Why does ether inhibit nerve impulses

Potassium leaves the neuron with the concentration gradient and electrostatic pressure. Potassium channels remain open for a brief period of time beyond that necessary to return to the resting state of polarization. The extra efflux of potassium ions from the neuron results in a brief approximately 1 millisecond period of Hyperpolarization.

During this period of hyperpolarization, another action potential cannot be triggered. The rate law of action potentials indicates that communication within the nervous system occurs via the timing or frequency of discharges and duration of pauses. The duration of hyperpolarization is the limiting factor in the rate at which action potentials can be initiated. This duration of approximately 1 millisecond means that the fastest rate for propagation of an impulse along an axon is approximately 1, per second.

Synthetic and natural molecules may affect different phases of the action potential, and thereby, affect the transmission of discharges. For example, scorpion venom acts to keep the sodium channels open and the potassium channels closed.

This results in a prolonged state of depolarization. Local anesthetics such as Novocain and Xylocaine attach to the sodium channels , and thus prevent the flow of sodium into the cell.

The net result is the blockage of neuronal stimulation. General anesthetics such as ether and chloroform function in a different fashion. Hypotheses that propose that local anesthetics act by expanding the nerve membrane and causing a change in protein conformation that blocks sodium permeability are vague in conception and difficult to test experimentally.

Evidence from voltage-clamp studies of single nerve fibers indicates that anesthetic molecules interact with the sodium channels directly, from the inner side of the nerve membrane. Anesthetics bind within sodium channels which have opened during membrane depolarization, preventing the normal sodium ion flux.

Anesthetic molecules can dissociate from open channels, but not from channels that remain closed when the nerve is kept at rest. The "gating" properties that regulate the opening and closing of sodium channels are reversibly modified during anesthesia. Specifically, the inactivation function responds more slowly and requires more negative membrane potential changes to reach the same values as in unanesthetized nerves.

A second, slow inactivation is observed following external application of tertiary amine anesthetics. Anesth Prog. Local anaesthetic systemic toxicity. Dubin AE, Patapoutian A. Nociceptors: the sensors of the pain pathway. J Clin Invest. Updated: October 14, Accessed: February 19, Essentials of local anesthetic pharmacology. Subcutaneous Infiltration of Local Anesthetics.

In: Post TW, ed. Last updated: January 3, Guay J. Methemoglobinemia related to local anesthetics: a summary of episodes. Anesth Analg.