurotransmitters. Endorphins, enkephalins, and substance P are considered peptidergic transmitters. There are many compounds that imitate the action of these neurotransmitters. 

Levy, E, Kendrick, K.M., Goode, J.A., Guevara-Guzman, R., and Keverne, E.B. (1995) Oxytocin and vasopressin release in the olfactory bulb of parturient ewes changes with maternal experience and effects on acetylcholine, gamma-aminobutyric acid, glutamate and noradrenaline release. Brain Res 669 197-206. 

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