Behavioral effects of corpus callosum transection and environmental enrichment in adult rats.

A common assumption about the corpus callosum transection (CCX) is that it only affects behaviors heavily relying on interhemispheric communication. However, cerebral laterality is ubiquitous across motor and perceptual, cognitive and emotional domains, and the corpus callosum is important for its establishment. Several recent studies showed that the partial denervation of the sensorimotor isocortex through CCX derepressed neural growth processes that were sensitive to motor demand (experience-dependent neural plasticity). We investigated whether the facilitatory effects of CCX on cortical neural plasticity, shaped by differential housing, extended beyond the motor domain. Adult rats were housed in enriched (EE), standard (SE) or impoverished environments (IE) for 10 weeks, that is, 2 weeks before they underwent CCX or sham surgery, and, then, 8 weeks throughout the experiments. After they recovered from surgery, the behavioral performance of rats was tested using open-field, spontaneous alternation in the T-maze, paw preference, Morris water maze, and tone fear conditioning. The results indicated that the effects of CCX and housing on open-field behavior were independent, with CCX increasing the time spent in the center of the field at the beginning of the observation (i.e., emotionality), and EE and IE increasing rearing (emotionality) and reducing teeth-chattering (habituation), respectively. CCX reduced the frequency of spontaneous alternation, denoting spatial working memory deficits, while housing did not influence this performance. Neither CCX, nor housing significantly affected paw preference lateralization, although CCX was associated with a leftward bias in paw preference. In the Morris water maze, housing had effects on spatial acquisition, while CCX reduced activity, without interfering with spatial memory. CCX did not influence tone fear conditioning, but context fear conditioning seemed to benefit from EE. We conclude that CCX in adult rats has subtle, but specific behavioral effects pertaining to emotionality, spatial working memory, and, possibly, aversively motivated exploration, and these effects are either independent or only peripherally interact with the effects of housing.

Have no fear, erythropoietin is here: erythropoietin protects fear conditioning performances after functional inactivation of the amygdala.

This study investigated the capacity of erythropoietin (EPO) to protect fear conditioning performances against functional inactivation of the amygdala. We infused an excitotoxic dose of glutamate in the lateral nucleus of the amygdala (LA) of adult rats in order to block the output projections to brainstem areas controlling the expression of conditioned fear responses. Subsequently, animals with excitotoxic lesions in the LA displayed altered short and long-term fear conditioned responses, but the integrity of their general emotional reactivity was preserved, as indicated by their open-field behavior. EPO infused immediately after glutamate succeeded to protect the conditioned fear performances of rats. This effect was reliably represented on both short, and long-term memory tests of conditioned fear. This and other studies have supported the potent neuroprotective activity of EPO, discriminable both morphologically, and behaviorally.

A behavioral and ultrastructural dissection of the interference of aluminum with aging.

The persistence of neuroscientists in exploring aluminium's (Al) possible contribution to the pathogenesis of Alzheimer's disease (AD) has resulted in a wealth of researches detailing the biological toxicity of this metal. However, to date, there have been few accounts of the interference of Al with aging and its relevance to the pathogenesis of AD. We investigated the behavioral and the ultrastructural signatures of Al in the hippocampus on young and aging rats which were exposed for three months to aluminium gluconate. The aging animals displayed decreased scores of activity and emotionality, and the Al-exposed aging males had altered emotional reactivity behaviors. The electron-microscopic analysis indicated that Al promoted in the aging hippocampus a variety of cellular and ultrastructural degenerative signs, such as granulo-vacuolar degenerations, deposition of lipofuscin and amyloid in the cytoplasm of neurons and astrocytes, and in extracellular compartments, Hirano bodies, demyelination and the atrophy of the mitochondria. Moreover, the quantitation of myelin sheath width and the diameter of mitochondria measured on randomly selected samples confirmed that myelin and mitochondria are primary targets of Al's toxicity. Demyelination and mitochondrial atrophy seemed more advanced in the hippocampus of Al-exposed aging males, supporting the effect of sex suggested by the behavioral results. These findings and other collateral results also reported here are discussed in the context of a possible involvement of Al in AD, mediated by aging and catalyzed by hepatic morphopathology.

A behavioral and histological study of the effects of long-term exposure of adult rats to aluminum.

Aluminum (Al) has been etiologically and epidemiologically related to several neurologic conditions, including Alzheimer's disease (AD). The effects of Al long-term exposure were investigated to describe the associated behavioral and brain modifications. Adult rats were intraperitoneally injected three times a week for 6 months with ecological doses of Al gluconate (0.85 mg/kg). The Al overload was confirmed by the significantly increased level of Al in serum. We assessed fear conditioning, spatial memory and emotional reactivity by shuttle-box task, Morris water maze, and open-field, respectively. The performance of the experimental animals at the shuttle-box task was significantly lower (p <.01) compared to that of control. The experimental animals had impaired spatial memory, with lower and more fluctuant performance at Morris water maze. The noxious-driven behavior of the experimental animals was also altered, with significantly lower activity scores (p <.05), and high emotionality scores (p <.01) at the open-field. We recovered and processed the brain for aluminum and amyloid deposits. The brains of experimental animals, studied by optical microscopy, displayed a massive cellular depletion in the hippocampal formation, particularly, the CAl field, and also in the temporal and parietal cortex. We observed numerous ghost-like neurons with cytoplasmic and nuclear vacuolations, and with Al deposits. The hippocampus contained extracellular accumulations of Al and amyloid surrounded by nuclei of degenerating cells, which we interpreted as neuritic plaques. The cerebrovasculature was distorted, with a significant thickening of the wall of capillaries, associated with amyloid deposits. These behavioral and neuropathological modifications associated with long-term exposure to Al are reminiscent of those observed in AD.