Central nervous system nicotine

Central nervous system Nicotine, strychnine, arsenic, halogenated hydrocarbons, organic phosphates, dinitro-phenols, fluoroacetate (1080)... 

Exposure to disulfoton can result in inhibition of acetylcholinesterase activity, with consequent accumulation of acetylcholine at nerve synapses and ganglia leading to central nervous system, nicotinic, and muscarinic effects (see Section 2.2.1.4 for more extensive discussion). 

Oswald RE, Ereeman JA (1981) Alpha-bungarotoxin binding and central nervous system nicotinic acetylchohne receptors. Neuroscience 6 1-14... 

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]. 

Mode of Motion. Nicotine, anabasine, and imidocloprid affect the ganglia of the insect central nervous system, faciUtating transsynaptic conduction at low concentrations and blocking conduction at higher levels. The extent of ionisation of the nicotinoids plays an important role in both their penetration through the ionic barrier of the nerve sheath to the site of action and in their interaction with the site of action, which is befleved to be the acetylcholine receptor protein. There is a marked similarity in dimensions between acetylcholine and the nicotinium ion. 

General types of physiological functions attributed to quaternary ammonium compounds are curare action, muscarinic—nicotinic action, and ganglia blocking action. The active substance of curare is a quaternary that can produce muscular paralysis without affecting the central nervous system or the heart. Muscarinic action is the stimulation of smooth-muscle tissue. Nicotinic action is primary transient stimulation and secondary persistent depression of sympathetic and parasympathetic ganglia. 

Cholinergic Transmission is the process of synaptic transmission which uses mainly acetylcholine as a transmitter. Cholinergic transmission is found widely in the peripheral and central nervous system, where acetylcholine acts on nicotinic and muscarinic receptors. 

The various stimulants have no obvious chemical relationships and do not share primary neurochemical effects, despite their similar behavioral effects. Cocaines chemical strucmre does not resemble that of caffeine, nicotine, or amphetamine. Cocaine binds to the dopamine reuptake transporter in the central nervous system, effectively inhibiting dopamine reuptake. It has similar effects on the transporters that mediate norepinephrine and serotonin reuptake. As discussed later in this chapter in the section on neurochemical actions mediating stimulant reward, dopamine is very important in the reward system of the brain the increase of dopamine associated with use of cocaine probably accounts for the high dependence potential of the drug. 

Clinical signs and symptoms of toxicity are related to the overstimulation of muscarinic, nicotinic, and central nervous system receptors in the nervous system. Muscarinic receptors are those activated by the alkaloid drug muscarine. These receptors are under the control of the parasympathetic nervous system, and their hyperactivity results in respiratory and gastrointestinal dysfunction, incontinence, salivation, bradycardia, miosis, and sweating. Nicotinic receptors are those activated by nicotine. Hyperactivity of these receptors results in muscle fasciculations even greater stimulation results in blockade and muscle paralysis (Lefkowitz et al. 1996 Tafliri and Roberts 1987). Hyperactivity of central nervous system receptors results in the frank neurological signs of confusion, ataxia, dizziness, incoordination, and slurred speech, which are manifestations of acute intoxication. Muscarine and nicotine are not... 

Neonicotinoids are potent broad-spectrum insecticides that exhibit contact, stomach and systemic activity. Acetamiprid, imidacloprid, nitenpyram, thiamethoxam and thiacloprid are representatives of the neonicotinoid insecticides (Figure 1). The mechanism of action is similar to that of nicotine, acting on the central nervous system causing irreversible blocking of postsynaptic nicotinic acetylcholine receptors (nAChR). Neonicotinoid insecticides are often categorized as antagonists of the... 

Since nicotine has wide ranging effects on the central nervous system it seems likely that pharmacogenomic effects on the development of nicotine dependence will span several neurotransmitter systems. One study found an association between a polymorphism in dopamine /1-hydroxylase and level of tobacco consumption [20]. This enzyme is important in noradrenaline synthesis and it is tempting to speculate that genetically regulated variations in activity might influence susceptibility to nicotine withdrawal symptoms mediated by noradrenergic pathways, but more information is required on the molecular effects of the polymorphism. 

The symptoms that followed the daily intramuscular administration of D.F.P. for 5 days mimicked most of the muscarine-like and nicotine-like effects (see p. 37) of cholinergic drugs. There were also effects on the central nervous system. 

D.F.P., a moderately inhibiting effect on the symptoms in the central nervous system, and no effect on the nicotinic symptoms. 

Pomerleau OF. (1992). Nicotine and the central nervous system biobehavioral effects of cigarette smoking. Am J Med. 93(1A) 2S-7S. 

Wada E, Wada K, Boulter J, Deneris E, Heinemann S, et al. 1989. Distribution of al, a3, a4, and 32 neuronal nicotinic receptor subunit mRNAs in the central nervous system a hybridization histochemical study in the rat. J Comp Neurol 284 314-335. 

Vallejo YE, Buisson B, Bertrand D, Green WN (2005) Chronic nicotine exposure upregulates nicotinic receptors by a novel mechanism. J Neurosci 25 5563-5572 Vemino S, Amador M, Luetje CW, Patrick J, Dani JA (1992) Calcium modulation and high calcium permeability of neuronal nicotinic acetylcholine receptors. Neuron 8 127-134 Vizi ES, Lendvai B (1999) Modulatory role of presynaptic nicotinic receptors in synaptic and non-synaptic chemical communication in the central nervous system. Brain Res Brain Res Rev 30 219-235... 

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