PDE-7 Inhibitor BRL-50481 Reduces Neurodegeneration and Long-Term Memory Deficits in Mice Following Sevoflurane Exposure

2020 ◽  
Vol 11 (9) ◽  
pp. 1353-1358 ◽  
Author(s):  
Yingle Chen ◽  
Shunyuan Li ◽  
Xianmei Zhong ◽  
Zhenming Kang ◽  
Rulei Chen
Keyword(s):  
Memory Deficits ◽  
Long Term Memory ◽  
Term Memory

Abstract P783: Alpha 7 -Acetylcholine Receptor Signaling Reduces Neuronal Apoptosis After Subarachnoid Hemorrhage

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Ari Dienel ◽  
Remya A Veettil ◽  
Kanako Matsumura ◽  
Peeyush Kumar T. ◽  
Spiros Blackburn ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Acetylcholine Receptor ◽  
Neuronal Apoptosis ◽  
Neuronal Survival ◽  
Memory Function ◽  
Memory Deficits ◽  
Long Term Memory ◽  
Term Memory ◽  
Receptor Knockout Mouse

Subarachnoid hemorrhage induces neuronal apoptosis which causes acute and long-term memory deficits. Ourhypothesis is that agonism of α7-acetylcholine receptors attenuates neuronal apoptosis and improves memorydeficits in SAH mice. Mice were randomly assigned into the experimental groups. One cohort was euthanizedone day after SAH to assess neuronal apoptosis and signaling pathways. A second cohort survived for 30 dayspost-SAH to test long-term memory function. Inhibitors and an α7-acetylcholine receptor knockout mouse wereused. Neurobehavioral performance was assessed on days 1-3, 5, 7, and 23-28. All outcomes were performedand all data was analyzed by a blinded investigator. The α7-acetylcholine receptor agonist prevented neuronalapoptosis and improved acute memory deficits caused by SAH via activation of the PI3K/Akt pathway in neurons.Agonism of the α7-acetylcholine receptor was beneficial in both male and female mice, although the protectionin females was significantly better than in male mice. α7-acetylcholine receptor agonism did not provide anybenefit in α7-acetylcholine receptor knockout mice subjected to SAH. Treatment with the α7-acetylcholinereceptor agonist for 3 days after SAH led to improved working memory one month after SAH suggesting thatacutely improving neuronal survival can have long-lasting benefits. The α7-acetylcholine receptor may be atherapeutic target for SAH which can promote neuronal survival acutely after SAH, but also confer long-lastingmemory benefits. The findings of this study support the α7-acetylcholine receptor as a treatment target whichmay attenuate the long-term memory deficits which SAH patients suffer from.

Developmental exposure to methylmercury elicits early cell death in the cerebral cortex and long‐term memory deficits in the rat

2008 ◽  
Vol 27 (2) ◽  
pp. 165-174 ◽  
Author(s):  
Luca Ferraro ◽  
Maria Cristina Tomasini ◽  
Sergio Tanganelli ◽  
Roberta Mazza ◽  
Addolorata Coluccia ◽  
...  
Keyword(s):  
Cell Death ◽  
Cerebral Cortex ◽  
Memory Deficits ◽  
Long Term Memory ◽  
Developmental Exposure ◽  
Term Memory

scholarly journals SU30. Long-Term Memory Deficits in Schizophrenia: Are All Things Equal?

2017 ◽  
Vol 43 (suppl_1) ◽  
pp. S171-S172
Author(s):  
Susan Rossell
Keyword(s):  
Memory Deficits ◽  
Long Term Memory ◽  
Term Memory

scholarly journals Selenofuranoside improves long-term memory deficits in rats after exposure to monosodium glutamate: Involvement of Na+, K+-ATPase activity

2018 ◽  
Vol 184 ◽  
pp. 27-33 ◽  
Author(s):  
Juliana Bernera Ramalho ◽  
Aryele Pinto Izaguirry ◽  
Melina Bucco Soares ◽  
Cristiano Chiapinotto Spiazzi ◽  
Natasha Frasson Pavin ◽  
...  
Keyword(s):  
Atpase Activity ◽  
Monosodium Glutamate ◽  
Memory Deficits ◽  
Long Term Memory ◽  
Term Memory

scholarly journals Long-Term Memory Deficits are Associated with Elevated Synaptic ERK1/2 Activation and Reversed by mGluR5 Antagonism in an Animal Model of Autism

2014 ◽  
Vol 39 (7) ◽  
pp. 1664-1673 ◽  
Author(s):  
Ronald R Seese ◽  
Anna R Maske ◽  
Gary Lynch ◽  
Christine M Gall
Keyword(s):  
Animal Model ◽  
Memory Deficits ◽  
Long Term Memory ◽  
Term Memory

Long-term memory deficits in patients with malignant gliomas

1995 ◽  
Vol 25 (3) ◽  
pp. 227-238 ◽  
Author(s):  
P�r Salander ◽  
Thomas Karlsson ◽  
Tommy Bergenheim ◽  
Roger Henriksson
Keyword(s):  
Malignant Gliomas ◽  
Memory Deficits ◽  
Long Term Memory ◽  
Term Memory

scholarly journals CREB overexpression in dorsal CA1 ameliorates long-term memory deficits in aged rats

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Xiao-Wen Yu ◽  
Daniel M Curlik ◽  
M Matthew Oh ◽  
Jerry CP Yin ◽  
John F Disterhoft
Keyword(s):  
Molecular Mechanisms ◽  
Pyramidal Neurons ◽  
Dorsal Hippocampus ◽  
Memory Deficits ◽  
Camp Response Element Binding ◽  
Intrinsic Excitability ◽  
Long Term Memory ◽  
Term Memory ◽  
Age Related

The molecular mechanisms underlying age-related cognitive deficits are not yet fully elucidated. In aged animals, a decrease in the intrinsic excitability of CA1 pyramidal neurons is believed to contribute to age-related cognitive impairments. Increasing activity of the transcription factor cAMP response element-binding protein (CREB) in young adult rodents facilitates cognition, and increases intrinsic excitability. However, it has yet to be tested if increasing CREB expression also ameliorates age-related behavioral and biophysical deficits. To test this hypothesis, we virally overexpressed CREB in CA1 of dorsal hippocampus. Rats received CREB or control virus, before undergoing water maze training. CREB overexpression in aged animals ameliorated the long-term memory deficits observed in control animals. Concurrently, cells overexpressing CREB in aged animals had reduced post-burst afterhyperpolarizations, indicative of increased intrinsic excitability. These results identify CREB modulation as a potential therapy to treat age-related cognitive decline.

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