Marked differences in extent of diffusion have been shown with the fluorescence histochemical method between guanethidine and 6-OHDA(64 mug in 2 mul) when injected acutely or chronically into the lateral hypothalamus, the substantia nigra or the amygdala of the rat brain. Cannulation damage up to 1 mm in diameter and attributed to the implantation of cannulae and placebo injection was observed. A further area of generalized damage occurred following the injection of drugs and was far greater for 6-OHDA (2 mm) than for guanethidien (0.3 mm). Guanethidine, but not 6-OHDA, caused specific damage to catecholamine-containing nerurons up to a distance of at least 3 mm and more from the cannula tip. These striking differences between the effects of intracranial injection of 6-OHDA and guanethidine are discussed in terms of the uptake and degradation of the two drugs and the anatomical features of the injection site; they are not explicable in terms of experimental conditions such as concentration, volume of injection, molecular weight or lipid solubility. The different patterns of damage would not easily be distinguished by biochemical analyses and the catecholamine specificity of 6-OHDA in studies of the central nervous system must be seriously questioned. Vascularization of chronically implanted cannula tracks and the presence of anatomical diffusion barriers are also discussed in relation to the diffusion of drugs injected intracranially.

Amygdala↗

PubMedDate not supplied

Primary demyelination in cat optic nerves associated with surgically induced axonal degeneration.

Localized Wallerian degeneration was induced in cat optic nerves by the gentle scratching of the exposed retinas. At intervals ranging up to 103 days after operation, the cats were killed and microscopic examination of the optic nerves showed, in addition to axonal degeneration, the presence of both demyelinating and demyelinated normal axons. The tongues of oligodendroglial cytoplasm were still associated with these demyelinated axons. This phenomenon is considered to reflect a change in the homeostasis of the oligodendroglial cell imposed by degeneration of a few axons from a state of maintaining the myelin sheath to one of resorption from adjacent normal axons. No evidence for the involvement of microglia in this process was found. It is concluded also that oligodendrocytes alone can be responsible for the removal of myelin debris during Wallerian degeneragion. This observation may be important to the understanding of certain demyelinating diseases of the central nervous system.

Animals↗

PubMedDate not supplied

Observations on focal demyelinating lesions in cat optic nerves.

A demyelinating perivascular condition has been observed in the optic nerves of three cats, the lesions of which included the following features: thinly myelinated and demyelinated axons, few normal oligodendrocytes, astroglial scar tissue, lymphocytes, plasma cells, mononuclear phagocytic cells and lipid-laden cells. Also present were tubular inclusion bodies which had morphological features similar to the nucleocapsids of some paramyxoviruses. These lesions are compared with some other demyelinating diseases of the central nervous system, and similarities to the lesions of multiple sclerosis are suggested.

Animals↗

PubMedDate not supplied

Changes in nervous tissue in bovine generalized glycogenosis type II.

Generalized Glycogenosis type II has been diagnosed in seven calves from a herd of cattle maintained at the Murdoch University Veterinary School Farm. The syndromes seen are equivalent to the infantile and childhood forms of the disease in humans. In the brain and spinal cord of the calves acid alpha-glucosidase activity was depressed and glycogen deposition was markedly increased. Swelling, vacuolation and glycogen deposition was present in neurones of the central and autonomic nervous systems and retina, in glia and in Schwann cells and fibroblasts within peripheral nerves. The distribution was similar to that seen in human cases. The glycogen was both membrane bound and free within the cytoplasm. Changes similar to those seen in axonal dystrophy were present and some nerve fibres showed Wallerian degeneration. Evidence of nerve cell destruction and nerve cell loss were not seen and the predominant clinical signs were related to muscle weakness.

Animals↗

PubMedDate not supplied

The effect of age on biochemical and morphological changes in the semitendinosus muscle of cattle with generalized glycogenosis type II.

Progressive changes in acid alpha-glucosidase activity, glycogen content and light microscopical and ultrastructural features in skeletal muscle of calves affected by generalized glycogenosis type II were assessed in biopsies from semitendinosus muscle of nine affected, twenty-six carrier and fifteen normal calves taken at varying times between birth and 17 months of age. Affected animals could be identified by using the PAS technique on paraffin and epon embedded material or by electron microscopy. However, estimation of acid alpha-glucosidase activity was required for precise diagnosis of generalized glycogenosis type II or to distinguish between normal and carrier animals. The glycogen content of the semitendinosus muscle of affected animals was approximately three times that in non-affected animals and although storage of glycogen reached a plateau soon after birth, the muscle fibre damage seen in very young calves increased with age. Morphological evidence of glycogen accumulation, both within the cytoplasm and within membrane bound structures, was present at birth. In some animals evidence of muscle fibre regeneration and damage was seen in the same sections.

Age Factors↗

PubMedDate not supplied

Primary demyelination in the central nervous system of cats.

Primary demyelinating lesions have been observed in the central nervous system of 16 (approximately 7%) of a total of 235 clinically normal cats. The size of the lesions varied from small perivascular lesions in white matter to a large lesion occupying the diameter of an optic nerve. Intracytoplasmic inclusions consisting of tubular structures were common to all lesions examined by electron microscopy. The features of these feline lesions are briefly compared with those seen in multiple sclerosis.

Animals↗

PubMedDate not supplied

Light and electron microscopical studies of the immunoperoxidase staining of multiple sclerosis plaques using antisera to a feline-derived agent and to galactocerebroside.

Antibodies have been raised to two agents (CCA147 and MV631) that were isolated from central nervous tissue of cats. The cells co-cultivated with these agents are characterized by the presence of cytoplasmic inclusions consisting of 16-18 nm diameter tubular elements morphologically similar to inclusions seen in a demyelinating condition in cats and to inclusions described as 'curved linear profiles' in multiple sclerosis (MS) plaques. The peroxidase-labelled antibodies to CCA147 and MV631 stain these inclusions in MS plaques as well as small virus-like particles. The antisera do not stain normal white matter either in MS or non-MS brain tissue. The staining reaction of one agent is blocked by pretreatment with antisera to the other agent and also by pretreatment with MS sera but not by normal human sera. Peroxidase-labelled antibody to galactocerebroside stains normal myelin and myelin debris within MS plaques but does not stain the 'curved linear profiles' that are stained by the labelled antibodies to the feline-derived agents. The results show that the 'curved linear profiles' described in MS plaques are not myelin degradation products, but are comparable to the nucleocapsids of morbilliviruses. In addition, the small virus-like particles are morphologically similar to morbillivirus virions. The results are discussed with particular emphasis on the features of the morbilliviruses, canine distemper and measles viruses.

Animals↗