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Brain Protective Roles Of Neurosteroids In Temporal Lobe Epileptic Male Rats

Posted on:2005-11-19Degree:DoctorType:Dissertation
Country:ChinaCandidate:J M LiangFull Text:PDF
GTID:1104360125450003Subject:Neurology
Abstract/Summary:PDF Full Text Request
Epilepsy is one of the common diseases in nervous system and repeatedly manifests unexpectedly transient brain disfunction caused by abnormally hyperactive and/or hypersynchronous neuronal discharges in brain, accompanied by various clinical or electroencepalogram abnormality, and often result in brain injury due to intercurrent relapse. By statistics, about 53.4% patiens accompany with dysnoesia in different degree, thus bring socially and their family serious burden. Therefore, cognitive damage following by epilepsy becomes focus, which gradually abstracts interests of more and more scholars. Plasticity is one of the potentialities or properties in structure and function of nervous system throughout life. Synaptic plasticity in nervous system underlies behavioral adaptation including learning and memory. At present, synaptic long-term-potentiation (LTP) has been regarded as physiologic symbol and primary mechanism underlying learning or memory, as well as ideal model obtaining information. For this, the potentiality of synaptic plasticity may be used as ideal label, which mirroring cognitive ability in cerebrum. But synaptic remodeling may also implicate in establishing epileptic pathway and subsequently decrease the potentialities of synaptic plasticity, which have close correlation with cognitive disturbance following epilepsy. Nowadays, the elements related to synaptic plasticity are used as standards to evaluate and screen antiepileptic drugs. Epilepsy is still relied on pharmaceutical therapy so far, but about 20%-30% cases of epilepsy yet show no sound effects following drug treatment, which naming intractable epilepsy. Temporal lobe epilepsy is one of the intractable epilepsies, mainly developing complex partial seizures, which commonly selected and applied surgical resection or other ruination upon epileptic focus, but always side with complications caused by synchronously damaging some of functioning structures. Therefore, in a sense, people have high-quality requirement on developing new type antiepileptic. Thus make neurologists faced with great challenges, such as investigating epileptic mechanisms deeply, developing new type antiepileptic provided with efficiency, being able to ameliorate impaired cognition or having no side effects on cognitive function.In recent years, some scholars have researched in epileptogenesis in many ways,including neurology, endocrinology and immunology etc, the roles of neurotransmitters and endocrine hormone on epilepsy have been followed with interests. Available data showing that, the imbalance between excitatory and inhibitory system in central nervous system is the foundation of epileptogenesis. Excitatory amino acids (EAA) and steroid hormone may have important roles in epileptic mechanisms. Neurosteroids not only have close correlation with synaptic plasticity and epilepsy, but also always influenced by epileptic activities, especially involving gonadal hormones and corticoids. The discovery of neurosteroid enzymes make scholars gradually realize the complexity of neurosteroids on functioning regulation in central nervous system. Neurosteroids including glucocorticoid (GCs), mineralocorticoid and gonadal hormones, together with peptide hormone and nervous medium, have same nervous cell targets in brain. GCs is very important on neuroendocrine and behavioral regulating, and has more other important roles in nervous system owing to its higher blood concentration, permeability through blood brain barrier, and widely distribution of its receptors in brain as well as its ability to influence cerebral physiological function. GCs has specific regulative mechanism in other histocytes, and excreted in blood by adrenal cortex. It is converted active or inactive forms by microsome enzyme 11 ?HSD in target cells, regulating GCs binding with its receptors (MR.GR), subsequently affecting post-receptor effects. Today, there are tow forms of 11 P -HSD have been detected, 11 P -HSDI mainly distributes in neuron in hippocampus, and only presenting reductive activity, may ampli...
Keywords/Search Tags:male rat, kainic acid, temporal lobe epilepsy, learning and memory, hippocampus, dexmethasone, estradiolNR2A, NR2B, zi?68 I ?HSD, a -reductas, aromatas, testosteon, cortil
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