Changes in the paired-pulse ratio after long-term potentiation induced by 2- and 100-Hz tetanus in rat visual cortical slices

2004 ◽  
Vol 1021 (1) ◽  
pp. 146-150 ◽  
Author(s):  
Bin Pan ◽  
Dong-Wei Yang ◽  
Tai-Zhen Han ◽  
Wen Xie
Keyword(s):  
Long Term Potentiation ◽  
Paired Pulse ◽  
Pulse Ratio ◽  
Term Potentiation ◽  
Visual Cortical ◽  
Cortical Slices

Visual deprivation decreases long-term potentiation in rat visual cortical slices

1993 ◽  
Vol 628 (1-2) ◽  
pp. 99-104 ◽  
Author(s):  
Richard L. Berry ◽  
A. Thomas Perkins ◽  
Timothy J. Teyler
Keyword(s):  
Long Term Potentiation ◽  
Visual Deprivation ◽  
Term Potentiation ◽  
Visual Cortical ◽  
Cortical Slices

scholarly journals Copper Inhibits NMDA Receptor-Independent LTP and Modulates the Paired-Pulse Ratio after LTP in Mouse Hippocampal Slices

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Nina L. Salazar-Weber ◽  
Jeffrey P. Smith
Keyword(s):  
Nmda Receptor ◽  
Ampa Receptors ◽  
Neurotransmitter Release ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Dependent Manner ◽  
Paired Pulse ◽  
Pulse Ratio ◽  
Term Potentiation

Copper misregulation has been implicated in the pathological processes underlying deterioration of learning and memory in Alzheimer's disease and other neurodegenerative disorders. Supporting this, inhibition of long-term potentiation (LTP) by copper (II) has been well established, but the exact mechanism is poorly characterized. It is thought that an interaction between copper and postsynaptic NMDA receptors is a major part of the mechanism; however, in this study, we found that copper (II) inhibited NMDA receptor-independent LTP in the CA3 region of hippocampal slices. In addition, in the CA3 and CA1 regions, copper modulated the paired-pulse ratio (PPR) in an LTP-dependent manner. Combined, this suggests the involvement of a presynaptic mechanism in the modulation of synaptic plasticity by copper. Inhibition of the copper-dependent changes in the PPR with cyclothiazide suggested that this may involve an interaction with the presynaptic AMPA receptors that regulate neurotransmitter release.

scholarly journals Pre- and Postnatal Propylthiouracil-Induced Hypothyroidism Impairs Synaptic Transmission and Plasticity in Area CA1 of the Neonatal Rat Hippocampus

Endocrinology ◽  
2003 ◽  
Vol 144 (9) ◽  
pp. 4195-4203 ◽  
Author(s):  
Li Sui ◽  
M. E. Gilbert
Keyword(s):  
Thyroid Hormone ◽  
Synaptic Transmission ◽  
Long Term Potentiation ◽  
Synaptic Function ◽  
Learning Deficits ◽  
Paired Pulse ◽  
Area Ca1 ◽  
Term Potentiation ◽  
Paired Pulse Depression

Abstract Thyroid hormones are essential for neonatal brain development. It is well established that insufficiency of thyroid hormone during critical periods of development can impair cognitive functions. The mechanisms that underlie learning deficits in hypothyroid animals, however, are not well understood. As impairments in synaptic function are likely to contribute to cognitive deficits, the current study tested whether thyroid hormone insufficiency during development would alter quantitative characteristics of synaptic function in the hippocampus. Developing rats were exposed in utero and postnatally to 0, 3, or 10 ppm propylthiouracil (PTU), a thyroid hormone synthesis inhibitor, administered in the drinking water of dams from gestation d 6 until postnatal day (PN) 30. Excitatory postsynaptic potentials and population spikes were recorded from the stratum radiatum and the pyramidal cell layer, respectively, in area CA1 of hippocampal slices from offspring between PN21 and PN30. Baseline synaptic transmission was evaluated by comparing input-output relationships between groups. Paired-pulse facilitation, paired-pulse depression, long-term potentiation, and long-term depression were recorded to examine short- and long-term synaptic plasticity. PTU reduced thyroid hormones, reduced body weight gain, and delayed eye-opening in a dose-dependent manner. Excitatory synaptic transmission was increased by developmental exposure to PTU. Thyroid hormone insufficiency was also dose-dependently associated with a reduction paired-pulse facilitation and long-term potentiation of the excitatory postsynaptic potential and elimination of paired-pulse depression of the population spike. The results indicate that thyroid hormone insufficiency compromises the functional integrity of synaptic communication in area CA1 of developing rat hippocampus and suggest that these changes may contribute to learning deficits associated with developmental hypothyroidism.

Interaction between paired-pulse facilitation and long-term potentiation during the stimulation of the cannabinoid and vanilloid systems in the dentate gyrus

2016 ◽  
Vol 1643 ◽  
pp. 27-34 ◽  
Author(s):  
Lida Tahmasebi ◽  
Alireza Komaki ◽  
Ruhollah Karamian ◽  
Siamak Shahidi ◽  
Abdolrahman Sarihi ◽  
...  
Keyword(s):  
Dentate Gyrus ◽  
Long Term Potentiation ◽  
Paired Pulse ◽  
Paired Pulse Facilitation ◽  
Term Potentiation ◽  
Stimulation Of
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