This is the solution for the CTQ #2. Listed under the page for CTQ #2 is the solution for this problem, #5. Sensory nervous stimuli, including pain stimuli are transmitted from the the CNS by action potential, In the nervous system action potentials are generated when voltage-gated sodium channels pen and permit sodium ions to pass through the plasma membrane into the neuron. The influx of sodium has the effect of making the cells negative and moves the membrane potential closer to threshold potential which is about -70-mV. When the threshold potential ( about -50 mV) is reached the cell depolarise or fires, that is, an action potential is created and the propagated along the axon , transmitting the neural stimulus.. Local anesthetics act to inhibit the generation and propagation of action potentials. They do so by blocking the sodium ion channel, preventing the inflow of sodium ions and preventing cell depolarization. This inhibits or prevents the transmission of pain or other stimuli to centers in the CNS. General anesthetics are some of the most important drugs in modern medicine. There are many types of general anesthetics from alcohol and ethyl ether to thiopental and isoflurane. Nevertheless there is no unitary theory that explains the mechanism of action of all the general anesthetics. The effect of these drugs is multifaceted, including analgesia, amnesia, immobility, unconsciousness , and sedation.
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Local anesthetics like lidocaine, and novocain bind to open Na+ channels on the cytoplasmic side and decrease the membrane permeability to Na+ ions-- or blocks the entry of Na + ions altogether. The result is that the inside of the neuron gets more negative and the membrane potential goes fro -70mV to -100mV or more. This hyperpolarization of the cell takes the membrane potential farther from threshold and makes it harder to generate an action potential. Thus the local anesthetic block the transmission of sensory neural messages. There are many different general anesthetics and there effects are multifaceted. There is no single explanation for the molecular modality( modalities) of the the effects of general anesthetics . However, it is known that many general anesthetic act at presynaptic membranes of axon terminals. There they activate chemically-gated ion channels. by binding to neurotransmitter receptors. Some channel receptors that they bind to include GABA(A) receptor, Glycine receptor, nACHr( ACH nicotinic receptor), as well as n-Acetyl-d-Aspartate and (NMDA) and amino methyl propionic acid receptors(AMPA). General anesthetics act at multiple sites in the CNS. including spinal cord, brain stem, cerebellum, thalamus , reticular activating system (RAS), and the hypothalamus. One mode of action of general anesthetics is to activate chemically-gated Cl- channels. This allows chloride ions to flow into the neuron and increase the intercellular negativity. This hyperpolarizes the cell and makes the generation of and action potential more difficult or impossible. There are several other mechanisms by which some general anesthetics act . They also affect the potassium 2pore channel, as well as,calcium, and sodium channels. But there is no unitary theory to explain all the actions of the several different types of general anesthetics.