Differential long-lasting potentiation of the NMDA and non-NMDA synaptic currents induced by metabotropic and NMDA receptor coactivation in cerebellar granule cells.
نویسندگان
چکیده
UNLABELLED Whole-cell patch-clamp recordings in rat cerebellar slices were used to investigate the effect of metabotropic glutamate receptor activation on mossy fibre-granule cell synaptic transmission. Transient application of 20 microM 1S, 3R-aminocyclopentane-1, 3-dicarboxylic acid simultaneously with low-frequency NMDA receptor activation induced long-lasting non-decremental potentiation of both NMDA and non-NMDA receptor-mediated synaptic transmission. Potentiation could be prevented by application of the metabotropic glutamate receptor antagonist (+)-O-methyl-4-carboxyphenyl-glycine at 500 microM. Characteristically, NMDA potentiation was two to three times as large as non-NMDA current potentiation, occurred only in a slow subcomponent, and was voltage-independent. This result demonstrates a pivotal role of NMDA receptors in the metabotropic potentiation of transmission, which may be important in regulating cerebellar information processing. KEYWORDS cerebellum, LTP, metabotropic receptors, NMDA receptors, patch-clamp, rat
منابع مشابه
P6: Metabotropic Glutamate Receptor-Dependent Role in the Formation of Long-Term Potentiation
Long-term potentiation (LTP) is a reflection of synaptic plasticity that induced by specific patterns of synaptic activity and has an important role in learning and memory. The first clue of the potential role of glutamate receptors in LTP was in 1991 with the observation that the mGluR agonists 1-amino-1, 3-cyclopentanedicarboxylic acid (ACPD), increased LTP. Studies have shown that ACPD induc...
متن کاملP19: Long-Term Potentiation
The term synaptic plasticity points to a series of persistent changes related to the activity of synapses. Long-term potentiation (LTP) is a reflection of synaptic plasticity that has an important role in learning and memory. LTP is a long-lasting increase of synaptic activity due to enhancement of excitatory synaptic transmission after a high-frequency train of electrical stimulations. Differe...
متن کاملThe effect of ketamine on NMDA receptor-mediated LTP depends on ketamine effects on non-NMDA-mediated synaptic transmission in CA1 area of rat hippocampal slices
It has been reported that ketamine as an uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist has also non-NMDA receptor antagonist properties. We recently found that ketamine (20 ?M) affected differently induction of NMDA receptor-mediated long-term potentiation (LTP) when administered 30 min prior to tetanic Primed-Bursts (PBs) stimulation. On the other hand, ketamine also influenced...
متن کاملThe effect of ketamine on NMDA receptor-mediated LTP depends on ketamine effects on non-NMDA-mediated synaptic transmission in CA1 area of rat hippocampal slices
It has been reported that ketamine as an uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist has also non-NMDA receptor antagonist properties. We recently found that ketamine (20 ?M) affected differently induction of NMDA receptor-mediated long-term potentiation (LTP) when administered 30 min prior to tetanic Primed-Bursts (PBs) stimulation. On the other hand, ketamine also influenced...
متن کاملEvidence for NMDA and mGlu receptor-dependent long-term potentiation of mossy fiber-granule cell transmission in rat cerebellum.
Long-term potentiation (LTP) is a form of synaptic plasticity that can be revealed at numerous hippocampal and neocortical synapses following high-frequency activation of N-methyl--aspartate (NMDA) receptors. However, it was not known whether LTP could be induced at the mossy fiber-granule cell relay of cerebellum. This is a particularly interesting issue because theories of the cerebellum do n...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- The European journal of neuroscience
دوره 8 6 شماره
صفحات -
تاریخ انتشار 1996