Nervous system nicotinic acetylcholine receptor binding

Orth M, Amann B, Robertson MM, RothweU JC (2005) ExcitabUity of motor cortex inhibitory circuits in Tourette syndrome before and after single dose nicotine. Brain 128 1292-1300 Oswald RE, Freeman JA (1981) Alpha-bungarotoxin binding and central nervous system nicotinic acetylcholine receptors. Neuroscience 6 1-14... 

Histrionicotoxin, 342, and synthetic analog inhibition of ligand binding at sites associated with the sodium, potassium, and calcium channels in brain membrane preparations has been investigated [721]. The effects of 342 on the ion channel of central nervous system nicotinic acetylcholine receptors [722], and on post-tetanic potentiation of mouse and rat phrenic nerve diaphram preparations have been described [723]. 

Nicotine affects the nervous system, interacting with the nicotinic acetylcholine receptors, and the tight binding is partially accounted for by the structural similarity between acetylcholine and nicotine. Curare-like antagonists also block nicotinic acetylcholine receptors (see Box 6.7). There are other acetylcholine receptors, termed muscarinic, that are triggered by the alkaloid muscarine. The tropane alkaloid hyoscyamine (see Box 10.9) binds to muscarinic acetylcholine receptors. 

The modes of action of different alkaloids are diverse. For example, nicotine binds to and affects nicotinic acetylcholine receptors and shows toxicity. A recent molecular 3D model suggests that both acetylcholine and nicotine bind to the same pocket formed in a nicotinic acetylcholine receptor.15 Morphine binds to and activates opioid receptors, transmembrane-spanning G protein-coupled receptors, in the central nervous system of humans.16 Caffeine, which is structurally similar to adenine, inhibits cyclic AMP phosphodiesterase activity and inhibits the degradation of cAMP, thus exerting a toxic effect on insects 17 in human beings, binding of caffeine to the adenosine A2A receptor induces wakefulness.18 Atropine binds to muscarinic acetylcholine receptors, competing with acetylcholine, and blocks neurotransmission.1... 

Taiget Sites in the Nervous System Neonicotinoids target nicotinic acetylcholine receptors, as has mainly been demonstrated by studies with imidadoprid (8). Compared with imidadoprid and the other neonicotinoid sales products, thiame-thoxam (13) binds in a different way, possibly to a different site of the receptor in aphids [55-58]. 

Atropine, an alkaloid from Atropa belladonna, is the classical parasympatholytic compound. It competes with acetylcholine for the binding at the muscarinic receptor. Its affinity towards nicotinic receptors is very low, so that it does not interfere with the ganglionic transmission or the neuromotor transmission, at least in therapeutic dosages. However, in the central nervous system muscarinic receptor do play an important role and while atropine can penetrate the blood-brain barrier it exerts pronounced central effects. Atropine, like all other antagonists of the muscarinic acetylcholine receptor inhibit the stimulatory influence of the parasympathetic branch of the autonomous nervous system. All excretory glands (tear, sweat, salivary, gasto-intestinal, bronchi) are... 

Mecfianism of Action A cholinergic-receptor agonist that binds to acetylcholine receptors, producing both stimulating and depressant effects on the peripheral and central nervous systems. Therapeutic Effect Provides a source of nicotine during nicotine withdrawal and reduces withdrawal symptoms. 

Nicotine is known to bind to acetylcholine receptors (the receiving areas on cells) that are located throughout the central nervous system as well as the peripheral nervous system. Acetylcholine is a neurotransmitter it transmits nerve impulses from one nerve fiber to another. The pleasurable effects of nicotine are a... 

As with the mental effects of nicotine, the physiological effects are brought about by its actions on the nervous system, both peripheral and central. Nicotine changes the transmission of nerve impulses by binding to acetylcholine receptors, and induces the release of several chemical messengers, which in turn affect several body systems. 

The nicotinic acetylcholine (ACh) receptor is a well-characterized receptor of this type consisting of five subunits. It is present on the skeletal muscle cell end-plate in the neuromuscular junction, at all autonomic ganglia, and in the central nervous system (CNS). The function of this receptor is to convert ACh binding into an electrical signal via increased Na+ or K+ permeability across the cell membrane (i.e., membrane depolarization). When two molecules of ACh bind to the a subunit of the receptor, a conformational change in the receptor induces opening of the channel to at least 0.65 nm for approximately 1-2 ms. 

Nicotine binds to a type of receptor, now called a nicotinic receptor, and causes the same effects as a release of the neurotransmitter acetylcholine at nerve endings. In this it is similar to organophosphates, which lead to excess acetylcholine at nerve endings (see pp. loo-ioi). Nicotine first excites and then inhibits the central nervous system it first stimulates and then paralyses nerves. It reacts with receptors in muscle and nerves, and is able to enter the brain from the bloodstream and interact with nicotinic receptors. At first there is a stimulation, with the smoker experiencing alertness and decreased irritability, aggression, and anxiety. With higher doses there is depression of the brain as a result of saturation of the receptors. 

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