MRNA differential display identification of thyroid hormone-responsive protein (THRP) gene in association with early phase of long-term potentiation

Hippocampus ◽  
2001 ◽  
Vol 11 (6) ◽  
pp. 637-646 ◽  
Author(s):  
Y.P. Tang ◽  
Y.L. Ma ◽  
S.K. Chen ◽  
E.H.Y. Lee
Keyword(s):  
Thyroid Hormone ◽  
Differential Display ◽  
Early Phase ◽  
Long Term Potentiation ◽  
Mrna Differential Display ◽  
Term Potentiation

Expression of Bcl2 Family Genes in the Early Phase of Long-Term Potentiation

2014 ◽  
Vol 158 (1) ◽  
pp. 77-79 ◽  
Author(s):  
P. D. Lisachev ◽  
V. O. Pustyl’nyak ◽  
M. B. Shtark
Keyword(s):  
Early Phase ◽  
Long Term Potentiation ◽  
Bcl2 Family ◽  
Term Potentiation

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.

scholarly journals The biophysical basis underlying the maintenance of early phase long-term potentiation

2020 ◽  
Author(s):  
Moritz F. P. Becker ◽  
Christian Tetzlaff
Keyword(s):  
Receptor Binding ◽  
Early Phase ◽  
Morphological Changes ◽  
Long Term Potentiation ◽  
Biophysical Model ◽  
Recycling Endosomes ◽  
Term Potentiation ◽  
Wide Range ◽  
Synaptic Changes

AbstractThe maintenance of synaptic changes resulting from long-term potentiation (LTP) is essential for brain function such as memory and learning. Different LTP phases have been associated with diverse molecular processes and pathways, and the molecular underpinnings of LTP on the short, as well as long time scales, are well established. However, the principles on the intermediate time scale of 1-6 hours that mediate the early phase of LTP (E-LTP) remain elusive. We hypothesize that the interplay between specific features of postsynaptic receptor trafficking is responsible for sustaining synaptic changes during this LTP phase. We test this hypothesis by formalizing a biophysical model that integrates several experimentally-motivated mechanisms. The model captures a wide range of experimental findings and predicts that synaptic changes are preserved for hours when the receptor dynamics are shaped by the interplay of structural changes of the spine in conjunction with increased trafficking from recycling endosomes and the cooperative binding of receptors. Furthermore, our model provides several predictions to verify our findings experimentally.Author summaryThe cognitive ability of learning is associated with plasticity-induced changes in synaptic transmission efficacy mediated by AMPA receptors. Synaptic changes depend on a multitude of molecular and physiological mechanisms, building complex interaction networks. By formalizing and employing a biophysical model of AMPAR trafficking, we unravel and evaluate the interplay between key mechanisms such as receptor binding, exocytosis, morphological changes, and cooperative receptor binding. Our findings indicate that cooperative receptor binding in conjunction with morphological changes of the spine and increased trafficking from recycling endosomes leads to the maintenance of synaptic changes on behaviorally relevant time spans. Characterizing the principles underlying synaptic changes will provide insight into the role of synaptic dynamics in neurodegenerative diseases.

scholarly journals The biophysical basis underlying the maintenance of early phase long-term potentiation

2021 ◽  
Vol 17 (3) ◽  
pp. e1008813
Author(s):  
Moritz F. P. Becker ◽  
Christian Tetzlaff
Keyword(s):  
Early Phase ◽  
Structural Changes ◽  
Long Term Potentiation ◽  
Biophysical Model ◽  
Term Potentiation ◽  
Wide Range ◽  
Long Time ◽  
Synaptic Changes ◽  
Experimental Findings

The maintenance of synaptic changes resulting from long-term potentiation (LTP) is essential for brain function such as memory and learning. Different LTP phases have been associated with diverse molecular processes and pathways, and the molecular underpinnings of LTP on the short, as well as long time scales, are well established. However, the principles on the intermediate time scale of 1-6 hours that mediate the early phase of LTP (E-LTP) remain elusive. We hypothesize that the interplay between specific features of postsynaptic receptor trafficking is responsible for sustaining synaptic changes during this LTP phase. We test this hypothesis by formalizing a biophysical model that integrates several experimentally-motivated mechanisms. The model captures a wide range of experimental findings and predicts that synaptic changes are preserved for hours when the receptor dynamics are shaped by the interplay of structural changes of the spine in conjunction with increased trafficking from recycling endosomes and the cooperative binding of receptors. Furthermore, our model provides several predictions to verify our findings experimentally.

Gene Expression in the Conversion of Early-Phase to Late-Phase Long-Term Potentiation

2005 ◽  
Vol 1048 (1) ◽  
pp. 259-271 ◽  
Author(s):  
PHILIP R. LEE ◽  
JONATHAN E. COHEN ◽  
KEVIN G. BECKER ◽  
R. DOUGLAS FIELDS
Keyword(s):  
Gene Expression ◽  
Early Phase ◽  
Late Phase ◽  
Long Term Potentiation ◽  
Term Potentiation

scholarly journals Expression of p53 Target Genes in the Early Phase of Long-Term Potentiation in the Rat Hippocampal CA1 Area

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Vladimir O. Pustylnyak ◽  
Pavel D. Lisachev ◽  
Mark B. Shtark
Keyword(s):  
Synaptic Plasticity ◽  
Early Phase ◽  
Target Genes ◽  
P53 Protein ◽  
Long Term Potentiation ◽  
Protein Levels ◽  
Basal Expression ◽  
Term Potentiation ◽  
Ca1 Area

Gene expression plays an important role in the mechanisms of long-term potentiation (LTP), which is a widely accepted experimental model of synaptic plasticity. We have studied the expression of at least 50 genes that are transcriptionally regulated by p53, as well as other genes that are related to p53-dependent processes, in the early phase of LTP. Within 30 min after Schaffer collaterals (SC) tetanization, increases in the mRNA and protein levels of Bax, which are upregulated by p53, and a decrease in the mRNA and protein levels of Bcl2, which are downregulated by p53, were observed. The inhibition of Mdm2 by nutlin-3 increased the basal p53 protein level and rescued its tetanization-induced depletion, which suggested the involvement of Mdm2 in the control over p53 during LTP. Furthermore, nutlin-3 caused an increase in the basal expression of Bax and a decrease in the basal expression of Bcl2, whereas tetanization-induced changes in their expression were occluded. These results support the hypothesis that p53 may be involved in transcriptional regulation during the early phase of LTP. We hope that the presented data may aid in the understanding of the contribution of p53 and related genes in the processes that are associated with synaptic plasticity.

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