Summary

The Physiology of Control: Neurons and Endocrine Cells Compared

• Control by a nervous system involves neurons that send axons to discrete postsynaptic cells. Neurons generate rapidly conducting action potentials to control the specific targets on which they end. They exert fast, specific control by releasing neurotransmitters at synapses.
• Endocrine cells release hormones into the bloodstream to mediate endocrine control. All body cells are potential targets of a hormone, but only those with specific receptors for the hormone actually respond. Hormonal control is slower, longer lasting, and less specific than neural control.

The Cellular Organization of Neural Tissue

• Neurons are the principal cells of nervous systems. They have long processes (dendrites and axons) that are specialized to receive signals from other neurons (via dendrites) and to generate and propagate action potentials (via axons).
• Glial cells are the support cells of the nervous system. Schwann cells (in the PNS) and oligodendrocytes (in the CNS) form sheaths around neuronal axons, including insulating myelin sheaths around myelinated axons. Astrocytes surround capillaries and act as metabolic intermediaries between neurons and their circulatory supply. Microglial cells serve immune and scavenging functions.

The Ionic Basis of Membrane Potentials

• Cell membranes have properties of electrical resistance and capacitance, which allow them to maintain a voltage (membrane potential) and regulate current flow across the membrane. Cells have inside-negative resting membrane potentials. The passive electrical properties of membranes determine how membrane potentials change with time (the time constant, τ) and with distance (the length constant, λ).
• Membrane potentials depend on selective permeability to ions. Any ion species to which the membrane is permeable will tend to drive the membrane potential toward the equilibrium potential for that ion. The Nernst equation calculates the equilibrium potential of a single ion species in terms of its concentrations on both sides of the membrane.
• All cells have higher concentrations of K⁺ inside than outside, higher concentrations of Na⁺ outside than inside, and higher concentrations of Cl^– outside than inside. Ion concentrations inside and outside cells are maintained by active ion pumps, as well as by passive Donnan-equilibrium effects.
• Membrane potentials depend on the permeabilities to and concentration gradients of several ion species: The resting membrane is dominated by permeability to K⁺, so the resting membrane potential is near E_K. The Goldman equation describes how changing the membrane permeability of an ion species changes the membrane potential.
• In addition to their major role of maintaining the nonequilibrium concentrations of ions, electrogenic ion pumps generate a current that makes a small, direct contribution to V_m. In addition, only those ions that are freely diffusible contribute to V_m, so corrections for bound ions may be necessary.

The Action Potential

• An action potential is a voltage change—a brief, transient reversal of membrane potential from inside-negative to inside-positive. Action potentials are all-or-none responses to any depolarization beyond a voltage threshold and are each followed by a brief refractory period.
• Action potentials result from voltage-dependent changes in membrane permeability to ions. Depolarization first opens voltage-gated Na⁺ channels, allowing Na⁺ ions to flow in and further depolarize the membrane toward E_Na. The voltage-gated Na⁺ channels rapidly become inactivated to terminate the rising phase of the action potential; then voltage-gated K⁺ channels open to repolarize the membrane.
• The effects of depolarization on membrane permeability to ions can be studied at the level of single channels by patch clamp, and at the whole-cell level by voltage clamp.
• Ongoing investigations are clarifying the molecular structures of voltage-gated channels. The principal protein subunit of a K⁺ channel is a single chain with six transmembrane regions; a K⁺ channel consists of four of these protein subunits around a central pore. Na⁺ and Ca²⁺ channels consist of a single polypeptide chain with four similar domains; each domain corresponds to one of the four subunits of the K⁺ channel. Functional attributes of the channels can be localized to particular regions of the proteins.
• Nonspiking neurons do not generate action potentials, and the ionic mechanisms of action potentials in excitable cells can vary. Calcium ions can make substantial contributions to action potentials in cardiac muscle cells and in some neurons. Other varieties of voltage-gated channels modify the excitable properties of neurons.

The Propagation of Action Potentials

• Action potentials propagate because the membrane’s underlying permeabilities to ions are voltage-dependent. Local circuits of current flow spread the depolarization along the axon, depolarizing a new region to threshold. Behind an advancing action potential, Na⁺ channels remain inactivated long enough to prevent reexcitation by the local currents.
• The conduction velocity of an action potential depends on axon diameter, myelination, and temperature. Larger-diameter axons have higher conduction velocities because their length constants are longer, so local currents spread farther along the axon. Myelin greatly increases conduction velocity by increasing R_m (increasing the length constant) while decreasing C_m (preventing an increase in the time constant). Increasing temperature speeds the gating of channels so that the membrane responds faster to the local currents.

Copyright 2016 Sinauer Associates