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Carrageenin-induced pedal inflammation in rats, was found to significantly enhance brain levels of prostaglandin (PG) E2 and PGF2α. PG levels increased after 30 min of induction of the inflammation, peaked at 1 h, and attained normal levels by 4 h. Bilateral adrenalectomy had little effect on carrageenin-induced increase in rat brain PGs. The pattern of elevation of central PGs and the time course of carrageenin inflammation were at variance, the latter peaking between 3 and 4 h. The findings lend credence to the postulate that inflammatory hyperalgesia involves participation of central pain circuits, and that fever accompanying inflammation is caused by the central release of PGs. The central nociceptive and hyperthermic actions of PGs are well documented. However, the increase in central PG levels may well be caused by stress induced by the peripheral inflammation, since the pattern of elevation in either case is qualitatively similar.

The frog dorsal root provides a useful model for the study of axonal regeneration in an adult vertebrate CNS. We have used the model to compare the regeneration of two very different types of axons within the same CNS environment and have found that regenerating dorsal root, as well as rerouted motoneuron axons, display similar growth patterns in the spinal cord. Both sensory and motor axons grow preferentially in some regions and not in others. They both regenerate effectively longitudinally as well as radially within the dorsolateral fasciculus (DLF). By contrast, fewer sensory and motor axons regenerate longitudinally or radially in the dorsal funiculus (DF). This similar preferential growth of two very different populations of axons suggests that the growth patterns reflect regional differences in the cellular environment of the cord. The DLF has fascicles of unmyelinated axons separated by radial glial processes and, after dorsal root injury, is mildly gliotic. By contrast, DF has very large myelinated axons, which widely separate the radial glial processes that traverse the region. After dorsal root injury, this region is markedly gliotic and contains myelin, debris and oligodendroglia, and microglial macrophages. Our data suggest that unmyelinated axons and radial glial processes are more preferred substrates for axonal growth than myelin debris, oligodendroglia and macrophages. It is not surprising, then, that regions of the adult mammalian CNS that are characterized by large myelinated axons fail to support axonal growth. Moreover, there is some evidence that regions of the adult mammalian CNS that are characterized by unmyelinated axons support axonal growth.

The patient was a 31-yr-old white male who developed behavioral abnormalities 6 months prior to death. He became progressively lethargic, socially withdrawn and somnolent. Over the 2 months prior to death his memory worsened, he exhibited an increasingly stumbling gait, and he developed multiple cranial nerve deficits. he became comatose, developed respiratory insufficiency, and died. The brain had gross and microscopic appearances consistent with a sudanophilic leukodystrophy. No specific intracellular inclusions were seen with electron microscopy. Water, total lipid, neutral lipid, phospholipid, cholesterol, and cholesterol ester contents of cerebral cortex were all normal. Levels of galactolipid and phospholipid were much lower than normal in affected white matter, but it contained almost three times the normal amount of neutral lipid. Cholesterol esters made up 75% of the total sterol in white matter, but very long chain fatty acids were not seen in this fraction. This case probably represents a type of sudanophilic leukodystrophy in which cholesterol esters accumulate in white matter to degrees not previously reported for other conditions.

Experimental allergic encephalomyelitis (EAE), accompanied by demyelinating central nervous system (CNS) lesions, can be induced in guinea pigs sensitized with whole guinea pig CNS tissue, but not in animals sensitized with purified myelin basic protein (BP). This type of chronic demyelinating EAE is presumably a result of a combination of a cell-mediated immune response to the encephalitogenic BP and a separate response to other nonencephalitogenic CNS antigens. We report here that demyelinating EAE can be induced when separate sensitizations are used to induce a cell-mediated response to BP and a second immune response to nonencephalitogenic CNS antigens. Animals sensitized in separate sites with guinea pig BP and whole chicken brain develop CNS demyelinating lesions. Animals sensitized only to BP or chicken brain do not develop demyelination. The antigen(s) responsible for demyelination are found in the myelin fraction of chicken brain.