Explain how autonomic neurotransmitter influence the actions of effector cells.?
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Neurotransmitter of sympathetic neurons is acetylcholine (ACh). It stimulates action potentials in the postganglionic neurons.\n\nThe neurotransmitter released by the postganglionic neurons is noradrenaline\nThe action of noradrenaline on a particular gland or muscle is excitatory in some cases, inhibitory in others. (At excitatory terminals, ATP may be released along with noradrenaline.)\nAcetylcholine (ACh) is the neurotransmitter at all the pre- and many of the postganglionic neurons of the parasympathetic system. However, some of the postganglionic neurons release nitric oxide (NO) as their neurotransmitter.
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my father just passed away May 1,dopamine is to control the shaking and tremors Mussel movement in Parkinson's disease patients. Yet, I had just seen a new report on  CNN from a neurosurgeon in Las Vegas. They did not know until recently that it also affect the behavioral. You two trans motors for mussel movement or on the outer side of the behavioral motor and there for when the dopamine cross over it can cause a compulsive behavioral problem. There were two of this neurosurgeon's patients that had compulsive gambling to come on after starting to take the Leve-Dopa and lost lots of money (but it can be other things that they take compulsive) so there for the Dr. went to checking and he had 12 patients that had the same pattern,so therefor he had to take these patients off the Leve-Dopa. Be careful and God Bless you. Let me add this. Talk to your Dr., But I do know that in recent studies the vitamin COQ10 is suppose to be great for early Parkinson's Diseas patients. It's also great for the circulartory system, the heart. Don't let you Dr. discourage you from this vitamin. Get you pharmaciest, Dr. or Alternative Medicene person to cross reference ALL of your medications. And don't just get one opinion. WEBMD,the are alot of places to research medication..From what I can remember an early detection of Parkinson's you shoul take 300 to work up to 1200mg of COQ10 a day. If you do start taking this after cross refercing the medications you are on and it's ok. Say you start taking 300mg of COQ10 and you feel tired of worse, don't stop taking in vitamin.....just cut the dose back and go at a more gradual approach until you work up to the recommended dose. I was a caregiver for both of my parents and researched a lot of stuff. Of course my mother's cancer and heart were to far gone. And Daddy had Parkinson's for over 25 years. My father had no surgery, moved around until the day he passed away. My 1st cousin was diagnosed at 33,now47 had 5 surgery's and barely gets by. If he undoes his batteries on the right he has no control what so ever pm the left, if he undoes the batteries on the left he has no control on the right. I seen my 69 year old father able to still move and talk after going for a while as my cousin can only go for so long. Again, check with your Dr. before you do anything. And always second and third opinions and other info helps. God Bless you
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THE AUTONOMIC NERVOUS SYSTEM \n\n1. THE AUTONOMIC NERVOUS SYSTEM REGULATES ACTIVITIES THAT ARE AUTOMATIC, OR INVOLUNTARY. \n\n2. The Nerves of the Autonomic Nervous System CONTROL Functions of the body that are NOT UNDER CONSCIOUS CONTROL. \n\n3. The Autonomic Nervous system seems to be concerned with striking a balance or MAINTAINING HOMEOSTASIS IN THE FUNCTIONING OF MANY ORGANS OF THE BODY. \n\n    EXAMPLES:  CONTRACTION IN THE HEART, DIGESTION, HEART RATE, BREATHING, SALIVATION, AND BLADDER. \n\n4. THE AUTONOMIC NERVOUS SYSTEM IS FURTHER SUBDIVIDED INTO TWO PARTS: \n\n    A. THE SYMPATHETIC DIVISION \n\n    B. THE PARASYMPATHETIC DIVISION \n\n5. The TWO parts have OPPOSITE EFFECTS on the ORGANS they control. (See Table 49-1) \n\n6. Most organs controlled by the Autonomic Division are under control of both Sympathetic and Parasympathetic Neurons. \n\nEXAMPLE:   Heart Rate is SPEEDED UP by the Sympathetic Nervous System, and it is \n                       SLOWED DOWN by the Parasympathetic Nervous System. \n\n7. The Sympathetic Division generally ACTIVATES ORGANS or SPEEDS UP. \n\n8. The Parasympathetic Division generally RETARDS ORGANS or SLOWS DOWN.
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it has much to do with the formation of memories, but it also deals with emotional responses and motovation.  It does so by sending signals via the endocrine system (hormones) and the autonomic nervous system.
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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
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It is a neurotransmitter in the catecholamine family that mediates chemical communication in the sympathetic nervous system, a branch of the autonomic nervous system. Like other neurotransmitters, it is released at synaptic nerve endings to transmit the signal from a nerve cell to other cells. Norepinephrine is almost identical in structure to epinephrine, which is released into the bloodstream from the adrenal medulla under sympathetic activation. The sympathetic nervous system functions in response to short-term stress; hence norepinephrine and epinephrine increase the heart rate as well as blood pressure. Other actions of norepinephrine include increased glycogenolysis (the conversion of glycogen to glucose) in the liver, increased lipolysis (the conversion of fats to fatty acids; in adipose (fat) tissue, and relaxation of bronchial smooth muscle to open up the air passages to the lungs. All of these actions represent a mobilization of the body's resources in order to meet the stressful challenge–such a response is often termed the "flight or fight" syndrome.
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neurotransmitter are found in the terminal buttons. The terminal buttons are balls at the end of axons that contain little vacuoles (vesicles i believe is the term for the pockets in brain cells) point is, there are pockets, each with neurotransmitters inside.  Lets back up for a moment... the most important concept to acknowledge, is that all emotions, cognitons, every action and behavior is due to some form of chemical change in our brain and or body.  Our bodies are complex chemical reactors.  Now, neurotransmitters are responsible for a lot and even most of of what we do both unconditionally and conditionally.  When the neurotransitter is released, it crosses a fluid filled gap known as the synaptic cleft.  The releasing neuron is known as the presynaptic neuron and the recieving neuron is known as the post synaptic neuron.  The N.T. docks at a receptor site- like a key in a lock and transferrs the information.  Lets say for instance, that this N.T. is designed to heat up the body in response to cold.  This message will reach a particular module of the brain n then send the message to the spine and then the sympathetic nervous system will activate bodily parts and efferent nerves will bring the message to muscles and u will start to shiver to heat up your body.  And that is an 1 example of how a N.T. can cause a behavior(shaking)
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I answered that same question yesterday:\nThe impulse reaches the terminal end of the motor neuron and breaks open the synaptic vesicles, releasing the neurotransmitter acetylcholine into the synaptic cleft.\nACh then binds to receptor molecules in the motor end plate of the muscle fiber.\nThe action potential is started in sarcolemma and passes along the membrane until it reaches the sarcoplasmic reticulum releasing calcium. Calcium diffuses in sarcoplasm and binds to the troponin in the thin filaments.\nThe binding sites on the actin molecules are freed, allowing\nthe heads of myosin (thick filaments) to attach on the binding sites forming the cross-bridges connections.\nThe cross-bridges shift their angle causing the thin filaments to slide over the thick filaments; this produces the contraction.\nATP is needed for the last step. ATP is bound to myosin; calcium activates ATP breakdown into ADP and phosphate.\nPart of the energy produced is used to move bridges, the other part is released as heat, increasing the body temperature.\nMore ATP breaks the bond between thick and thin filaments in the cross bridge; calcium returns to thesarcoplasmic reticulum and the thin filaments return to their original position, closing off the binding site to cross bridges and causing the muscle to relaxe.
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The hypothalamus in the brain controls the pituitary gland, which releases hormones that often affect the release of other hormones by other endocrine glands. \n\nMost of the time, however, it's a direct response to the conditions in the body and environment. For instance, when your brain preceives that you are in danger, you get the fight-or-flight response. Your adrenal glands release epinephrine, aka adrenaline, which speeds up your heart rate and gets you ready for action.
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To trigger a biological response.
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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.
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Proteins can not penetrate plasma membranes\nCyclic AMP (mediates neurotransmitters)\nHormone (first messenger) binds to receptor\nReceptor binds G-protein\nG-protein binds GTP, releasing GDP (has GTPase)\nActivated G-protein moves along membrane binds to Adenalyte cyclase,\nhydrolyzes it’s bound GTP to GDP.\ncAMP generated from ATP (secondary messenger)\nCyclic AMP (cAMP) diffuses throughout cell, triggering protein kinases\n(enzymes)\nExample: Epinephrine (adrenaline) on fat cell-break down glycogen and fat.\nPhosphodiesterase (intercellular enzyme) degrades cAMP\nImplications\nMultiplier effect: 1 Adenylate cyclase: ?? cAMP\nKinase catalyzes hundreds of reactions\nSingle hormone may catalyze millions of product molecules\nSequence regulated by:\nTarget cell type, specific protein kinases, and the initiating hormone\nSecondary messenger system: The PIP-Calcium signal mechanism\nSome hormones (e.g. epinephrine) mediated by Calcium, not cAMP.\nHormone binds to receptor\nG protein activated as GTP binds, displacing GDP\nG protein binds to and activates a membrane bound phospholipase, and\ninactivates\nPhospholipase splits PIP2 into IP3 and diacylglycerol (secondary messengers)\nPIP2 : phosphatidyl inositol biphosphate; IP3: inositol triphosphate\nIP3: Calcium from ER (endoplasmic reticulum)\nDiacylglycerol: Protein kinases\nCa2+: alters plasma membrane ion channels and also binds to Calmodulin, which\namplifies cellular response (decreases the energy of activation)\n\nalso see:
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Ok, Franko got it started-The action potential is propagated along the sensory axons, through the ulnar or other nerve (depending on exactly what part of your hand touched the stove), through the dorsal root ganglia (which is where the cell bodies for the sensory axon live) to the spinal cord.  There, they will release neurotransmitters at synapses with secondary sensory dendrites and cell bodies (which will send a signal on up the spinal cord to the brain) In addition, they will release neurotransmitters at synapses with interneurons, which synapse with motor neurons.  There motorneurons send axons to a number of muscles, such as the bicep.  A signal is generated at the motorneuron, sent down the axon, which then terminates on motor end-plates, which stimulate the muscle to contract, and thus pull the hand away.
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"Many nerve cells are of the basic type illustrated above. Some kind of stimulus triggers an electric discharge of the cell which is analogous to the discharge of a capacitor. This produces an electrical pulse on the order of 50-70 millivolts called an action potential. The electrical impulse propagates down the fiber-like extension of the nerve cell (the axon). The speed of transmission depends upon the size of the fiber, but is on the order of tens of meters per second - not the speed of light transmission that occurs with electrical signals on wires. Once the signal reaches the axon terminal bundle, it may be transmitted to a neighboring nerve cell with the action of a chemical neurotransmitter. "\n\ni studied this once when i was in matriculation college. i found this quite useful. hope this will help ya..\n\ngood luck
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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
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When the electrical impulse reaches the end of the axon it is transferred to the next nerve cell so the message can continue. At the end of the axon the cell widens out and forms a bulb which comes close to but does not touch the next nerve cell. It is this tiny space between the two cells that is referred to as a synapse. Transmission of the signal across a synapse involves the release of a chemical, called a neurotransmitter, which passes from one cell to the other across the synapse. The neurotransmitter acts on receptor sites on the second cell's membrane, changing its permeability to sodium ions and thus stimulating depolarization. In this manner the nerve impulse is transferred to the second cell.
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"Upregulation is the process by which a cell increases the number of receptors to a given hormone or neurotransmitter to improve its sensitivity to this molecule. A decrease of receptors is called downregulation."\n\n\n"Upregulation: An increase in the number of receptors on the surface of target cells, making the cells more sensitive to a hormone or another agent. For example, there is an increase in uterine oxytocin receptors in the third trimester of pregnancy, promoting the contraction of the smooth muscle of the uterus."