Key Concepts
     1. Like other cells of the body, neurons at rest exhibit an electrical potential across the cell membrane.
     2. This resting potential is the consequence of the differential concentrations of ions inside and outside the neuron, and the semipermeable nature of the membrane. The membrane is primarily permeable to potassium ions, and when equilibrium is reached between the diffusion pressure forcing potassium out of the cells and the electrostatic pressure forcing potassium into the cell, the resting membrane potential is about ?70 mV.
     3. Neurons must actively maintain this ion balance, due to the gradual leakage of ions across the membrane.
     4. Perturbations of the resting potential that cause it to become more negative, or hyperpolarized, reduce the probability that a nerve impulse will be produced. Perturbations that depolarize the membrane increase the probability that a nerve impulse will be produced. Such perturbations spread passively from the site of stimulation, decreasing with time and distance.
     5. Depolarizations that exceed an individual neuron’s threshold will cause the production of a nerve impulse, or action potential, in the axon. The action potential has an amplitude of about 100 mV and is generated in an all-or-none fashion—its size is independent of stimulus magnitude.
     6. For a brief period of time after producing an action potential, the axonal membrane is completely insensitive to further stimuli; this is called the absolute refractory phase. This phase is immediately followed by a brief period of reduced sensitivity called the relative refractory phase.
     7. During the peak of the action potential, the membrane potential approaches +40 mV, due to sodium permeability that results from the opening of gated sodium channels. These channels close rapidly and the resting potential is restored.
     8. Gating currents are tiny electrical currents across the cell membrane that induce voltage-gated channels to open. The gated sodium channels of the axonal membrane are voltage-gated. These channels contain an activation gate, which opens as a consequence of depolarization, and an inactivation gate that closes slowly with depolarization. In the resting state, the activation gate is closed, and the inactivation gate is open.
     9. Cell bodies and dendrites contain few voltage-gated ion channels and thus cannot propagate action potentials.
     10. The structure and function of ion channels has been studied using molecular genetic approaches, the use of toxins, and the patch-clamp technique, in which individual channels may be studied in isolation.
     11. Action potentials arise at the axon hillock and spread down the axon through a regenerative process at speeds ranging from 1 to 120 m/s. Conduction velocity is increased in axons with large diameters, and particularly in axons that are myelinated. In the latter case, the action potential jumps between nodes of Ranvier; this is called saltatory conduction.
     12. The arrival of an action potential at the axon terminals of a presynaptic neuron, and the subsequent release of neurotransmitter, results in a small graded depolarization (excitatory postsynaptic potential; EPSP) or graded hyperpolarization (inhibitory postsynaptic potential; IPSP) of the membrane of the postsynaptic cell (depending on whether the presynaptic cell is excitatory or inhibitory, respectively). If enough EPSPs are received, the postsynaptic cell’s threshold is reached and an action potential is produced.
     13. The IPSPs and EPSPs produced in a postsynaptic neuron sum temporally and spatially. If relatively more and/or greater EPSPs occur, the cell’s threshold is exceeded at the axon hillock and an action potential is generated. This integration is the basis of information processing by the neuron.
     14. At chemical synapses, the arrival of an action potential causes voltage-gated calcium channels to open in the membrane of the axon terminal. Calcium influx induces vesicles to fuse to the synaptic membrane and release transmitter; the amount released is proportional to the size of the calcium current.
     15. Transmitter diffuses across the synaptic cleft, binds to receptors, and alters the permeability of the postsynaptic membrane, resulting in a change in membrane potential. The action of the transmitter is stopped rapidly, either by chemical inactivation or reuptake.
     16. Transmitter receptors operate like a lock and key; a particular transmitter “key” may open several different types of receptor “locks” (receptor subtypes).
     17. Ionotropic receptors are ligand-gated ion channels. Metabotropic receptors involve the liberation of chemical second messengers, which may have numerous effects within the cell.
     18. Some synapses are electrical, rather than chemical, and provide a direct electrical coupling between neurons.
     19. Neurons accomplish complex information processing by acting together in circuits, such as neural chains, feedback circuits, and oscillator circuits.
     20. The electrical activity of populations of neurons can be measured using scalp electrodes. EEG measures spontaneous electrical activity, whereas ERPs reflect the reaction of populations of neurons to discrete stimuli. Both techniques have important diagnostic applications (such as in epilepsy [EEG] and auditory testing [ERP]), as well as applications in basic research (such as sleep research [EEG] and studies of cognitive processing [ERP]).
     21. Future research is likely to focus on combining data on electrical activity with spatial coordinates within the brain to produce three-dimensional activity maps—this is being accomplished with techniques such as BEAM, combinations of ERPs and fMRI, and a new technique that uses light scattering through the skull to detect changes in blood flow and electrical activity.
     22. Under some circumstances, the electrical activity of large populations of neurons may become synchronized, resulting in seizures. The behavioral characteristics of the seizures depend on the site at which the seizures originate and the degree to which the seizure activity spreads to other regions of the brain.