Hyaluronic Acid Conjugated with 17β-Estradiol Effectively Alleviates Estropause-Induced Cognitive Deficits in Rats.

Women are at a higher risk of cognitive impairments and Alzheimer's disease (AD), particularly after the menopause, when the estrous cycle becomes irregular and diminishes. Numerous studies have shown that estrogen deficiency, especially estradiol (E2) deficiency, plays a key role in this phenomenon. Recently, a novel polymeric drug, hyaluronic acid-17β-estradiol conjugate (HA-E2), has been introduced for the delivery of E2 to brain tissues.

Modulation of striatal glutamatergic, dopaminergic and cholinergic neurotransmission pathways concomitant with motor disturbance in rats with kaolin-induced hydrocephalus.

Background: Hydrocephalus is characterized by abnormal accumulation of cerebrospinal fluid in the cerebral ventricles and causes motor impairments. The mechanisms underlying the motor changes remain elusive. Enlargement of ventricles compresses the striatum of the basal ganglia, a group of nuclei involved in the subcortical motor circuit.

The effect of astaxanthin treatment on the rat model of fetal alcohol spectrum disorders (FASD).

Fetal alcohol spectrum disorder (FASD) caused by mother's exposure to alcohol during pregnancy is a congenital neurological disease of the fetus resulting in fetal developmental and intellectual disabilities, cognitive impairment, and coordination disorder. Excess oxidative stress and neuroinflammatory responses were an important factor in neuropathological changes in FASD. Astaxanthin (AST) was a potent antioxidant and anti-inflammatory carotenoid.

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.

Role of hypothalamic leptin-LepRb signaling in NPY-CART-mediated appetite suppression in amphetamine-treated rats.

Leptin is an adipose tissue hormone which plays an important role in regulating energy homeostasis. Amphetamine (AMPH) is a drug of appetite suppressant, which exerts its effect by decreasing the expression of hypothalamic neuropeptide Y (NPY) and increasing that of cocaine- and amphetamine-regulated transcript (CART). This study investigated whether leptin, the leptin receptor (LepRb) and the signal transducer and activator of transcription-3 (STAT3) were involved in NPY/CART-mediated appetite suppression in AMPH-treated rats.

Knockdown of the transcript of ERK in the brain modulates hypothalamic neuropeptide-mediated appetite control in amphetamine-treated rats.

Background And Purpose: Amphetamine is a releaser of dopamine stored in synaptic terminals, which can suppress appetite by changing the expression levels of neuropeptide Y (NPY) and proopiomelanocortin (POMC) in the hypothalamus. This study explored whether ERKs are involved in appetite control mediated by cAMP response element binding protein (CREB), NPY and POMC in amphetamine-treated rats.

Experimental Approach: Rats were given amphetamine for 4 days, and changes in feeding behaviour and expression levels of phosphorylated-ERK (pERK), pCREB, NPY and melanocortin MC receptors were examined and compared.

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.

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.

Fabrication of bioactive conduits containing the fibroblast growth factor 1 and neural stem cells for peripheral nerve regeneration across a 15 mm critical gap.

Nerve conduits are often used in combination with bioactive molecules and stem cells to enhance peripheral nerve regeneration. In this study, the acidic fibroblast growth factor 1 (FGF1) was immobilized onto the microporous/micropatterned poly (D, L-lactic acid) (PLA) nerve conduits after open air plasma treatment. PLA substrates grafted with chitosan in the presence of a small amount of gold nanoparticles (nano Au) showed a protective effect on the activity of the immobilized FGF1 in vitro.

The distribution of muscles fibers and their types in the female rat urethra: cytoarchitecture and three-dimensional reconstruction.

An attempt to explore urethral cytoarchitecture including the distribution of smooth muscles and fast and slow striated muscles of adult female Sprague Dawley rat--a popular model in studying lower urinary tract function. Histological and immunohistochemical stainings were carried out to investigate the distribution of urethral muscle fibers and motor end plates. The urethral sphincter was furthermore three-dimensionally reconstructed from serial histological sections.

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.

Sciatic nerve regeneration by microporous nerve conduits seeded with glial cell line-derived neurotrophic factor or brain-derived neurotrophic factor gene transfected neural stem cells.

Neurotrophic factors such as the glial cell line-derived neurotrophic factor (GDNF) and brain-derived neurotrophic factor (BDNF) promote nerve cell survival and regeneration, but their efficacy in repairing a longer gap defect of rat sciatic nerve (15 mm) has not been established. In this study, two recombinant mammalian vectors containing either rat GDNF gene or BDNF gene were constructed and each was transfected into neural stem cells (NSCs). It was found that the transfection of GDNF or BDNF gene into NSCs led to significantly enhanced expression of GDNF or BDNF mRNA.

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.

Transplanted bone marrow stromal cells migrate, differentiate and improve motor function in rats with experimentally induced cerebral stroke.

Bone marrow stromal cells are multipotential cells that can be induced to differentiate into osteoblasts, chondrocytes, myocytes and adipocytes in different microenvironments. Recent studies revealed that bone marrow stromal cells could improve neurological deficits of various damages or diseases of the central nervous system such as Parkinson's disease, brain trauma, spinal cord injury and multiple sclerosis, and promote glia-axonal remodeling in animal brain subjected to an experimentally induced stroke. In the present study, bone marrow stromal cells were intracerebrally transplanted into the cerebrum following a transient middle cerebral artery occlusion.

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.

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.

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.