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Laser-Doppler flowmetry is a new technique for noninvasive and continuous measurement of local microcirculatory cerebral and spinal-cord blood flow. The flow estimate by this technique is based on the assessment of the Doppler shift of low-power laser light, which is scattered by moving red blood cells. Laser-Doppler flowmetry has been validated for various organs, including the central nervous system. These studies revealed a linear relationship between relative changes of the Doppler signal and blood flow over a wide range of pharmacological as well as pathological flow alterations, including cerebral ischemia. The usefulness of laser-Doppler flowmetry in experimental as well as clinical applications has received growing attention. The superiority of the technique lies in its high spatial and temporal resolution. Disadvantages are the difficulty of obtaining absolute flow values and the sensitivity to artifacts. The versatility and on-line capacity of laser-Doppler flowmetry might allow new insights into the pathophysiology of alterations of the cerebral and spinal-cord microcirculation.

Although a variety of potential sources for reactive oxygen species (ROS) exist in the CNS, brain macrophages, i.e., the microglia, generate large quantities of these reactive species, particularly in response to injury or inflammatory signals. In order to understand how microglia contribute to changes in oxidative status of the CNS and how this might relate to disease states, such as Alzheimer disease (AD), we have examined the regulation of superoxide anion and nitric oxide production from rodent and human microglia. Our results indicate that microglia from all species we have studied release superoxide anion, but produce significantly different amounts in response to the same activating agents. Species differences are also found in the ability to generate nitric oxide (NO). In particular, mouse microglia generate large quantities of NO when stimulated, but human and hamster microglia do not produce measurable amounts under the same stimulation conditions. These species differences are important to consider when modeling human disease processes from rodent studies.

The effect of acrylamide treatment on the immunocytochemical localization of microtubule-associated proteins (MAP1 and MAP2) was studied in different brain regions (cerebellum, cerebral cortex, and hippocampus) of adult rats. Animals were treated with acrylamide (estimated mean dose: 15 mg/kg/d) orally for 2 wk when they showed slight hindlimb weakness. Immunoreactivity for MAP1 and MAP2 was detected in tissue sections with monoclonal antibodies according to the Sternberger’s peroxidase-antiperoxidase technique. Intense MAP1 immunoreactivity was observed in neuronal perikarya and dendrites, with faint staining in axons. By contrast, MAP2 immunostaining was selectively observed in dendrites and neuronal perikarya. Treatment of animals with acrylamide reduced immunoreactivity for both MAP1 and MAP2 in hippocampus and cerebellum, with relatively little change in cerebral cortex. Loss of MAPs immunoreactivity in affected brain areas likely proceeded from dendrite to perikaryon. The results of this study indicate that hippocampal compromise is part of the neurotoxic picture associated with rodent exposure to acrylamide.

Arylsulfatase A (ASA) and cerebroside-β-galactosidase activities in leukocytes serve as a diagnostic tool for determining the presence of metachromatic leukodystrophy and globoid cell leukodystrophy, respectively. It has not been demonstrated whether a delay in blood processing and the presence of mixed cell types in different proportions in leukocytes affect the activities of the two enzymes in these cells. We have in the present study determined the specific activity in leukocytes and lymphocytes (T-cells) prepared from blood samples processed immediately after, 4, and 24 h after collection. In order to determine whether the enzyme activitiies in lymphocytes reflect expression of genetic trait, and not environmental or “state” influence, the activities of the two enzymes in interleukin 2-stimulated T-cells and resting T-cells were compared. A delay of up to 24 h in blood processing did not significantly change the specific activities of the two enzymes in both leukocytes and lymphocytes. The specific activity of ASA and β-galactosidase in lymphocytes was 1.4–1.8 times that in leukocytes. The activities of the two enzymes in interleukin 2-stimulated T-cells did not differ from those in resting T-cells. These results indicate that blood-processing delay had no significant effects on ASA and β-galactosidase activity. The data further indicate that the ASA and β-galactosidase activity in interleukin 2-stimulated T-cells was not significantly different from resting lymphocytes from either normal or psychiatric subjects exposed to various medications. The activity levels in lymphocytes from psychiatric subjects thus reflect expression of genetic trait, rather than environmental or state influence.

The asymmetric pincer and snapper claws in the snapping shrimp differ in external morphology and musculature. The snapper is a massive claw used for displays and defense; the pincer is small and slender, used for feeding and burrowing. The snapper has only slow muscle fibers; the pincer has both slow and fast. Removal or denervation of the snapper claw induces transformation of the contralateral pincer to a snapper type of claw at the subsequent molt. A removed claw regenerates as a pincer type, as long as the innervation of the remaining claw is intact. Fast muscle fibers, found exclusively in the pincer claw, normally degenerate completely within 10 d after the moult, which transforms the pincer to a snapper. Morphological transformation of the pincer following removal of the snapper claw can occur even if the pincer claw is denervated. Denervation of the pincer, however, delays degeneration of the fast fibers, increasing the estimated half-time for muscle degeneration, from 4.4±0.2 to 19.5±0.8. d after the transforming moult. Neural influences there-fore are involved both in the determination of the morphology of the claw and in the induction of degenerative changes during the remodeling of an existing claw.

CARIBRO was founded in response to the United Nations declaration that the 1990s be designated the Decade of the Brain. The Program of Action is: In the same program, a CARIBRO Laboratory was created in one of the Medical Faculties of Havana with the aim to teach students from the Caribbean in neuroscience research. As part of this program, we have been working in lateralized motor functions. Preliminary results in rats show that reaching acquisition allows classification of the animals as right-handed (40%), left-handed (40%), and ambidextrous (20%). Electrolytic lesion of caudate nucleus or amygdala impairs lateralized response. Contralateral lesions increase reaching attempts. Ipsilateral lesions to the preferred forepaw do not affect the reaction. The results remain the same 10, 20, and 90 d after the interference. Pharmacological experiments showed that trihexiphenidil (0.1 mg/kg ip) induced handedness reversion in 50% of the animals, whereas haloperidol (1 mg/kg ip) produced immobility, tremor, and autonomic symptoms. This effect remained the same in young as well as in old animals. We are also working on mathematical modelation. In this sense, preliminary reports about a model for synaptic modification in the framework of the Fukushima hypothesis is discussed.

A laminectomy was performed at the T5−T6 vertebral level in adult, male, Sprague-Dawley rats and the spinal cord transected with a scalpel. A group of sham animals was subjected to the same surgery without the transection step. A group of unhandled control rats was also included. A subgroup of transected animals received a subcutaneous osmotic minipump that dispensed IL-1 receptor antagonist protein (IRAP) at the transection site for 7 consecutive days. Another transected subgroup received a minipump that infused the vehicle only. IRAP-treated rats displayed a significant reduction in body temperature (p<0.05) compared with vehicle-treated rats. The IRAP-treated rats were also less active when assessed for locomotor behavior using an HVS computerized tracking system (p<0.01). IRAP treatment had no effect on serum corticosterone, β-endorphin levels, Con A, PHA, or LPS-induced splenocyte mitogenesis when compared with vehicle-treated animals. However, half of the IRAP-treated animals exhibited a substantive reduction in the number of reactive astrocytes near the transection site, suggesting a possible effect of IRAP on astrocyte activation.