Neurons are the central building blocks of the nervous system, 100 billion strong at birth. Like all cells, neurons consist of several different parts, each serving a specialized function (Figure 3.8). A neuron’s outer surface is made up of a semipermeable membrane. This membrane allows smaller molecules and molecules without an electrical charge to pass through it, while stopping larger or highly charged molecules. Figure 3.8 This illustration shows a prototypical neuron, which is being myelinated by a glial cell. The nucleus of the neuron is located in the soma, or cell body. The soma has branching extensions known as dendrites. The neuron is a small information processor, and dendrites serve as input sites where signals are received from other neurons. These signals are transmitted electrically across the soma and down a major extension from the soma known as the axon, which ends at multiple terminal buttons. The terminal buttons contain synaptic vesicles that house neurotransmitters, the chemical messengers of the nervous system. Axons range in length from a fraction of an inch to several feet. In some axons, glial cells form a fatty substance known as the myelin sheath, which coats the axon and acts as an insulator, increasing the speed at which the signal travels. The myelin sheath is not continuous and there are small gaps that occur down the length of the axon. These gaps in the myelin sheath are known as the Nodes of Ranvier. The myelin sheath is crucial for the normal operation of the neurons within the nervous system: the loss of the insulation it provides can be detrimental to normal function. To understand how this works, let’s consider an example. PKU, a genetic disorder discussed earlier, causes a reduction in myelin and abnormalities in white matter cortical and subcortical structures. The disorder is associated with a variety of issues including severe cognitive deficits, exaggerated reflexes, and seizures (Anderson & Leuzzi, 2010; Huttenlocher, 2000). Another disorder, multiple sclerosis (MS), an autoimmune disorder, involves a large-scale loss of the myelin sheath on axons throughout the nervous system. The resulting interference in the electrical signal prevents the quick transmittal of information by neurons and can lead to a number of symptoms, such as dizziness, fatigue, loss of motor control, and sexual dysfunction. While some treatments may help to modify the course of the disease and manage certain symptoms, there is currently no known cure for multiple sclerosis. In healthy individuals, the neuronal signal moves rapidly down the axon to the terminal buttons, where synaptic vesicles release neurotransmitters into the synaptic cleft (Figure 3.9). The synaptic cleft is a very small space between two neurons and is an important site where communication between neurons occurs. Once neurotransmitters are released into the synaptic cleft, they travel across it and bind with corresponding receptors on the dendrite of an adjacent neuron. Receptors, proteins on the cell surface where neurotransmitters attach, vary in shape, with different shapes “matching” different neurotransmitters. How does a neurotransmitter “know” which receptor to bind to? The neurotransmitter and the receptor have what is referred to as a lock-and-key relationship—specific neurotransmitters fit specific receptors similar to how a key fits a lock. The neurotransmitter binds to any receptor that it fits. Figure 3.9 (a) The synaptic cleft is the space between the terminal button of one neuron and the dendrite of another neuron. (b) In this pseudo-colored image from a scanning electron microscope, a terminal button (green) has been opened to reveal the synaptic vesicles (orange and blue) inside. Each vesicle contains about 10,000 neurotransmitter molecules. (credit b: modification of work by Tina Carvalho, NIH-NIGMS; scale-bar data from Matt Russell)