What are neurons in biological psychology?
In the latter part of the nineteenth century, there were two competing theoretical approaches toward explaining the composition of the brain. The reticular theory, championed by the Italian scientist Camillo Golgi , proposed that the brain consisted of a dense, netlike structure of nerve wires with no individual cells. The neuron doctrine, as advocated by the Spanish scientist Santiago Ramón y Cajal , asserted that the brain was composed of individual cells, just like other structures of the body, and that these cells were separated from one another by small gaps. The best microscopic views of that era could not provide evidence to determine which theory was correct, and a contentious debate ensued.
Ironically, it was a staining technique developed by Golgi in the late 1800s that enabled Ramón y Cajal eventually to demonstrate the existence of individual cells in the brain, confirming the neuron doctrine. Ramón y Cajal called these cells neurons, nerve cells that are specialized to receive information and electrochemically transmit it to other cells. In 1906, the gaps between these neurons were termed “synapses” by Charles Sherrington , who deduced many of the properties of synaptic functioning.
There are an estimated one trillion neurons in the human nervous system, with somewhere around one hundred billion in the brain. Neurons share many of the same features as other cells. For example, they are surrounded by a membrane, have a nucleus that contains the chromosomes, are provided metabolic energy by mitochondria, and synthesize proteins at sites called ribosomes. What makes neurons structurally different from other cells is a unique tripartite structure.
Most neurons contain a soma, many dendrites, and only one axon. The soma or cell body is a rounded swelling of the neuron that contains the cell nucleus. Electrical messages, also called impulses or action potentials, are collected in the soma, which, in turn, may cause the discharge of electricity to another cell.
Input to the soma usually comes from dendrites. Most neurons have many of these branching fibers whose surface is lined with receptors specialized to receive impulses. Some dendrites have small outgrowths called spines, which increase the places available for connection to other cells.
The axon is a thin fiber, usually longer than the dendrites, that is specialized to send messages from the soma to other cells. Axons have many branches, each of which enlarges at the tip, forming the terminal end bulb. It is from this end bulb that chemicals are released into the synaptic cleft (gap).
Neurons can be distinguished from one another in several ways. Axonal length is long in projection neurons, but short or even absent in local neurons. The function of neurons is different in sensory neurons, which are specialized to detect physical information from the environment, and in motor neurons, which are specialized to activate muscles and glands. A third function of neurons, found in interneurons, is to communicate only with other neurons. The direction of the neural impulse is toward a structure in afferents, away from a structure in efferents, and within a structure in intrinsic neurons. Finally, neurons can be distinguished on the basis of polar dimensions. Unipolar neurons carry a message in one direction only, bipolar neurons convey an impulse in two directions, and multipolar neurons can transmit information in many directions.
Each neuron has the capability of producing an electrical charge called the resting potential. Neurons in their resting (nondischarging) state generate voltage by creating an imbalance of positive (sodium, potassium, and calcium) and negative (chloride) electrically charged particles called ions. Four factors contribute to this ion imbalance between the inside and the outside of the neuron’s membrane. First, the membranes of neurons have small gaps in them called ion channels. Potassium and chloride ions pass through these channels more readily than sodium ions, resulting in more negative ions on the inside of the neuron than on the outside. Second, the sodium-potassium pump forces three sodium ions out of the neuron for every two potassium ions allowed inside the cell, resulting in less positively charged ions inside the neuron. Third, proteins on the inside of the neuron carry a negative charge. Finally, the gradient balance between entropy—ions will move toward a place of less density—and enthalpy—ions will move toward a place of opposite electrical charge—results in a further negatively charged environment inside the neurons. Combining these four factors together yields approximately a −70 millivolt resting potential for each neuron. In other words, the neuron is like a battery that carries a charge of −70 millivolts.
Stimulation from the environment or other neurons can disturb the balance that creates the neuron’s resting potential and produce a reversal of electrical polarity that leads the neuron to discharge an electrical impulse. This process is called the action potential and occurs in three phases. The first phase begins with a depolarization—a reduction of the electrical charge toward zero—of the neuron. When this depolarization is sufficient to cause the neuron to be approximately 10 to 15 millivolts less negative, the threshold of excitation is reached and the sodium ion gates, responding to the voltage change, will be opened. This results in a sudden influx of positively charged ions resulting in a reversal of polarity. One millisecond after the sodium gates open, they immediately shut, cutting off the sodium influx, and the gates cannot be opened for another millisecond or so, ending the first phase of the process.
The second phase begins with the opening of the potassium ion channels. Because the inside of the neuron is now positively charged and dense with potassium ions, the positively charged potassium ions flow out of the neuron. Unlike the sodium gates, the potassium gates do not snap shut quickly, and this results in fewer potassium ions inside the neuron than during the resting state. The net effect is that the second phase produces a hyperpolarization, which means that the neuron has an increased charge of approximately −110 millivolts.
In the third phase, the sodium and potassium gates return to their normal conditions, restoring the ion flow conditions that create the resting potential. As a result of the action potential, slightly more sodium ions and slightly fewer potassium ions are found in the neuron at the beginning of the third phase. The sodium-potassium pump eventually corrects this small imbalance and restores the original resting potential conditions.
Between the peak of the action potential and the restoration of the resting potential, the neuron resists generating an action potential. This resistance of refractory period is first absolute—it is impossible for an action potential to occur—and then relative—action potentials can happen, but require stronger-than-normal stimulation.
In motor neurons, but not all interneurons or sensory neurons, the action potential begins where the axon exits the soma, a place called the axon hillock. Basically, each point along the axon regenerates the sodium-ion influx as it travels down the axon like a ripple caused by throwing a stone in a pond. Because the sodium-ion gates snap shut shortly after they open, the action potential will not travel back to the soma and the impulse is ensured to move toward the synapse. Unlike the small ripple on the pond, the traveling wave down the axon does not diminish in size or velocity and is independent of the size of the stimulus that generates it. This axonal (not dendritic or somatic) phenomenon is called the all-or-none law.
The speed of the impulse down the axon is affected by two factors. First, the larger the diameter of the axons, the more rapidly the impulse is transmitted. Second, many axons are covered with an insulating material called myelin. In myelinated axons, neural impulses “jump” from one break in the myelin sheath—called a node of Ranvier—to another break, resulting in conduction speeds of up to 270 miles per hour. This node-to-node jumping, called saltatory conduction, is much faster than conduction in unmyelinated axons, which produces speeds of only 2 to 22 miles per hour.
Because a small gap separates one neuron from another, the traveling electrical charge down the axon cannot affect the next neuron electrically: The “wire” is cut. What allows the gap to be bridged is a chemical process that can be described as a sequence that begins with presynaptic events (what occurs in the sending neuron) and ends with postsynaptic events (what occurs in the receiving neuron).
Presynaptically, when the action potential reaches the terminal end bulb, it opens ion channels for calcium ions that then enter the axon. Calcium activates tiny bubbles called vesicles, which contain chemicals called neurotransmitters. The neurotransmitters are chemicals synthesized in the somas of sending neurons that will cause changes in receiving neurons. The activated vesicles will then excrete neurotransmitters into the synaptic cleft. These chemicals will diffuse across the cleft to the postsynaptic neuron. The total process takes approximately two milliseconds.
Postsynaptically, neurotransmitters attach to places on the receiving neuron called receptors. Different receptors are specialized to pick up different kinds of neurotransmitters. Additionally, most of the many kinds of neurotransmitters will have several different types of receptors with which they can interact. Once the neurotransmitter activates the receptor, it may have an excitatory effect, making the postsynaptic cell more likely to produce an impulse, or an inhibitory effect, making the receiving neuron less likely to generate an action potential. Although most neurotransmitters are predominantly excitatory or inhibitory, the ultimate effect of the neurotransmitter depends on the particular receptor. Furthermore, neurotransmitters can alter the activity of the postsynaptic neuron iontropically, by opening ion gates (a quick but brief process), or metabotropically, by initiating metabolic changes (a slow but long-lasting process). Neurotransmitters that do not bind to receptors are usually reabsorbed into the presynaptic neuron or enzymatically broken down, thereby preventing overactivity of the postsynaptic neuron.
Most neurons are on the receiving end of input from many other neurons. How often a synapse is activated (temporal summation), how many innervating synapses are activated (spatial summation), what neurotramsitters are released, and what receptors are involved all combine to determine whether a neuron will produce an action potential.
The synaptic network that links neurons is a dynamic system that is highly responsive to the organism’s experience. The more synapses are stimulated, the more efficient they become in their activity. Furthermore, repeated synaptic stimulation increases the number of synapses and induces dendritic branching. This phenomenon, called long-term potentiation, is the neuronal substrate of learning. Long-term potentiation is one reason that those who frequently engage in intellectually stimulating habits, such as reading, develop denser brains than less intellectually stimulated individuals. In other words, an active mind makes for a better brain.
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