Ketamine blocks an NMDA receptor-mediated component of synaptic transmission in rat hippocampus in a voltage-dependent manner

1988 ◽  
Vol 92 (2) ◽  
pp. 213-217 ◽  
Author(s):  
S.N. Davies ◽  
S.T. Alford ◽  
E.J. Coan ◽  
R.A.J. Lester ◽  
G.L. Collingridge
Keyword(s):  
Nmda Receptor ◽  
Synaptic Transmission ◽  
Rat Hippocampus ◽  
Dependent Manner ◽  
Voltage Dependent

scholarly journals NMDA receptor dependence of mGlu-mediated depression of synaptic transmission in the CA1 region of the rat hippocampus

1996 ◽  
Vol 119 (6) ◽  
pp. 1239-1247 ◽  
Author(s):  
Jenni Harvey ◽  
Mary J. Palmer ◽  
Andrew J. Irving ◽  
Vernon R.J. Clarke ◽  
Graham L. Collingridge
Keyword(s):  
Nmda Receptor ◽  
Synaptic Transmission ◽  
Rat Hippocampus ◽  
Ca1 Region

β-Amyloid produces a delayed NMDA receptor- dependent reduction in synaptic transmission in rat hippocampus

Neuroreport ◽  
1996 ◽  
Vol 8 (1) ◽  
pp. 87-92 ◽  
Author(s):  
William K. Cullen ◽  
Jianqun Wu ◽  
Roger Anwyl ◽  
Michael J. Rowan
Keyword(s):  
Nmda Receptor ◽  
Synaptic Transmission ◽  
Rat Hippocampus ◽  
Β Amyloid

scholarly journals Laminar Specific Distribution of Lateral Excitatory Connections in the Rat Superior Colliculus

2004 ◽  
Vol 92 (6) ◽  
pp. 3500-3510 ◽  
Author(s):  
Yasuhiko Saito ◽  
Tadashi Isa
Keyword(s):  
Signal Processing ◽  
Nmda Receptor ◽  
Synaptic Transmission ◽  
Superior Colliculus ◽  
Neuronal Population ◽  
Wide Field ◽  
Specific Distribution ◽  
Excitatory Network ◽  
Voltage Dependent ◽  
Whole Cell Recordings

Premovement activities in neurons in the intermediate gray layer [stratum griseum intermediale (SGI)] of the mammalian superior colliculus (SC) are essential for initiation of orienting behaviors such as saccades. Our previous study demonstrated that burst activities are induced by synchronous activation of SGI neurons communicating within a local excitatory network, which depends on NMDA-receptor–dependent synaptic transmission and release from GABAA inhibition. Furthermore, dual whole cell recordings from adjacent neurons in SGI revealed that application of 10 μM bicuculline (Bic) and reduction of extracellular Mg2+ concentration (to 0.1 mM) induce spontaneous depolarization that is synchronous between neuron pairs, suggesting the recruitment of a large number of neurons communicating through intense excitatory connections. In the present study, we investigated the properties of synchronous depolarization and the fundamental structure of the lateral excitatory network that recruits a neuronal population in SC to synchronous activation, by analyzing the synchronicity of spontaneous depolarization induced in the presence of Bic plus low Mg2+. We found that 1) spontaneous depolarization exhibits bidirectional horizontal propagation among the SGI neuron pairs; 2) induction of spontaneous depolarization is not caused by activation of intrinsic voltage-dependent conductances; 3) neurons exposed to low Mg2+ alone exhibit spontaneous depolarization, although in this case the depolarization is less synchronous; and 4) neurons exposed to Bic alone exhibit synchronous depolarization, but less frequently than those exposed to both Bic and low Mg2+. Analysis of the synchronicity of spontaneous depolarization indicates that the distribution of lateral excitatory connections is markedly different among layers of SC; the SGI neurons form extensive lateral excitatory connections, whereas they are sparse or limited within subsets of neurons in the stratum griseum superficiale (SGS). Wide-field vertical neurons in the stratum opticum have features intermediate between neurons in the SGS and SGI. Such differences in the structure of lateral excitatory connections may reflect the different way signal processing is achieved in each layer of SC.

β-Amyloid selectively augments NMDA receptor-mediated synaptic transmission in rat hippocampus

Neuroreport ◽  
1995 ◽  
Vol 6 (17) ◽  
pp. 2409-2413 ◽  
Author(s):  
Jianqun Wu ◽  
Roger Anwyl ◽  
Michael J. Rowan
Keyword(s):  
Nmda Receptor ◽  
Synaptic Transmission ◽  
Rat Hippocampus ◽  
Β Amyloid

scholarly journals The sigma-1 receptor modulates NMDA receptor synaptic transmission and plasticity via SK channels in rat hippocampus

2006 ◽  
Vol 578 (1) ◽  
pp. 143-157 ◽  
Author(s):  
Marzia Martina ◽  
Marie-Eve B. Turcotte ◽  
Samantha Halman ◽  
Richard Bergeron
Keyword(s):  
Nmda Receptor ◽  
Synaptic Transmission ◽  
Rat Hippocampus ◽  
Sk Channels ◽  
Sigma 1 Receptor ◽  
Sigma 1

Effects of cytochrome c on the mitochondrial apoptosis-induced channel MAC

2004 ◽  
Vol 286 (5) ◽  
pp. C1109-C1117 ◽  
Author(s):  
Liang Guo ◽  
Dawn Pietkiewicz ◽  
Evgeny V. Pavlov ◽  
Sergey M. Grigoriev ◽  
John J. Kasianowicz ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Outer Membrane ◽  
Cell Types ◽  
Rnase A ◽  
Mitochondrial Outer Membrane ◽  
Dependent Manner ◽  
Mitochondrial Apoptosis ◽  
Noise Type ◽  
Voltage Dependent

Recent studies indicate that cytochrome c is released early in apoptosis without loss of integrity of the mitochondrial outer membrane in some cell types. The high-conductance mitochondrial apoptosis-induced channel (MAC) forms in the outer membrane early in apoptosis of FL5.12 cells. Physiological (micromolar) levels of cytochrome c alter MAC activity, and these effects are referred to as types 1 and 2. Type 1 effects are consistent with a partitioning of cytochrome c into the pore of MAC and include a modest decrease in conductance that is dose and voltage dependent, reversible, and has an increase in noise. Type 2 effects may correspond to “plugging” of the pore or destabilization of the open state. Type 2 effects are a dose-dependent, voltage-independent, and irreversible decrease in conductance. MAC is a heterogeneous channel with variable conductance. Cytochrome c affects MAC in a pore size-dependent manner, with maximal effects of cytochrome c on MAC with conductance of 1.9–5.4 nS. The effects of cytochrome c, RNase A, and high salt on MAC indicate that size, rather than charge, is crucial. The effects of dextran molecules of various sizes indicate that the pore diameter of MAC is slightly larger than that of 17-kDa dextran, which should be sufficient to allow the passage of 12-kDa cytochrome c. These findings are consistent with the notion that MAC is the pore through which cytochrome c is released from mitochondria during apoptosis.

scholarly journals GPI-1046 Increases Presenilin-1 Expression and Restores NMDA Channel Activity

2010 ◽  
Vol 37 (4) ◽  
pp. 457-467 ◽  
Author(s):  
Joseph P. Steiner ◽  
Kathryn B. Payne ◽  
Christopher Drummond Main ◽  
Sabrina D'Alfonso ◽  
Kirsten X. Jacobsen ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Synaptic Transmission ◽  
Brain Slices ◽  
Synaptic Activity ◽  
Presenilin 1 ◽  
Receptor Function ◽  
Channel Function ◽  
Nmda Channel ◽  
Nmda Receptor Function ◽  
6 Hydroxydopamine

Background:Previously we showed that 6-hydroxydopamine lesions of the substantia nigra eliminate corticostriatal LTP and that the neuroimmunolophilin ligand (NIL), GPI-1046, restores LTP.Methods:We used cDNA microarrays to determine what mRNAs may be over- or under-expressed in response to lesioning and/or GPI-1046 treatment. Patch clamp recordings were performed to investigate changes in NMDA channel function before and after treatments.Results:We found that 51 gene products were differentially expressed. Among these we found that GPI-1046 treatment up-regulated presenilin-1 (PS-1) mRNA abundance. This finding was confirmed using QPCR. PS-1 protein was also shown to be over-expressed in the striatum of lesioned/GPI-1046-treated rats. As PS-1 has been implicated in controlling NMDA-receptor function and LTP is reduced by lesioning we assayed NMDA mediated synaptic activity in striatal brain slices. The lesion-induced reduction of dopaminergic innervation was accompanied by the near complete loss of NDMA receptor-mediated synaptic transmission between the cortex and striatum. GPI-1046 treatment of the lesioned rats restored NMDA-mediated synaptic transmission but not the dopaminergic innervation. Restoration of NDMA channel function was apparently specific as the sodium channel current density was also reduced due to lesioning but GPI-1046 did not reverse this effect. We also found that restoration of NMDA receptor function was also not associated with either an increase in NMDA receptor mRNA or protein expression.Conclusion:As it has been previously shown that PS-1 is critical for normal NMDA receptor function, our data suggest that the improvement of excitatory neurotransmission occurs through the GPI-1046-induced up-regulation of PS-1.

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