No abstract available.
Animals ; Brain* ; Glutamic Acid* ; Glycine* ; Rats*

Sixty years elapsed since Chang (Hsiang-Tung Chang, Xiang-Tong Zhang) presented his seminal report "Cortical neurons with particular reference to the apical dendrite" at the Cold Spring Harbor Symposium. Thanks to the development of elaborated techniques through the 6 decades, our understanding of the dendrite has been pushed forward greatly: the backward and forward conductions during excitation, sodium and calcium conductances, chemical excitation by uncaging glutamate at a dimension of micrometer, and the quantitative study of chemical organization of postsynaptic density (PSD), etc. Though the progression is great, there are still tough problems in dendritic research, especially the integration through dendritic spine.
Calcium Signaling ; Dendrites ; physiology ; Glutamic Acid ; metabolism

No abstract available.
Amino Acid Transport System X-AG* ; Anesthetics* ; Glutamic Acid*

No abstract available.
Animals ; Cerebral Cortex* ; Glutamic Acid* ; Glycine* ; Kynurenic Acid* ; Perfusion* ; Rats*

No abstract available.
Brain* ; Glutamic Acid* ; Intracranial Aneurysm ; Ischemia* ; Prosencephalon* ; Rats, Inbred SHR*

Several decades of research attempting to explain schizophrenia regarding dopamine hyperactivity hypothesis have produced disappointing results. New hypotheses focusing on serotonin-dopamine interactions and hypofunction of the NMDA glutamate transmitter system have been emerging as potentially more promising concepts. The next generation of treatments for schizophrenia, whether they are based on dopamine, serotonin, or glutamate etc., should be effective on negative symptoms and cognitive deficits as well as positive symptoms. In this article, I review the brief overview of these hypotheses and new drugs based on the hypotheses.
Dopamine ; Glutamic Acid* ; N-Methylaspartate ; Receptors, Glutamate* ; Schizophrenia ; Serotonin

No abstract available.
Brain Ischemia* ; Glutamic Acid* ; Microdialysis ; Nitric Oxide Synthase* ; Nitric Oxide*

Tianeptine is an antidepressant effective in reducing depressive symptoms and combined anxiety symptoms. Tianeptine has drawn much attention, because this compound challenges traditional monoaminergic hypothesis of depression. The involvement of glutamate in the mechanism of action of tianeptine is consistent with glutamate hypothesis of depression which demonstrating the key function of glutamate in the mechanism of altered neuroplasticity that underlies the symptoms of depression. This article reviews the evidence of tianeptine's mechanism of action with a focus on the glutamatergic system in an attempt to provide a possible explanation for the observed beneficial clinical profile of tianeptine in patients with depression.
Anxiety ; Depression ; Glutamic Acid ; Humans ; Neuronal Plasticity ; Thiazepines

Glutamate as an excitatory neurotransmitter in the central nervous system, participate in initiation and maintaining of sleep and wakefulness. The paper presents an overview of the research progress of glutamate in the regulation of sleep and wakefulness, especially focuses on its role in the brainstem, lateral hypothalamus and basal forebrain. Glutamate in the brain stem regulates the brain activity and maintains muscle tone during the wakefulness, as well as adjusts the electroencephalograph (EEG) in rapid eye movement phase and leads to muscle weakness. Glutamate in the lateral hypothalamus participates in the lateral hypothalamic arousal system by activating orexins neurons. The basal forebrain glutamatergic neurons take part in EEG synchronization and cause the decrease of sleep. Finally,The glutamatergic neurons of the cerebral cortex is not just a target of the arousal system, but itself contribute to regulation of arousal. Meantime, the glutamatergic neurons can regulate sleep stages through interaction with other types of neurons, which forms a complex sleep-wake regulation network in the brain. These indicate that the switches between different phases of sleep and wakefulness have different neuronal circuits.So we also reviewed the neuronal circuits and mechanisms that glutamate may be involved in. This review will help us to get a better understanding of the roles of glutamate in sleep and wakefulness.
Glutamic Acid ; physiology ; Humans ; Sleep ; physiology ; Wakefulness ; physiology

OBJECTIVE: Obsessive compulsive and related disorders are a collection of debilitating psychiatric disorders in which the role of glutamate dysfunction in the underpinning neurobiology is becoming well established. N-acetyl cysteine (NAC) is a glutamate modulator with promising therapeutic effect. This paper presents a systematic review of clinical trials and case reports exploring the use of NAC for these disorders. A further objective was to detail the methodology of current clinical trials being conducted in the area. METHODS: PubMed, Web of Science and Cochrane Library Database were searched for human clinical trials or case reports investigating NAC in the treatment of obsessive compulsive disorder (OCD) or obsessive compulsive related disorders. Researchers with known involvement in NAC studies were contacted for any unpublished data. RESULTS: Four clinical trials and five case reports/series were identified. Study durations were commonly 12-weeks, using 2,400-3,000 mg/day of NAC. Overall, NAC demonstrates activity in reducing the severity of symptoms, with a good tolerability profile and minimal adverse effects. Currently there are three ongoing randomized controlled trials using NAC for OCD (two adults and one pediatric), and one for excoriation. CONCLUSION: Encouraging results have been demonstrated from the few pilot studies that have been conducted. These results are detailed, in addition to a discussion of future potential research.
Adult ; Cysteine* ; Glutamic Acid ; Humans ; Neurobiology ; Obsessive-Compulsive Disorder