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The hippocampus is essentially involved in learning and memory, and is known to be a target for androgen actions. As neuron-astrocyte interactions play a crucial role during development and in the adult brain, it is thought that astrocytes support learning and memory through specific mechanisms. In this study, the effect of testosterone-induced impairment of acquisition and retrieval of long-term memory, on the number of astrocytes was studied. Adult male albino Wistar rats were bilaterally cannulated into the CA1 region and received 80 microg/0.5 microl of testosterone enanthate dissolved in DMSO as vehicle. In trained groups injection was done 30 min before training. Our results showed that pre-training administration of testosterone increased escape latency and the traveled distance, as compared to intact or DMSO administered (sham-operated) counterparts. Testosterone administration also increased the number of astrocytes in rats, compared to sham-operated and intact animals in both trained and non-trained groups. We have also found that spatial learning could increase the number of astrocytes in the hippocampus as a center of long-term learning and memory and recall. It is concluded that, testosterone-induced impairment in learning and memory, causes an increase in the number of astrocytes in the CA1 region of rat hippocampus., (Copyright 2009 Elsevier B.V. All rights reserved.)

The aim of this study was to evaluate changes of both peripheral motor function and histology of spinal anterior horn in adult rats after unilateral sciatectomy. Ten adult healthy rats served as control group, while in the ten rat experimental group the right sciatic nerve was severed. We followed-up nerve motor function using a sciatic function index and electromyography activity of the gastrocnemious muscle. The rats of the experimental group presented the expected gross locomotor deficit and leg muscle atrophy. At 12 weeks post sciatectomy, L4 and L5 spinal cord segments were removed from the twenty rats and were analysed by istological stereological methods. In the axotomized animals volume of the anterior horn and its content of motor neurons decreased, while the content of astrocytes increased (p < 0.05). Thus, in adult rats, beside the obvious peripheral nerve disfuction, the sciatic nerve axotomy have severe consequences on the soma of the injured motor neurons in the spinal anterior horn. All these quantitative analyses may be usefull to quantify changes occurring in adult animals after axotomy and eventual management to modify the final outcomes in peripheral nerve disorders. [ABSTRACT FROM AUTHOR]

Introduction: Previous studies have suggested that the cerebellum is a primary site of motor learning. The cerebellar cortex has a particular glial architecture with large astroglial cells. In addition, more recent works have revealed that astrocytes play a more active role in neuronal activity. The aim of this study was to evaluate the number of astrocytes in the molecular layer of rat's cerebellum after spatial learning. Methods: 21 male albino wistar rats were used in this study. Reference and working memory methods of Morris Water Maze (MWM) were used. Following behavioral testing, animals were decapitated under diethyl ether anesthesia. Brains were removed and fixed for 2 weeks for histological assessment. Finally, 7 µm thick coronal slices were cut and stained with PTAH staining for showing the astrocytes. Results: Our results showed a significant difference in the number of astrocytes between the control, reference and working memory groups. On the other hand, the number of astrocytes in the working memory group was more than the other groups. There was no difference in density of astrocytes between the lateral and medial parts of the cerebellum in any group. It seems that the distribution of astrocytes in the lateral and medial parts of cerebellum is similar. Discussion: We concluded that spatial learning such as reference or working memory methods, can increase the number of astrocytes in the cerebellum and this increase is similar in the cerebellar cortex. [ABSTRACT FROM AUTHOR]

Objective: Epilepsy is accompanied by inflammation, and the anti-inflammatory agents may have anti-seizure effects. In this investigation, the effect of deep brain stimulation, as a potential therapeutic approach in epileptic patients, was investigated on seizure-induced inflammatory factors. Materials and Methods: In the present experimental study, rats were kindled by chronic administration of pentylenetetrazol (PTZ; 34 mg/Kg). The animals were divided into intact, sham, low-frequency deep brain stimulation (LFS), kindled, and kindled +LFS groups. In kindled+LFS and LFS groups, animals received four trains of intra-hippocampal low-frequency deep brain stimulation (LFS) at 20 minutes, 6, 24, and 30 hours after the last PTZ injection. Each train of LFS contained 200 pulses at 1 Hz, 200 µA, and 0.1 ms pulse width. One week after the last PTZ injection, the Y-maze test was run, and then the rats’ brains were removed, and hippocampal samples were extracted for molecular assessments. The gene expression of two pro-inflammatory factors [interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α)], and glial fibrillary acidic protein (GFAP) immunoreactivity (as a biological marker of astrocytes reactivation) were evaluated. Results: Obtained results showed a significant increase in the expression of of interleukin-6 (IL-6), tumor necrosis factor (TNF)-α, and GFAP at one-week post kindling seizures. The application of LFS had a long-lasting effect and restored all of the measured changes toward normal values. These effects were gone along with the LFS improving the effect on working memory in kindled animals. Conclusion: The anti-inflammatory action of LFS may have a role in its long-lasting improving effects on seizure-induced cognitive disorders. [ABSTRACT FROM AUTHOR]