Taurine can Decrease Phosphorylated Tau Protein Levels in Alzheimer's Model Rats' Brains.

Background Microtubule formation is a dynamic process and Tau proteins promote the assembly of tubulin monomers into microtubules. Hyperphosphorylation of some amino acids in tau proteins causes neuron starvation and finally cell death. Taurine is found in the brain and has neuroprotective effects. Objective Since the protective and therapeutic effects of Taurine on phosphorylated tau proteins level in the cerebellum and prefrontal cortex of rats induced by scopolamine have not been studied, we examined these effects. Method Adult male Wistar rats were randomly distributed into nine groups. For two weeks, Taurine-treated rats received different doses of Taurine (25, 50, and 100 mg/kg/ day) before or after scopolamine injection. The phosphorylated tau protein level in the cerebellum and prefrontal cortex was determined by the enzyme-linked immunosorbent assay (ELISA) technique. Result Pretreatment with three doses of Taurine significantly decreased the phosphorylated tau protein level that increased by scopolamine in the prefrontal cortex (p < 0.001), as well as the cerebellum (p < 0.001). Moreover, high-dose administration of Taurine (100 mg/kg/day) after scopolamine injection significantly decreased phosphorylated tau protein level in the cerebellum (p < 0.01), as well as the prefrontal cortex (p < 0.05). However, there was not any significant change in the level of phosphorylated tau protein after Taurine treatment (25 and 50 mg/kg/day) in the cerebellum and prefrontal cortex. Conclusion It can be concluded that Taurine could attenuate the increase in phosphorylated tau protein induced by scopolamine in the brain of rats and usage of Taurine as a pretreatment complement could be more useful in the protection of neurons.

Effects of hCG on reduced numbers of hCG receptors in the prefrontal cortex and cerebellum of rat models of Alzheimer's disease.

Age-associated changes in the levels of luteinizing hormone and human chorionic gonadotropin (hCG) are potential risk factors for Alzheimer's disease (AD); hCG concentration is related to the incidence of AD. The highest density of hCG receptors is in zones of the brain that are vulnerable to AD and streptozotocin (STZ) can decrease the density of this receptor. We investigated the effects of different doses of hCG on hCG receptor density in the prefrontal cortex and cerebellum in a rat model of STZ-induced AD. AD was induced by intracerebroventricular injection of 3 mg/kg STZ. The resulting AD rats were treated for 3 days with 50, 100 or 200 IU/200 µl hCG, or with saline as a control. Sections of prefrontal cortex and cerebellum were stained immunohistochemically and hCG receptor-immunoreactive (ir) neurons were counted. STZ injected into the lateral ventricles of rat brains reduced the density of hCG receptor-ir neurons in the prefrontal cortex and cerebellum. hCG administration resulted in a significant dose-dependent increase in the number of hCG receptor-ir neurons in the prefrontal cortex and cerebellum. The maximum increase in the number of receptors occurred following the 200 IU dose of hCG. Administration of hCG ameliorated the lowered density of hCG receptor-ir neurons in the cerebellum and prefrontal cortex in STZ-induced AD rats.

α2-Adrenoceptor-ir neurons' density changes after single dose of clonidine and yohimbine administration in the hippocampus of male rat.

OBJECTIVE: Despite the important role of α2-adrenoceptors in pain modulation processes, the impact of administration of α2-adrenoceptor agonist and antagonist on the density of hippocampal α2-adrenoceptor-immunoreactive neurons has not been investigated. Therefore, we aimed to determine the effect of single doses of clonidine and yohimbine on the density of α2-adrenoceptor-immunoreactive neurons in rat hippocampus. MATERIALS AND METHODS: Adult male Wistar rats received a single dose of clonidine (0.7 mg/kg) alone or 5 min after intraperitoneal (1 mg/kg) and/or intracerebroventricular (5 µg/kg) injection of yohimbine. After histological processing, neurons with α2-adrenoceptor immunoreactivity were identified and counted through immunohistochemical analysis of hippocampal regions. RESULTS: Clonidine slightly increased the number of α2-adrenoceptor-immunoreactive neurons in the hippocampal subregions compared with the normal saline group. Intraperitoneal injection of yohimbine followed by injection of clonidine significantly increased the number of α2-adrenoceptor-immunoreactive neurons in subregions cornu ammonis 1 (CA1) and cornu ammonis 3 (CA3). Intracerebroventricular injection of yohimbine after injection of clonidine significantly reduced the number of α2-adrenoceptor-immunoreactive neurons in all hippocampal subregions. CONCLUSION: The present study demonstrates that intraperitoneal administration of α2-adrenoceptor agonist clonidine increases the density of α2-adrenoceptor-immunoreactive neurons in rat hippocampus, while intracerebroventricular injection of yohimbine decreases the density of these neurons.

Female rat hippocampal cell density after conditioned place preference.

The hippocampus is important for learning tasks, such as conditioned place preference (CPP), which is widely used as a model for studying the reinforcing effects of drugs with dependence liability. Long-term opiate use may produce maladaptive plasticity in the brain structures involved in learning and memory, such as the hippocampus. We investigated the phenomenon of conditioning with morphine on the cell density of female rat hippocampus. Forty-eight female Wistar rats weighing on average 200-250 g were used. Rats were distributed into eight groups. Experimental groups received morphine daily (three days) at different doses (2.5, 5, 7.5 mg/kg) and the control-saline group received normal saline (1 ml/kg), and then the CPP test was performed. Three sham groups received only different doses (2.5, 5, 7.5 mg/kg) of morphine without CPP test. Forty-eight hours after behavioural testing animals were decapitated under chloroform anaesthesia and their brains were fixed, and after tissue processing, slices were stained with cresyl violet for neurons and phosphotungstic acid haematoxylin for astrocytes. The maximum response was obtained with 5 mg/kg of morphine. The density of neurons in CA1 and CA3 areas of hippocampus after injection of morphine and CPP was decreased. The number of astrocytes in different areas of hippocampus was increased after injection of morphine and CPP. It seems that the effective dose was 5 mg/kg, as it led to the CPP. We concluded that both injection of mor phine and CPP can decrease the density of neurons and also increase the number of astrocytes in the rat hippocampus.