Figure 1132

Schematic drawing of blood-brain barrier. This drawing shows the blood-brain barrier, which consists of endothelial cells joined together by elaborate, complex tight junctions, endothelial basement membrane, and the end foot processes of astrocytes.

lamina (Fig. 11.32). The tight junctions eliminate gaps between endothelial cells and prevent simple diffusion of solutes and fluid into the neural tissue.

Evidence suggests that the tight junction depends on the normal functioning of the astrocyte. In several brain diseases, the blood-brain barrier loses effectiveness. Examination of brain tissue in these conditions by TEM reveals loss of the tight junctions as well as alterations in the morphology of the astrocytes. Other experimental evidence has revealed that astrocytes release soluble factors that increase barrier properties and tight junction protein content.

The presence of only a few small vesicles indicates that pinocytosis across the brain endothelial cells is severely restricted. The substances that do cross the capillary wall are actively transported by specific receptor-mediated endocy-tosis. Thus, the low permeability of the blood-brain barrier to macromolecules is due to a low level of expression of specific receptors on the endothelial cell surface.

Substances that are required for neuronal integrity must leave and enter the blood capillaries through the endothelial cells. Thus, certain lipid-soluble molecules as well as 02 and C02 easily penetrate the endothelial cell. Other substances such as glucose (which the neuron depends on almost exclusively for energy), amino acids, nucleosides, and vitamins are actively transported by specific transmembrane carrier proteins. In addition, several other proteins that reside within the plasma membrane of the endothelial cells protect the brain by rejecting drugs, foreign proteins, and other disruptive molecules from crossing the barrier.

Recent studies indicate that the end feet of astrocytes also play an important role in maintaining water homeostasis in brain tissue. Water channels (aquaporin AQP4) are found in end feet processes where water crosses the blood-brain barrier. In pathologic conditions such as brain edema, these channels play a key role in reestablishing osmotic equilibrium in the brain.

Some parts of the CNS, however, are not isolated from substances carried in the bloodstream. The barrier is ineffective or absent in the neurohypophysis (posterior pituitary), substantia nigra, and locus ceruleus. In these areas of the brain, sampling of materials circulating in the blood may be necessary to regulate neurosecretory control of parts of the nervous system and of the endocrine system.

v response of neurons to injury

Degeneration

The portion of a nerve fiber distal to a site of injury degenerates because of interrupted axonal transport

Degeneration of an axon distal to a site of injury is called anterograde (Wallerian) degeneration. In the PNS, the axon distal to the injury becomes beaded and frag ments into discontinuous segments within a few days (Fig. 11.33, a and b). In the CNS, breakdown of the isolated axon segments takes several weeks.

The myelin sheath also fragments, and the myelin fragments enclose the axon fragments. Phagocytotic cells, derived from the Schwann cells in the PNS, microglia in the CNS, and blood monocytes that migrate to the site of injury, remove the myelin and axon fragments. Some retrograde degeneration also occurs but extends for only a few internodal segments. In the PNS, the Schwann cells and their external laminae remain as tubular structures distal to the injury (Fig. 11.33c).

served within 1 to 2 days after injury and reaches a peak at about 2 weeks (Fig. 11.33b). The changes in the cell body are proportional to the amount of axoplasm lost by the injury; extensive loss of axoplasm can lead to death of the cell. When a motor fiber is cut, the muscle innervated by that fiber undergoes atrophy (Fig. 11.33c).

Before the development of modern dye and radioisotope tracer techniques, Wallerian degeneration and chromatoly-sis were used as research tools. These tools allowed researchers to trace the pathways and destination of axons and the localization of the cell bodies of experimentally injured nerves.

The cell body of an injured nerve swells, its nucleus moves peripherally, and there is loss of Nissl substance

Nerve injury leads to a loss of Nissl substance from the cell body, called chromatolysis. Chromatolysis is first ob

Scar Formation

In the PNS, connective tissue and Schwann cells form scar tissue in the gap between the ends of a severed or crushed nerve. If the amount of scar tissue is not too great or if sur-

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