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Brain slices were prepared from 17‐day old rats, and incubated with [3H]glycine or [3H]‐leucine to label proteins. Myelin was isolated from the slices, and the proteins were separated by discontinuous gel electrophoresis in buffers containing sodium dodecyl sulfate. Radioactive basic and Wolfgram proteins appeared in myelin at similar initial rates, and their entry was nearly linear between 15 and 120 min with no detectable lag. Radioactive proteolipid protein appeared in myelin at one‐fourth the rate of the basic and Wolfgram proteins between 0 and 30 min, then entered at a rate comparable to the other proteins between 45 and 120 min. When cycloheximide (0.2 mM) or puromycin (1.0 mM) was added, appearance of newly labeled basic and Wolfgram proteins in myelin stopped while proteolipid protein continued to appear in myelin at a normal rate for at least 30 min. Chase experiments with unlabeled glycine had similar effects. These results indicate the existence of a previously synthesized precursor pool of proteolipid protein with a 30‐min interval between synthesis of proteolipid protein and its appearance in myelin. Incorporation of [3H]fucose into glycoprotein of the myelin sheath was studied, as was inhibition of incorporation of radioactivity by the use of either cycloheximide, or dilution with unlabeled fucose. The results indicated fucosylation of a sizable pool of presynthesized protein and a delay of 30 min between fucosylation of these polypeptides and their subsequent appearance in myelin as glycoproteins.

The neurons of the nucleus centrum medianum and the neurons of the nucleus parafascicularis were studied in Golgi preparations of the adult monkey (Macaca mulatta). The cell bodies of the prinicipal neurons in the nucleus centrum medianum have a few somatic spines and vary in shape: some are cubical with protruding angles; some are egg-shaped; some are elongated and sausage-shaped. Four to six slightly branched dendrites of unequal thickness radiate from the cell body. Some dendrites extend for nearly 500 microns; all have dendritic spines. In the nucleus parafascicularis there are two varieties of principal neurons: (1) neurons with somatic spines and (2) neurons without somatic spines. The neurons with somatic spines are most numerous. They have polygonal-shaped cell bodies, prominent somatic spines and processes, larger than spines but considerably smaller than dendrites. These processes bear spines and are designated here "microdendrites." Spines and occasionally a "microdendrite" are found on the axon-hillocks. Five to six dendrites of unequal thickness emerge from the cell bodies. Some extend for more than 500 microns; all have prominent dendritic spines. The neurons without somatic spines are relatively few. Usually three exceptionally long, slightly branched dendrites, one apical and two basal, emerge from their elongated, slim cell bodies. Some dendrites extend for more than 800 microns; all have few scattered spines. The Golgi type II neurons found in both of these intralaminar nuclei have small cell bodies and a few, relatively long, undulating dendrites, which bear bulbous dendritic appendages and beaded axon-like processes. Distally on these dendrites, where the appendages and processes are more numerous, the dendritic appendages and axon-like processes form complex entanglements. Distally on these dendrites, where the appendages and processes are more numerous, the dendritic appendages and axon-like processes form complex entanglements. Beaded axons are found on some but not all of the cell bodies. Morphologically these neurons resemble the local interneurons that have been described in various thalamic nuclei.

We have developed and tested a rat (Wistar) model of moderate concussion. Concussion is produced by controlled and repeatable mechanical fixed, closed-head injury. Moderate concussion in this model is characterized by 4 to 10 minutes of unconsciousness, absence of skull fractures or brain contusions, and few, if any, acute neurologic symptoms. By 2 hours postinjury, the subsequent trauma is further characterized by regional and global increases in cerebrovascular permeability and decreases in cerebral blood flow. Such changes are accompanied by brain swelling and two phases of elevated intracranial pressure; one lasting about 5 hours with a peak of about 10 mmHg, the other lasting more than 3 days postinjury with a peak of about 30 mmHg. Regional neurohistologic damage detected between 3 and 4 days postinjury correlates for the most part with earlier changes in regional permeability and blood flow. Significant morphologic changes which are characterized by patchy neuronal degeneration can be found in numerous forebrain locations, particularly in the frontal (coup) and entorhinal (contre coup) cortices. These observations have important parallels in human head trauma and suggest that this reliable physiological model may be a useful, relatively simple and inexpensive tool for investigating the mechanisms and therapeutics of head trauma.