Development of the nervous system in the embryo begins with a series of divisions of precursor cells that can develop into neurons or glia. After the last cell division, each neuronal daughter cell differentiates, migrates to its final location, and sends out processes that will become its axon and dendrites. A specialized enlargement, the growth cone, forms the tip of each extending axon and is involved in finding the correct route and final target for the process.
As the axon grows, it is guided along the surfaces of other cells, most commonly glial cells. Which particular route is followed depends largely on attracting, supporting, deflecting, or inhibiting influences exerted by several types of molecules. Some of these molecules, such as cell adhesion molecules, reside on the membranes of the glia and embryonic neurons. Others are soluble neurotropic factors (growth factors for neural tissue) in the extracellular fluid surrounding the growth cone or its distant target.
Once the target of the advancing growth cone is reached, synapses are formed. The synapses are active, however, before their final maturation occurs, and this early activity, in part, determines their final use. During these intricate early stages of neural development, which occur during all trimesters of pregnancy and into infancy, alcohol and other drugs, radiation, malnutrition, and viruses can exert effects that cause permanent damage to the developing fetal nervous system.
A normal, although unexpected, aspect of development of the nervous system occurs after growth and projection of the axons. Many of the newly formed neurons and synapses degenerate. In fact, as many as 50 to 70 percent of neurons die by apoptosis in some regions of the developing nervous system! Exactly why this seemingly wasteful process occurs is unknown although neuroscientists speculate that in this way connectivity in the nervous system is refined, or "fine tuned."
Although the basic shape and location of existing neurons in the mature central nervous system do not change, the creation and removal of synaptic contacts begun during fetal development continue, albeit at a slower pace, throughout life as part of normal growth, learning, and aging. Division of neuron precursors is largely complete before birth, and after early infancy new neurons are formed at a slower pace to replace those that die.
Severed axons can repair themselves, however, and significant function regained, provided that the damage occurs outside the central nervous system and does not affect the neuron's cell body. After repairable injury, the axon segment now separated from the cell body degenerates. The proximal part of the axon (the stump still attached to the cell body) then gives rise to a growth cone, which grows out to the effector organ so that in some cases function is restored.
In contrast, severed axons within the central nervous system attempt sprouting, but no significant regeneration of the axon occurs across the damaged site, and there are no well-documented reports of significant function return. Either some basic difference of central nervous system neurons or some property of their environment, such as inhibitory factors associated with nearby glia, prevents their functional regeneration.
In humans, however, spinal injuries typically crush rather than cut the tissue, leaving the axons intact. In this case, a primary problem is self-destruction (apoptosis) of the nearby oligodendroglia, because when these cells die and their associated axons lose their myelin coat, the axons cannot transmit information effectively.
Researchers are attempting a variety of measures to provide an environment that will support axonal regeneration in the central nervous system. They are creating tubes to support regrowth of the severed axons, redirecting the axons to regions of the spinal cord that lack the growth-inhibiting factors, preventing apopto-sis of the oligodendrocytes so myelin can be maintained, and supplying neurotropic factors that support recovery of the damaged tissue.
PART TWO Biological Control Systems
Attempts are also being made to restore function to damaged or diseased brains by the implantation of precursor cells that will develop into new neurons that will replace missing neurotransmitters or neurotropic factors. Alternatively, pieces of fetal brain or tissues from the patient that produce the needed neurotransmitters or growth factors are implanted. For example, the adrenal medulla, which is part of the adrenal glands, synthesizes and secretes chemicals similar to some of the neurotransmitters found in the brain. When pieces of a patient's own adrenal medulla are inserted into damaged parts of the brain, the pieces continue to secrete these chemicals and provide the missing neurotransmitters.
We now turn to the mechanisms by which neurons and synapses function, beginning with the electrical properties that underlie all these events.
I. The basic unit of the nervous system is the nerve cell, or neuron. II. The cell body and dendrites receive information from other neurons. III. The axon (nerve fiber), which may be covered with sections of myelin separated by nodes of Ranvier, transmits information to other neurons or effector cells.
I. Neurons are classified in three ways:
b. Efferent neurons transmit information out of the CNS to effector cells.
II. Information is transmitted across a synapse by neurotransmitters, which are released by a presynaptic neuron and combine with receptors on a postsynaptic neuron.
I. The CNS also contains glial cells, which help regulate the extracellular fluid composition, sustain the neurons metabolically, form myelin, serve as guides for developing neurons, and provide immune functions.
Neural Growth and Regeneration
I. Neurons develop from precursor cells, migrate to their final location, and send out processes to their target cells.
II. Cell division to form new neurons is markedly slowed after birth.
III. After degeneration of a severed axon, damaged peripheral neurons may regrow the axon to their target organ. Damaged neurons of the CNS do not regenerate or restore significant function.
SECTION A KEY TERMS
central nervous system (CNS)
Schwann cell node of Ranvier axon transport afferent neuron efferent neuron interneuron sensory receptor nerve synapse presynaptic neuron postsynaptic neuron glial cell astroglia microglia neurotropic factor
1. Describe the direction of information flow through a neuron and also through a network consisting of afferent neurons, efferent neurons, and interneurons.
2. Contrast the two uses of the word "receptor."
Was this article helpful?
This guide will help millions of people understand this condition so that they can take control of their lives and make informed decisions. The ebook covers information on a vast number of different types of neuropathy. In addition, it will be a useful resource for their families, caregivers, and health care providers.