Effects of ventral hippocampal long-term potentiation and depression on the gamma-band local field potential in anesthetized rats

2004 ◽  
Vol 157 (2) ◽  
Author(s):  
Yoshinori Izaki ◽  
Masatoshi Takita ◽  
Masahiko Nomura ◽  
Tatsuo Akema
Keyword(s):  
Local Field ◽  
Local Field Potential ◽  
Field Potential ◽  
Long Term Potentiation ◽  
Gamma Band ◽  
Anesthetized Rats ◽  
Term Potentiation

Effects of hippocampus-induced prefrontal long-term depression on gamma-band local field potential in anesthetized rats

2002 ◽  
Vol 330 (2) ◽  
pp. 204-206 ◽  
Author(s):  
Yoshinori Izaki ◽  
Masatoshi Takita ◽  
Masahiko Nomura ◽  
Tatsuo Akema
Keyword(s):  
Local Field ◽  
Local Field Potential ◽  
Field Potential ◽  
Gamma Band ◽  
Long Term Depression ◽  
Anesthetized Rats

Anoxic LTP is mediated by the redox modulatory site of the NMDA receptor

1994 ◽  
Vol 72 (6) ◽  
pp. 3017-3022 ◽  
Author(s):  
H. Gozlan ◽  
D. Diabira ◽  
P. Chinestra ◽  
Y. Ben-Ari
Keyword(s):  
Nmda Receptor ◽  
Hippocampal Neurons ◽  
Field Potential ◽  
Extracellular Recording ◽  
Glucose Deprivation ◽  
Long Term Potentiation ◽  
Receptor Field ◽  
Oxygen And Glucose Deprivation ◽  
Term Potentiation

1. The effects of redox reagents, 5,5'-dithiobis-2-nitrobenzoic acid (DTNB) and tris(carboxyethyl)phosphine (TCEP), on anoxia-induced long-term potentiation (LTP) were investigated in CA1 hippocampal neurons using extracellular recording techniques. Experiments were performed in the presence of 0.1 mM MgCl2 and 10 microM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) to pharmacologically isolate N-methyl-D-aspartate (NMDA) receptor-mediated responses. 2. DTNB (200 microM), a thiol oxidizing reagent, reduces by 52 +/- 9% (mean +/- SE) (n = 9/9) NMDA-receptor field potentials evoked by electrical stimulation of Schaffer collaterals and this effect could not be reversed by extensive washing. Nearly the same reduction of the initial response was obtained with different concentrations of DTNB (100 and 500 microM), but the time required to reach the maximal inhibition was concentration-dependent. 3. In keeping with an earlier study oxygen and glucose deprivation for 2-3 min induced a long-term potentiation (LTP) of the NMDA receptor response (+65 +/- 16%, n = 4/6). This potentiation was reversed by DTNB (100-500 microM) (-47 +/- 18%; n = 4/4) and the initial LTP could not be restored upon extensive washing of the drug. 4. TCEP (200 microM), a reagent which reduces S-S bond, amplified the electrically evoked NMDA-receptor EPSP (+27 +/- 12%; n = 3). In addition, TCEP (200 microM), nearly completely reversed the effect of DTNB (200 microM) on anoxia-induced LTP (+56 +/- 19%; n = 3/3). Preliminary results also indicate that TCEP occlude anoxic-LTP (n = 3/4). 5. Following DTNB (200 microM) treatment, oxygen and glucose deprivation did not generate anoxic LTP and extensive washing did not restore a potentiated NMDA field potential. 6. These observations strongly suggest that the redox site of the NMDA receptor is involved in the induction and the maintenance of the anoxic LTP of the NMDA receptor-mediated response in CA1.

Isoflurane Impairs Learning and Hippocampal Long-term Potentiation via the Saturation of Synaptic Plasticity

2014 ◽  
Vol 121 (2) ◽  
pp. 302-310 ◽  
Author(s):  
Kazuhiro Uchimoto ◽  
Tomoyuki Miyazaki ◽  
Yoshinori Kamiya ◽  
Takahiro Mihara ◽  
Yukihide Koyama ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Western Blotting ◽  
Field Potential ◽  
Inhibitory Avoidance ◽  
Long Term Potentiation ◽  
Fear Learning ◽  
Male Rats ◽  
Avoidance Task ◽  
Term Potentiation

Abstract Background: General anesthesia induces long-lasting cognitive and learning deficits. However, the underlying mechanism remains unknown. The GluA1 subunit of AMPAR is a key molecule for learning and synaptic plasticity, which requires trafficking of GluA1-containing AMPARs into the synapse. Methods: Adult male rats were exposed to 1.8% isoflurane for 2 h and subjected to an inhibitory avoidance task, which is a hippocampus-dependent contextual fear learning paradigm (n = 16 to 39). The in vitro extracellular field potential of hippocampal synapses between the Schaffer collateral and the CA1 was evaluated using a multielectrode recorder (n = 6 per group). GluA1 expression in the synaptoneurosome was assessed using Western blotting (n = 5 to 8). The ubiquitination level of GluA1 was evaluated using immunoprecipitation and Western blotting (n = 7 per group). Results: Seven days after exposure to 1.8% isoflurane for 2 h (Iso1.8), the inhibitory avoidance learning (control vs. Iso1.8; 294 ± 34 vs. 138 ± 28, the mean ± SEM [%]; P = 0.002) and long-term potentiation (125.7 ± 6.1 vs. 105.7 ± 3.3; P < 0.001) were impaired. Iso1.8 also temporarily increased GluA1 in the synaptoneurosomes (100 ± 9.7 vs. 138.9 ± 8.9; P = 0.012) and reduced the GluA1 ubiquitination, a main degradation pathway of GluA1 (100 ± 8.7 vs. 71.1 ± 6.1; P = 0.014). Conclusions: Isoflurane impairs hippocampal learning and modulates synaptic plasticity in the postanesthetic period. Increased GluA1 may reduce synaptic capacity for additional GluA1-containing AMPARs trafficking.

scholarly journals Neuronal NT-3 Is not Required For Synaptic Transmission or Long-Term Potentiation in Area CA1 of the Adult Rat Hippocampus

1999 ◽  
Vol 6 (3) ◽  
pp. 267-275 ◽  
Author(s):  
Long Ma ◽  
Gerald Reis ◽  
Luis F. Parada ◽  
Erin M. Schuman
Keyword(s):  
Synaptic Transmission ◽  
Hippocampal Slices ◽  
Field Potential ◽  
Early Death ◽  
Long Term Potentiation ◽  
Wild Type ◽  
Adult Rat ◽  
Term Potentiation ◽  
Knockout Animals

Neurotrophic factors, including BDNF and NT-3, have been implicated in the regulation of synaptic transmission and plasticity. Previous attempts to analyze synaptic transmission and plasticity in mice lacking the NT-3 gene have been hampered by the early death of the NT-3 homozygous knockout animals. We have bypassed this problem by examining synaptic transmission in mice in which the NT-3 gene is deleted in neurons later in development, by crossing animals expressing the CRE recombinase driven by the synapsin I promoter to animals in which the NT-3 gene is floxed. We conducted blind field potential recordings at the Schaffer collateral–CA1 synapse in hippocampal slices from homozygous knockout and wild-type mice. We examined the following indices of synaptic transmission: (1) input-output relationship; (2) paired-pulse facilitation; (3) post-tetanic potentiation; and (4) long-term potentiation: induced by two different protocols: (a) two trains of 100-Hz stimulation and (b) theta burst stimulation. We found no difference between the knockout and wild-type mice in any of the above measurements. These results suggest that neuronal NT-3 does not play an essential role in normal synaptic transmission and some forms of plasticity in the mouse hippocampus.

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