Potential molecular mechanisms for decreased synaptic glutamate release in dysbindin-1 mutant mice

نویسندگان
چکیده

برای دانلود باید عضویت طلایی داشته باشید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Loss of dysbindin-1, a risk gene for schizophrenia, leads to impaired group 1 metabotropic glutamate receptor function in mice

The expression of dysbindin-1, a protein coded by the risk gene dtnbp1, is reduced in the brains of schizophrenia patients. Evidence indicates a role of dysbindin-1 in dopaminergic and glutamatergic transmission. Glutamatergic transmission and plasticity at excitatory synapses is critically regulated by G-protein coupled metabotropic glutamate receptor (mGluR) family members, that have been imp...

متن کامل

Abnormal association of mutant huntingtin with synaptic vesicles inhibits glutamate release.

In Huntington disease (HD), polyglutamine expansion causes the disease protein huntingtin to aggregate and accumulate in the nucleus and cytoplasm. The cytoplasmic huntingtin aggregates are found in axonal terminals and electrophysiological studies show that mutant huntingtin affects synaptic neurotransmission. However, the biochemical basis for huntingtin-mediated synaptic dysfunction is uncle...

متن کامل

Molecular Mechanisms in Synaptic Plasticity

Brain is a sophisticated information processing and storage system with capabilities unmatched by any manmade computers. Neurons, the primary building blocks of the brain are structurally and functionally specialized to do these functions. The neuronal membrane is equipped with several types of ion channel and ion pump proteins which enable it to conduct nerve impulses in the form of electroche...

متن کامل

ATP-dependent glutamate uptake into synaptic vesicles from cerebellar mutant mice.

The ATP-dependent glutamate uptake system in synaptic vesicles prepared from mouse cerebellum was characterized, and the levels of glutamate uptake were investigated in the cerebellar mutant mice, staggerer and weaver, whose main defect is the loss of cerebellar granule cells, and the nervous mutant, whose main defect is the loss of Purkinje cells. The ATP-dependent glutamate uptake is stimulat...

متن کامل

ALLN rescues an in vitro excitatory synaptic transmission deficit in Lis 1 1 mutant mice

25 LIS1 gene mutations lead to a rare neurological disorder, classical Lissencephaly, 26 characterized by brain malformations, mental retardation, seizures and 27 premature death. Mice heterozygous for Lis1 (Lis1) exhibit cortical 28 malformations, defects in neuronal migration, increased glutamate-mediated 29 synaptic transmission and spontaneous electrographic seizures. Recent work 30 demonst...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

ژورنال

عنوان ژورنال: Schizophrenia Research

سال: 2013

ISSN: 0920-9964

DOI: 10.1016/j.schres.2013.01.037