The electroencephalogram (EEG) records electrical activity of the cerebral cortex via electrodes placed on the skull. The EEG waves originate from alternating excitatory and inhibitory synaptic potentials that produce sufficient extracellular current flow across the cortex to be detected by surface electrodes. (EEG waves are not action potentials. Electrodes on the surface of the skull are not sufficiently sensitive to detect the small voltage changes of single action potentials.)
The normal EEG (Fig. 3-37) comprises waves with various amplitudes and frequencies. In a normal, awake adult with eyes open, the dominant frequency recorded over the parietal and occipital lobes is the beta rhythm (13–30 Hz), which consists of desynchronous low-voltage, high-frequency waves. With eyes closed, the dominant frequency is the alpha rhythm (8–13 Hz), which has more synchronous waves of higher voltage and lower frequency.
Figure 3–37 Electroencephalogram of an awake subject and of subjects in Stages 1, 2, 4, and REM sleep.
As a person falls asleep, he or she passes through four stages of slow-wave sleep. In Stage 1, the alpha waves seen in an awake adult with eyes closed are interspersed with lower-frequency theta waves. In Stage 2, these low-frequency waves are interspersed with high-frequency bursts called sleep spindles and large, slow potentials called K complexes. In Stage 3 (not shown in the figure), there are very low-frequency delta waves and occasional sleep spindles. Stage 4 is characterized by delta waves. Approximately every 90 minutes, the slow-wave sleep pattern changes to rapid eye movement (REM) sleep, in which the EEG becomes desynchronized, with low-voltage, high-frequency waves that resemble those in an awake person. REM sleep is sometimes called paradoxical sleep: Even though the EEG is most similar to that of the awake state, the person is (paradoxically) most difficult to awaken. REM sleep is characterized by loss of muscle tone, notably in the eye muscles resulting in rapid eye movements, loss of temperature regulation, pupillary constriction, penile erection, and fluctuations in heart rate, blood pressure, and respiration. Most dreams occur during REM sleep. The proportion of slow-wave sleep and REM sleep varies over the life span. Newborns spend half of their sleep in REM sleep; young adults spend about 25% of sleep in REM sleep; and the elderly have little REM sleep.
Learning and Memory
Learning and memory are higher-level functions of the nervous system. Learning is the neural mechanism by which a person changes his or her behavior as a result of experiences. Memory is the mechanism for storing what is learned.
Learning is categorized as either nonassociative or associative. In nonassociative learning, exemplified by habituation, a repeated stimulus causes a response, but that response gradually diminishes as it is “learned” that the stimulus is not important. For example, a newcomer to New York City may be awakened at first by street noises, but eventually the noises will be ignored as it is learned they are not relevant. The opposite of habituation is sensitization, where a stimulus results in a greater probability of a subsequent response when it is learned that the stimulus is important. In associative learning, there is a consistent relationship in the timing of stimuli. In classic conditioning, there is a temporal relationship between a conditioned stimulus and an unconditioned stimulus that elicits an unlearned response. When the combination is repeated, provided the temporal relationship is maintained, the association is learned; once learned (e.g., by Pavlov’s dog), the stimulus alone (e.g., the bell) elicits the unlearned response (e.g., salivation). In operant conditioning, the response to a stimulus is reinforced, either positively or negatively, causing the probability of a response to change.
Synaptic plasticity is the fundamental mechanism that underlies learning. That is, synaptic function is variable and depends on the prior level of activity or “traffic” through the synapse. The responsiveness of postsynaptic neurons (called synaptic strength) is not fixed, but rather depends on the previous level of synaptic traffic. For example, in the phenomenon of potentiation, repeated activation of a neuronal pathway leads to increased responsiveness of the postsynaptic neurons in that pathway. The period of enhanced responsiveness may be brief, lasting for only milliseconds, or it may last for days or weeks (i.e., long-term potentiation). Conversely, in habituation, increased synaptic activity causes decreased responsiveness of the postsynaptic neuron.
The mechanism of long-term potentiation involves synaptic pathways that use the excitatory neurotransmitter glutamate and its N-methyl-D-aspartate (NMDA) receptor. When the presynaptic neurons are activated, they release glutamate, which diffuses across the synapse and activates NMDA receptors on the postsynaptic membranes. The NMDA receptors are ligand-gated ion Ca2+ channels that, when open, allow Ca2+ to enter the postsynaptic cells. With high-frequency stimulation (increased activity of the pathway), more Ca2+ accumulates in the postsynaptic cells; the higher intracellular Ca2+ concentration leads to an increase in protein kinase activity and, by mechanisms that are not fully understood, increased responsiveness of those synapses.