The effects of astaxanthin treatment on a rat model of Alzheimer's disease.

Alzheimer's disease (AD), a progressive neurodegenerative disorder characterized by memory loss and dementia, could be a consequence of the abnormalities of cortical milieu, such as oxidative stress, inflammation, and/or accompanied with the aggregation of β-amyloid. The majority of AD patients are sporadic, late-onset AD, which predominantly occurs over 65 years of age. Our results revealed that the ferrous amyloid buthionine (FAB)-infused sporadic AD-like model showed deficits in spatial learning and memory and with apparent loss of choline acetyltransferase (ChAT) expression in medial septal (MS) nucleus.

Cortical compression rapidly trimmed transcallosal projections and altered axonal anterograde transport machinery.

Trauma and tumor compressing the brain distort underlying cortical neurons. Compressed cortical neurons remodel their dendrites instantly. The effects on axons however remain unclear.

Reproductive experience modified dendritic spines on cortical pyramidal neurons to enhance sensory perception and spatial learning in rats.

Behavioral adaptations during motherhood are aimed at increasing reproductive success. Alterations of hormones during motherhood could trigger brain morphological changes to underlie behavioral alterations. Here we investigated whether motherhood changes a rat's sensory perception and spatial memory in conjunction with cortical neuronal structural changes.

Hydrocephalus compacted cortex and hippocampus and altered their output neurons in association with spatial learning and memory deficits in rats.

Hydrocephalus is a common neurological disorder in children characterized by abnormal dilation of cerebral ventricles as a result of the impairment of cerebrospinal fluid flow or absorption. Clinical presentation of hydrocephalus varies with chronicity and often shows cognitive dysfunction. Here we used a kaolin-induction method in rats and studied the effects of hydrocephalus on cerebral cortex and hippocampus, the two regions highly related to cognition.

Rostral Intralaminar Thalamic Deep Brain Stimulation Triggered Cortical and Hippocampal Structural Plasticity and Enhanced Spatial Memory.

Background/aims: Rostral intralaminar thalamic nucleus (ILN) has been shown to modulate cognition through indirect connection with the hippocampus and prefrontal cortex. We explored the effects of deep brain stimulation (DBS) to the rostral ILN on spatial memory acquisition, brain neuronal activation and cortical and hippocampal synaptic changes in rats.

Methods: The Morris water maze (MWM) task was used to evaluate the spatial memory of the rats.

NMDA receptor triggered molecular cascade underlies compression-induced rapid dendritic spine plasticity in cortical neurons.

Compression causes the reduction of dendritic spines of underlying adult cortical pyramidal neurons but the mechanisms remain at large. Using a rat epidural cerebral compression model, dendritic spines on the more superficial-lying layer III pyramidal neurons were found quickly reduced in 12h, while those on the deep-located layer V pyramidal neurons were reduced slightly later, starting 1day following compression. No change in the synaptic vesicle markers synaptophysin and vesicular glutamate transporter 1 suggest no change in afferents.

Exogenous dehydroisoandrosterone sulfate reverses the dendritic changes of the central neurons in aging male rats.

Sex hormones are known to help maintaining the cognitive ability in male and female rats. Hypogonadism results in the reduction of the dendritic spines of central neurons which is believed to undermine memory and cognition and cause fatigue and poor concentration. In our previous studies, we have reported age-related regression in dendrite arbors along with loss of dendritic spines in the primary somatosensory cortical neurons in female rats.

Genistein partly eases aging and estropause-induced primary cortical neuronal changes in rats.

Gonadal hormones can modulate brain morphology and behavior. Recent studies have shown that hypogonadism could result in cortical function deficits. To this end, hormone therapy has been used to ease associated symptoms but the risk may outweigh the benefits.

Morphological changes of cortical pyramidal neurons in hepatic encephalopathy.

Background: Hepatic encephalopathy (HE) is a reversible neuropsychiatric syndrome associated with acute and chronic liver diseases. It includes a number of neuropsychiatric disturbances including impaired motor activity and coordination, intellectual and cognitive function.

Results: In the present study, we used a chronic rat HE model by ligation of the bile duct (BDL) for 4 weeks.

Methylcobalamin facilitates collateral sprouting of donor axons and innervation of recipient muscle in end-to-side neurorrhaphy in rats.

Using ulnar nerve as donor and musculocutaneous nerve as recipient we found earlier that end-to-side neurorrhaphy resulted in weak functional reinnervation after lengthy survival. End-to-side neurorrhaphy however is the sole choice of nerve repair at times and has the advantage of conserving donor nerve function. Here, we investigated whether myelination-enhancing agent methylcobalamin and motoneuron trophic factor pleiotrophin enhances the recovery after end-to-side neurorrhaphy.

Testosterone modulation of dendritic spines of somatosensory cortical pyramidal neurons.

Brain structures and functions are increasingly recognized to be directly affected by gonadal hormones, which classically determine reproductive functions and sexual phenotypes. In this regard, we found recently that ovariectomy trimmed the dendritic spines of female rat primary somatosensory cortical neurons and estradiol supplement reversed it. Here, we investigated whether in the male androgen also has a cortical modulatory effect.

Active endocytosis and microtubule remodeling restore compressed pyramidal neuron morphology in rat cerebral cortex.

Previous studies have shown that compression alone reduced the thickness of rat cerebral cortex and apical dendritic lengths of pyramidal neurons without apparent cell death. Besides, decompression restored dendritic lengths at different degrees depending on duration of compression. To understand the mechanisms regulating dendritic shortening and lengthening upon compression and decompression, we applied transmission electron microscopy to examine microtubule and membrane structure of pyramidal neurons in rat sensorimotor cortex subjected to compression and decompression.

Ascorbic acid and α-tocopherol supplement starting prenatally enhances the resistance of nucleus tractus solitarius neurons to hypobaric hypoxic challenge.

Hypobaric hypoxia, encountered at high altitude, could result in severe consequences. Ascorbic acid (AA) and α-tocopherol (αTC), the two readily available over-the-counter antioxidants, are known to protect nervous tissue against oxidative stress. Here we study whether AA or αTC supplement starting prenatally protects animals against hypobaric hypoxic challenge at adulthood.

Compression alters kinase and phosphatase activity and tau and MAP2 phosphorylation transiently while inducing the fast adaptive dendritic remodeling of underlying cortical neurons.

In traumatic brain injury (TBI) there is often compression of the cerebral cortex. Using a rat epidural bead implantation model we found that mechanical compression distorted the dendrites of underlying cortical pyramidal neurons, and that the deformed dendrites regained straight morphology in 3 days. This was accompanied by a transient increase in the phosphorylation of microtubule-associated proteins (MAPs) at sites known to destabilize microtubules, including MAP2 from 30 min to 1 h, and tau from 10 min to 12 h following compression.

The efficacy of end-to-end and end-to-side nerve repair (neurorrhaphy) in the rat brachial plexus.

Proximal nerve injury often requires nerve transfer to restore function. Here we evaluated the efficacy of end-to-end and end-to-side neurorrhaphy of rat musculocutaneous nerve, the recipient, to ulnar nerve, the donor. The donor was transected for end-to-end, while an epineurial window was exposed for end-to-side neurorrhaphy.

Gonadal hormones modulate the dendritic spine densities of primary cortical pyramidal neurons in adult female rat.

Adult dendritic arbors and spines can be modulated by environment and gonadal hormones that have been reported to affect also those of hippocampal and prefrontal cortical neurons. Here we investigated whether female gonadal hormones and estrous cycle alter the dendrites of primary cortical neurons. We employed intracellular dye injection in semifixed brain slices and 3-dimensional reconstruction to study the dendritic arbors and spines of the major cortical output cells, layer III and V pyramidal neurons, during different stages of the estrous cycle.

Proximity of lesioning determines response of facial motoneurons to peripheral axotomy.

We recently found that rubrospinal (RS) neurons, which typify central neurons projecting within the central nervous system (CNS), exhibited different neuronal and glial reactions to axotomy at proximal as opposed to distal sites. To determine whether distance also determines the reaction to axonal injury of central neurons projecting to the periphery, we studied the temporal expression of four free-radical-related enzymes as well as the severity of cell loss, perineuronal astrocytic and microglial reactions, and degeneration of the proximal central axons of facial motoneurons after axotomies performed at various sites on the brainstem surface and in the stylomastoid foramen, respectively. Distal lesions resulted in upregulation of these neurons' expression of nitric oxide synthase (NOS) and persistent downregulation of their expression of the NOS-activating enzyme calcineurin.

Neonatal toluene exposure alters N-methyl-D-aspartate receptor subunit expression in the hippocampus and cerebellum in juvenile rats.

Recent evidence indicates that toluene is a non-competitive inhibitor of N-methyl-d-aspartate (NMDA) receptor-mediated synaptic currents. The NMDA receptor plays a major role in neuronal development and differentiation. The present study characterized the long-term effects of toluene exposure during synaptogenesis on the expression of NMDA receptor subunits (NR1, NR2A and NR2B).

The effects of decompression and exogenous NGF on compressed cerebral cortex.

Using a rat epidural bead implantation model, we found that compression alone could reduce the overall and individual layer thicknesses of cerebral cortex with no apparent cell death. The dendritic lengths and spine densities of layer II/III and V pyramidal neurons started to decrease within 3 days of compression. Decompression for 14 days resulted in near complete to partial recovery of the cortical thickness and of the dendritic lengths of layer II/III and V pyramidal neurons, depending on the duration of the preceding compression.

Spinal axonal injury induces brief downregulation of ionotropic glutamate receptors and no stripping of synapses in cord-projection central neurons.

Spinal cord injury often damages the axons of cord-projecting central neurons. To determine whether their excitatory inputs are altered following axonal injury, we used rat rubrospinal neurons as a model and examined their excitatory input following upper cervical axotomy. Anterograde tracing showed that the primary afferents from the cerebellum terminated in a pattern similar to that of control animals.

Spinal axonal injury transiently elevates the level of metabotropic glutamate receptor 5, but not 1, in cord-projection central neurons.

In investigating the effect of spinal injury on cord-projection central neurons, we found that rat rubrospinal neurons retained glutamatergic afferents and, in general, ionotropic glutamate receptor expression following spinal axotomy. Since glutamate also acts on second-messenger-coupled metabotropic receptors, the expression of group I metabotropic glutamate receptors, mGluR1 and mGluR5, was examined following similar treatment. mGluR1 expression began to decline in the perikarya 2 days postlesion and a day later in the neuropil.

The effect of epidural compression on cerebral cortex: a rat model.

We developed a rat model of epidural plastic bead implantation to study the effect of physical compression on the cerebral cortex. Epidural implantation of a bead of appropriate size compressed the underlying sensorimotor cortex without apparent ischemia, since the capillary density of the cortex was increased. Although the thickness of all layers of the compressed cortex was significantly decreased, no apparent changes in the number of NADPH-diaphorase reactive neurons, reactive astrocytes, or microglial cells were observed, nor were apoptotic neurons observed.

Close axonal injury of rubrospinal neurons induced transient perineuronal astrocytic and microglial reaction that coincided with their massive degeneration.

To learn more about the pathophysiology of axonal injury and the significance of axon collaterals on the survival of axotomized cord-projection central neurons, we studied the survival rate, surrounding astrocytic and microglial reactions, and bouton coverage on rat rubrospinal cell bodies following their axonal lesion at the brain stem and upper cervical level. The brain stem lesion disconnected most rubrospinal neurons from all their targets, while the upper cervical lesion spared their supraspinal collaterals. Much higher cell loss accompanied by robust astrocytic and microglial reaction was found following brain stem than upper cervical lesion starting 4 days postaxotomy.

Fate of the soma and dendrites of cord-projection central neurons after proximal and distal spinal axotomy: an intracellular dye injection study.

We used rat rubrospinal neurons as a model to study the soma-dendritic morphology of cord-projection neurons following spinal axonal injury. We examined lumbar-projection neurons following both upper cervical and lower thoracic axotomy to find out whether changes were dependent on the proximity of the lesion to the cell body. Axotomized neurons were marked with retrograde tracer and studied 4 and 8 weeks later with intracellular dye injection technique.

Parvalbumin-containing neurons mediate the feedforward inhibition of rat rubrospinal neurons.

The calcium-binding protein, parvalbumin and glutamic acid decarboxylase immunohistochemistry were used to locate candidate neurons mediating the inhibition of rat rubral neurons. A group of cells with small to medium-sized cell bodies that reacted positively to both were found in the red nucleus and its immediate vicinity. At the caudal nuclear level, these neurons gathered in the reticular formation, the pararubral area dorsolateral to the nucleus.