The acetylcholine , shortened in Ach , is the first Neurotransmetteur discovered. He as well plays a big role in the central Nervous system where he is implied in the memory and the training, as in the peripheral Nervous system. This ester of the acetic Acid and the Choline, whose action is médiée by the nicotinic receivers and muscarinic has a molar Masse of 146,2 G/mol and for Chemical formula C H 3C O OCH2CH2 NR + (CH3) 3.
History
As of 1907, Reid Hunt shows the presence of acetylcholine in the Ergot of rye. The physiologist English Henry Hallett Dale insulates this compound in 1914 and shows in 1921, in collaboration with the German pharmacologist Otto Loewi that the acetylcholine is a mediator released by the parasympathetic Nervous system. Pave and Loewi will receive the Nobel Prize Physiologie and of Médecine in 1936 for their work on the chemical transmission of nervous information.
Physiology
During the nerve impulse, the acetylcholine is released on the level of the Synapse S of the Neuron S known as “cholinergic” of the peripheral nervous system, to transmit the nervous information of a neuron to the following. These synapses which use acetylcholine as neuro-transmitter are called cholinergic synapses . In the vegetative peripheral nervous system, the acetylcholine intervenes in the pre-ganglionic synapse of the sympathetic fibers and parasympathetic like in the neuro-effector synapse of the system parasympatic (see Figure 2). The acetylcholine is finally implied in the junctions neuromusculaires connecting the Motoneurone S to the skeletal Muscle S.Au level of each synapse is indicated the neuro-transmitter and the receiver impliqués.
Ach: Acetylcholine, G: Ganglia, Nad: Noradrenalin, SNC: Central nervous system.
Pharmacology
The acetylcholine is stored in the blisters of the termination of the axon, at a rate of 5 000 with 10 000 Molecule S by blister. On arrival of a Potentiel of action the entry of ions calcium (Ca2+) causes the fusion of the blisters with the cellular Membrane what releases neurotransmitters in the synaptic slit. The botulinic Toxine inhibits the acetylcholine release. The acetylcholine is fixed on the receivers present at the surface of the post-synaptic neuron. These receivers are mainly of two types: nicotinic and muscarinic.
Receivers muscarinic
See also Receiving muscarinic
The muscarinic receiving just like belong to the family of the receivers métabotropes to seven transmembrane fields (7TM) the receivers adrenergic. They are widely distributed in the organization and are very represented in the brain (M1, m3 and M4).
These receivers are responsible for the parasympathetic transmission postganglionnaire and are divided into five classes: M1, m3 and M5 which have an exiting activity, m2 and M4 which are inhibiting.
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the receivers M1 (central Nervous system, Stomach and ganglion S), m3 and M5 are coupled with a Phospholipase C (PLC) and have an exiting effect. The activation of the PLC can involve, according to fabrics, the muscular contraction, the release of adrenalin or the modulation of the exitability of the neurons.
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the receivers m2 (Heart, smooth muscles) and M4 inhibit the Adénylate cyclase via the activation of the sub-unit alpha of a Protéine Gi. They are also responsible for the opening of channels potassium creating a hyperpolarisation of the post-synaptic membrane.
Receivers nicotinic
to also see Receiving nicotinic
The nicotinic receiving are present in the Cerveau, the Spinal-cord, the ganglion S of the nervous systems sympathetic and parasympathetic and in the synapse between the sympathetic neurons and the Effecteur S. These pentameric receivers of a molecular mass of 280 kDa form a channel of a diameter of 6,5 Å, which opens only after fixing of two acetylcholine molecules. The activation of the receivers N1 (central nervous system and peripheral ganglia) produced the opening of permeable channels to the ions sodium and potassium. The important entry of ions sodium in the post-synaptic neuron creates a fast depolarization of the membrane and ensures the propagation of the nerve impulse. The receivers N2 located on the junctions neuromusculaires are coupled with sodic channels. That causes the entry of Na+, which produces a localized depolarization called potential of driving plate (PPM). This PPM opens voltage-dependant the Na+ channels and start a traditional potential of action. This one traverses muscle fiber and penetrates in the transverse tubule, or it will stimulate the release of the calcium contained in the reticulum sarcoplasmic. The rise in the intracellular concentration in ions calcium causes the contraction of the skeletal muscles.
Metabolism
The acetylcholine is synthesized in the Cytoplasme presynaptic neurons starting from Choline and of Acétyl-coenzyme has during a reaction catalyzed by the Choline acétyltransférase (CAT), a Enzyme. The acétyl coenzyme has comes from the Métabolisme of glucose in the Mitochondrie, during the Glycolyse), which leads to the Pyruvate, transformed in acétyl CoA by the Pyruvate déshydrogénase.
The choline, which is the limiting element of the acetylcholine synthesis, is collected in the extracellular medium by an active conveyer using the ions sodium. Choline acétyltransférase is synthesized in the cellular body of the presynaptic neuron and follows fast anterograde transport until the end of the axon, place of synthesis of the neuro-transmitter. This enzyme is used as specific marker of the presence of cholinergic neurons. Contrary to many neurotransmitters which are recaptured by the presynaptic neuron, the acetylcholine released after Exocytose is primarily degraded out of choline and acetate by the acétylcholinestérases of the synaptic slit. The half-life of acetylcholine in the synaptic slit is from 1 to 2 milliseconds.
See too
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