Are nicotonic receptors a type of Ligand Gated channels?
139472
I really don't know much about the subject but a Google search will reveal a world of information.  You might want to try Lexus Nexus as well.
869334
Since caffeine and other methyxanthines act as competitive antagonists to adenosine.  This means that they bond to the same receptor site but fail to activate it.  As they are bound to the receptor, the true agonist is unable to bind and activate that receptor.   Similar to carbon monoxide, caffeine could have a higher affinity to the receptor thus attaching to the receptor longer and/or displacing adenosine from the receptor to attach.\n\nAs for the role of adenosine in dilation of blood vessels, I have only found that it dilates coronary arteries and constricts the the afferent arterioles of the glomerulus.
980593
Dialysis tubing can come in various pore sizes that allow selective passage of materials. This is like a cell membrane that is also selective, but not really in terms of the size of the material. It has to do with the polarity (cell membrane is bipolar-has polar head with long, non-polar tail, but two chains of this with non-polar ends facing inward on the membrane and polar heads facing the outside of the membrane). Polar molecules (such as Na+ or K+) need to go through membrane-bound protein channels or receptors.
979404
Actually I think he meant, "What would reduced extracellular Ca++ concentration (hypocalcemia) do to the synaptic transmission at the NMJ?"\n\nIf this is what you mean, then here's my answer:\n\nCalcium is required for the release of acetylcholine at the NMJ.  If there is a large reduction of calcium in the body, eventual results include flaccid paralysis, poor pupillary response to light, and coma.  This occurs after a temporary bout of hyperexcitability and tetany.
759945
Alpha-bungarotoxin is a specific antagonist of a limited isoform of the nicotinic acetylcholine receptor. When used for skeletal muscle the toxin blocks all transmission induced by ACh. This is because the toxin reacts with the skeletal muscle alpha1, beta1, epsilon, delta subunit containing receptor. Bungarotoxin works on this receptor form and also on the alpha7-containing neuronal nicotinic receptor. Ganglionic AChRs and many neuronal cells do not contain subunits that are sensitive to bungarotoxin.
637350
INFORMATION IS CONDUCTED ELETROCHEMICALLY BY THE NEURONS THROUGH VARYING CONCENTRATIONAS OF Na and K ions across the myelin seath of the neurons.in a neuron at rest there is more conc. of k ions on the inner side(this is the polarised region) and more conc. of Na ions on the outer side(depolarised region) .thus the inner side is at a greater potential than the outer side .when a stimulas is received the conc. in a particular regin of the neuron begins to change. K IONS move to the outer side and Na ions move to the inner side.now in that part of the neuron the outer membrane is at a higher potential than the the inner membrane. in the outer region the Kions are surrounded by large number of Na ions due to this a current sink develops and the K ion move back to the inner side while Na ions move back to the outer region and this region gets repolarised.but the region next to this gets deolarised in the process.thus the nerve impulse travels across the neuron as a wave of polarisation, depolarisation and repolarisation.\n           as the nerve impulse reaches the terminals of the neuron called dendrites the vesicles present there release ascetylcholine and this neurotransmitter transfers messages from one neuron to another and the above process continues till the message reaches the concerned organ.
686729
By chemically blocking pain receptors
644652
I answered this already.\n\nhttp://answers.yahoo.com/question/index;_ylt=AmW0Em3eAdmFrnQMc4_Xilzsy6IX?qid=1006051323791\n\nWorks the same as if you were changing permeability. If you have more Na inside the cell, there is less drive for Na outside the cell to come in. Because Na only has a minor impact on the resting membrane potential, it won't change much, but it will hyperpolarize a bit (away from the Ena and towards Ek).
873225
I can't find any research on the subject at the moment.\n\nThe sensible answer is no, the amount of nicotine (the primary addictive component of cigarette smoke) found in second-hand smoker's urine is practically nothing compared to that found in those that do smoke (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17008197&query_hl=1&itool=pubmed_docsum).\n\nThe exception to this is maternal smoking during pregnancy where there is a theoretical risk that the foetus develops an 'addiction'. I cannot find any research on this though.
71177
Neurotransmitters - What They Do . . .\n\nNeurotransmitters are small molecules whose function is to transmit nerve signals (impulses) from one nerve cell (neuron) to another. Neurotransmitters are chemical messengers which neurons use to tell other neurons that they have received an impulse. There are many different neurotransmitters - some trigger the receiving neuron to send an impulse and some stop it from doing so. See this simplified diagram of a neuron: \n\n\nNerve impulses always flow in one direction - from the branched extensions called dendrites, down the neuron to the presynaptic terminals. The join between the presynaptic terminals of one neuron and the dendrites of another is called the synapse. \n\nThe two neurons do not actually touch each other but are separated by a space called the synaptic cleft. \n\nWhen a nerve impulse arrives at a presynaptic terminal it causes neurotransmitters to be released into the synaptic cleft. The neurotransmitters then bind with special "postsynaptic receptors" in the dendrites of the receiving neuron. \n\nWhen a postsynaptic receptor receives a neurotransmitter it can either cause a nerve impulse to travel down the neuron or it can inhibit a nerve impulse depending on the neurotransmitter released. \n\nNeurotransmitters which propagate nerve impulses in the receiving neuron are called excitatory neurotransmitters. Those which inhibit nerve impulses are called inhibitory neurotransmitters. \n\nNeurotransmitters are sythesized in the cell body (the soma) and migrate down the axon to the presynaptic terminals. Here they are stored in little packets called vesicles which fuse with the synaptic membrane. When a depolarizing current (the action potential) is received, these vesicles release their contents into the synaptic cleft. \n\nNeurotransmitters activate receptors by "sticking" to them and thus preventing other neurotransmitters from activating them. Inactivation of the transmitter happens in one of three ways: \n\n\nReabsorption of the neurotransmitter into the neuron. This is known as reuptake. \n\nDestruction of the neurotransmitter with special chemicals called enzymes. This is known as enzymatic degradation. \n\nBy the neurotransmitter becoming deteched from the receptor and drifting out of the synaptic cleft. This is known as diffusion.\nSubstances that effect neurotransmission but are not neurotransmitters can be broadly divided into two categories - agonists and antagonists. \n\nAgonists make transmission of nerve impulses more likely. They do this in a number of ways including preventing reuptake (cocaine works this way). \n\nActually triggering the receptor themselves (nicotine works this way) \n\nAnd by making the receptor more responsive (a lot of anti-anxiety drugs work like this). \n\nAntagonists do the opposite - they interfere with nerve transmission across the synapse sometimes by blocking receptor sites (many spider and snake venoms work this way) \n\nAnd sometimes by preventing release of the neurotransmitter from the presynaptic terminal (many anti-psychotic drugs operate like this). \n\nThe following is an partial list of neurotransmitters, together with the sites in which they work: \n\nNeurotransmitters Group Neurotransmitter Region of Operation \nAcetylcholine Acetylcholine Central Nervous System (CNS), Peripheral Nervous System (PNS) and Autonomic Nervous System (ANS)  \nSerotonin SerotoninCNS and PNS \nAmino acids Glutamate, GammaAminobutyric Acid (GABA), Glycine, Aspartate  CNS \nHistamine Histamine Hypothalamus \nCatecholamines Norpinephrine, Epinephrine (Adrenalin) CNS and Sympathetic Nervous System \nNeuropeptides Endorphins (Enkephalins and Dynorphins), Substance P CNS \nDopamine Dopamine CNS \nNucleotides Adenosine, Adenosine Triphosphate (ATP) CNS, PNS and ANS \nNitric oxide Nitric oxide CNS
932037
the signal transduction...\nsignal transduction is a process of the change of an extracellular stimuli into a intracellular signal which produce response towards that stimuli.\n\none of the example is the mechanism of non-steroid hormone via activation of cyclic AMP.\nbasically it's like this:\nthe non-steroid hormone such as andrenaline acts as the first mesenger which bind with a specific receptor in the plasma membrane. the hormone-receptor complex then binds with a relay molecule, a G protein. the G protein binds with GTP. the activated G protein in turn stinulate the enzyme adenylyl cyclase which converts ATP into cyclic AMP( cAMP). cAMP then triggers responses of target cell such as cascade reactions, permeability changes of cell membrane, increased production of glucose.
276026
"As the action potential envelops the bouton (the terminal bouton at the end of the axon), the synaptic vesicles attach to the bouton membrane at the active zone.  Once attached they release their chemical messenger into the synaptic cleft where it diffuses to the post synaptic membrane.  There the chemical messenger combines with a receptor protein, a process that alters the ionic conductance and consequently the membrane potential of the post synaptic cell.  This may initiate an action potential in the post synaptic neuron."\n\nTo summarize:\nThe action potential arrives at the synaptic junction.  There it stimulates the release of the chemical messenger, known as a neurotransmitter, into the synaptic cleft.  If enough neurotransmitter chemicals cross the synaptic cleft and attach to receptors on the 2nd neuron, a new action potential is initiated in the 2nd neuron.
386749
Local anaesthetics work by blocking singals that pass through neurons. They can do this through a few mechanisms, but the fastest acting ones do so by blocking ion channels in the neuron's cell membrane. Typically, an electrical impulse propagates itself by opening and closing ion channels in rapid succession. Without functioning ion channels, the electrical impulses halt, thus stopping transmission of signal.\n\nLidocaine, novocaine and cocaine all have this ability to temporarily stop ion channels. Correct me if I'm wrong, but I think it's a K+ channel?
816195
There is a new smoking cessation drug that was just approved by the FDA... Chantix is what it is called.  It actually binds to the receptors that nicotine binds to.  It is supposedly safe and does not interact with any other medications.  I think this could apply to young adults.
391224
There are two classes of acetylcholine receptors, muscarinic and nicotinic (see Molecular Biology, Pharmacology, and Brain Distribution of Subtypes of the Muscarinic Receptor). These receptors play major roles in the function of the body. In brain, evidence suggests a role for muscarinic receptors in memory function (28, 71) and in the pathophysiology of affective illness (46, 47, 79) and schizophrenia (24, 50, 85, 86). Because of their putative role in cognitive function, muscarinic receptors have been a focus of research in Alzheimer's disease (see Experimental Therapeutics).\n\nResearchers defined the two classes of cholinergic receptors early in this century on the basis of tissue responses to certain agonists and antagonists (22). A response caused by muscarine, an alkaloid derived from a poisonous mushroom (Amanita muscaria), and antagonism of a response caused by atropine, an alkaloid from the deadly nightshade (Atropa belladonna—a favorite of poisoners in past centuries), defined muscarinic receptors in a tissue. On the other hand, response to nicotine and blockade by d-tubocurarine (one of the alkaloids from the South American arrow poisons) defined nicotinic receptors. These definitions for the two types of cholinergic receptors are still used today.\n\nMuscarinic receptors are widely distributed throughout the body. They mediate various types of responses in many different tissues—such as cardiac tissue, smooth muscle, and exocrine glands—and in cells throughout the peripheral and central nervous system. Within the nervous system, muscarinic receptors are present on some axon endings (heteroreceptors and autoreceptors), regulating neurotransmitter release (1, 67, 68, 90). These receptors are also on the soma and dendrites of many types of neurons, including cholinergic and noncholinergic neurons (67, 95).\n\nIn the past several years, discoveries by molecular biologists have made the field of muscarinic receptors immensely interesting and complex. At a time when pharmacologists could identify at most three subtypes of muscarinic receptors, molecular biologists showed that at least five different muscarinic receptors exist on the basis of molecular cloning experiments (15, 16, 54, 55, 63). Much knowledge about these receptors has come from the use of transfected cell lines that have incorporated into their genome and express the gene encoding the specific muscarinic receptor.\n\nThis chapter will focus mainly on the biochemical events associated with activation of muscarinic receptors. The concepts of receptors, their effectors, and second messengers will be presented along with a general discussion of the types of membrane-bound receptors. Specific aspects of transduction at cholinergic receptors will be presented along with a brief discussion of the neuropsychopharmacology of muscarinic receptors.\n\nRECEPTORS\n\nThe concept of a receptor was put forth in the latter part of the nineteenth century and the early part of this century by Professors J. N. Langley and Paul Ehrlich. Professor Ehrlich has stated "the toxin must unite . . . with `receptors' in order for the toxin to have its effects" (30). Professor Langley used the term "receptive substance" (56).\n\nA receptor is a highly specialized protein, which, in most cases, is a transmembrane spanning protein on the cellular surface (receptors for steroid hormones are intracellular). This receptor protein has the unique ability to recognize (bind) specific molecules. All neurotransmitters, neuromodulators, and hormones have specific receptors. Many neurotransmitters are known to have more than one type of receptor to which they bind.\n\nCurrently, receptors may be classified into four groups based upon their signal transduction mechanisms: (i) receptors that are ligand-gated ion channels [e.g., the nicotinic acetylcholine (21, 65) and gamma-aminobutyric acid (GABA) receptors (13, 75)]; (ii) receptors that are enzymes [e.g., the ins
1135871
They work through signal transduction.
679433
cystic fibrosis transmembrane conductance regulator, or CTRF,gene;it codes for a molecule that acts as a chloride channel.Mutation in it   leads to impaired chloride secretion in airway epithelium. The low level of luminal chloride in the airways (and high levels of sodium) leads to the accumulation of hyper-concentrated, thickened secretions within the respiratory tree.