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*

Astrocytes and neurons are inseparable partners in the brain. Neurotransmitters released from neurons activate corresponding G protein-coupled receptors (GPCR) expressed in astrocytes, resulting in release of gliotransmitters such as glutamate, D-serine, and ATP. These gliotransmitters in turn influence neuronal excitability and synaptic activities. Among these gliotransmitters, ATP regulates the level of network excitability and is critically involved in sleep homeostasis and astrocytic Ca2+ oscillations. ATP is known to be released from astrocytes by Ca2+-dependent manner. However, the precise source of Ca2+, whether it is Ca2+ entry from outside of cell or from the intracellular store, is still not clear yet. Here, we performed sniffer patch to detect ATP release from astrocyte by using various stimulation. We found that ATP was not released from astrocyte when Ca2+ was released from intracellular stores by activation of Galpha(q)-coupled GPCR including PAR1, P2YR, and B2R. More importantly, mechanical stimulation (MS)-induced ATP release from astrocyte was eliminated when external Ca2+ was omitted. Our results suggest that Ca2+ entry, but not release from intracellular Ca2+ store, is critical for MS-induced ATP release from astrocyte.
Adenosine Triphosphate* ; Astrocytes* ; Brain ; Glutamic Acid ; Homeostasis ; Neurons ; Neurotransmitter Agents

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

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

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

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* ; Glutamic Acid* ; Intracranial Aneurysm ; Ischemia* ; Prosencephalon* ; Rats, Inbred SHR*