The composition of the extracellular fluid that surrounds CNS neurons is carefully regulated to protect them from extreme variations. One of the ways this is achieved is through the presence of the blood-brain barrier, which restricts the movement of large molecules and highly charged ions from the blood into the brain and spinal cord. Capillary endothelial cells and tight junctions play a role in this barrier function, and astrocytes also help limit the movement of certain substances. Additionally, glia cells provide buffering functions, regulate CNS circulation, and facilitate the exchange of substances between the cerebrospinal fluid and extracellular fluid of the CNS. Some pharmaceutical agents, such as penicillin, can be removed from the CNS through transport mechanisms.

When nervous tissue is injured, neurons and glia respond to the injury. Severe injury can lead to cell death, and once a neuron is lost, it cannot be replaced in most cases. However, there are exceptions to this, such as olfactory bulb and hippocampal neurons in animals. In humans, significant levels of neurogenesis in the adult CNS have only been found in the hippocampus.

When an axon is transected, the soma of the neuron may undergo chromatolysis, also known as "axonal reaction." This process involves the neuron attempting to repair the axon by producing new structural proteins. The rough endoplasmic reticulum becomes filled with the products of protein synthesis, causing disorganization of the ribosomes and weak staining of Nissl bodies by basic aniline dyes. The soma may also swell, become rounded, and the nucleus may shift to an eccentric position. These morphological changes reflect the cytological processes associated with increased protein synthesis.

Since the axon cannot synthesize new protein, the distal part of the axon beyond the transection site eventually dies. Within a few days, the axon and its synaptic endings disintegrate. In the CNS, if the axon was myelinated, the myelin sheath will fragment and be removed by phagocytosis. However, in the peripheral nervous system, the Schwann cells that formed the myelin sheath remain viable and can undergo cell division. This sequence of events is known as wallerian degeneration, named after the scientist Waller who first described it.
The local environment of most CNS neurons is controlled such that neurons are normally protected from extreme variations in the composition of the extracellular fluid that bathes them. Part of this control is provided by the presence of a blood-brain barrier (other mechanisms are the buffering functions of glia, regulation of CNS circulation, and exchange of substances between the CSF and extracellular fluid of the CNS). Movement of large molecules and highly charged ions from blood into the brain and spinal cord is severely restricted. The restriction is at least partly due to the barrier action of the capillary endothelial cells of the CNS and the tight junctions between them. Astrocytes may also help limit the movement of certain substances. For example, astrocytes can take up potassium ions and thus regulate [K+] in the extracellular space. Some pharmaceutical agents, such as penicillin, are removed from the CNS by transport mechanisms.
Nervous Tissue Reactions to Injury
Injury to nervous tissue elicits responses by neurons and glia. Severe injury causes cell death. Except in specific instances, once a neuron is lost it cannot be replaced because, in general,
CHAPTER 4 The Nervous System: Introduction to Cells and Systems 63
The blood-brain barrier can be disrupted by pathology of the brain. For example, brain tumors may allow substances that are otherwise excluded to enter the brain from the circulation. Radiologists can exploit this by introducing a substance into the circulation that normally cannot penetrate the blood-brain barrier. If the substance can be imaged, its leakage into the region occupied by the brain tumor can be used to demonstrate the distribution of the tumor.
neurons are postmitotic cells. In animals, two exceptions are olfactory bulb and hippocampal neurons; however, in humans, only for the hippocampus has evidence been found for significant levels of neurogenesis in the adult CNS.
When an axon is transected, the soma of the neuron may show chromatolysis, or “axonal reaction.” Normally, Nissl bodies stain well with basic aniline dyes, which attach to the RNA of ribosomes (
Fig. 4.10A ). After injury to the
Fig. 4.10B), the neuron attempts to repair the axon by making new structural proteins, and the cisterns of the rough endoplasmic reticulum become distended with the products of protein synthesis. The ribosomes appear to be disorganized, and the Nissl bodies are stained weakly by basic aniline dyes. This process, called chromatolysis, alters the staining pattern (see
Fig. 4.10C ). In addition, the soma may swell and become rounded, and the nucleus may assume an eccentric position. These morphological changes reflect the cytological processes that accompany increased protein synthesis.
Because it cannot synthesize new protein, the axon distal to the transection dies (see
Fig. 4.10C ). Within a few days the axon and all the associated synaptic endings disintegrate. If the axon had been a myelinated axon in the CNS, the myelin sheath would also fragment and eventually be removed by phagocytosis. However, in the PNS the Schwann cells that had formed the myelin sheath remain viable, and in fact they undergo cell division. This sequence of events was originally described by Waller and is called wallerian degeneration.