ArticleProceedings of the National Academy of Sciences of the United States of America2009
Learning-related postburst afterhyperpolarization reduction in CA1 pyramidal neurons is mediated by protein kinase A.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 61 citations in OpenAlex.
- Article
- Sex-dependent alterations in the physiology of entorhinal cortex neurons in old heterozygous 3xTg-AD mice.Biology of sex differences · 2020Article
- The role of intrinsic excitability in the evolution of memory: Significance in memory allocation, consolidation, and updating.Neurobiology of learning and memory · 2020Review
- Learning and aging affect neuronal excitability and learning.Neurobiology of learning and memory · 2020Review
- Electrophysiological and Imaging Calcium Biomarkers of Aging in Male and Female 5×FAD Mice.Journal of Alzheimer's disease : JAD · 2020Article
- Regulation of intrinsic excitability: Roles for learning and memory, aging and Alzheimer's disease, and genetic diversity.Neurobiology of learning and memory · 2019Review
- Senescent neurophysiology: CaNeurobiology of learning and memory · 2019Review
- CREB, cellular excitability, and cognition: Implications for aging.Behavioural brain research · 2017Review
- Article
- Linking Memories across Time via Neuronal and Dendritic Overlaps in Model Neurons with Active Dendrites.Cell reports · 2016Article
- Surface expression of hippocampal NMDA GluN2B receptors regulated by fear conditioning determines its contribution to memory consolidation in adult rats.Scientific reports · 2016Article
- Aging-Related Hyperexcitability in CA3 Pyramidal Neurons Is Mediated by Enhanced A-Type K+ Channel Function and Expression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Increased Excitability of Both Principal Neurons and Interneurons during Associative Learning.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2015Review
- Increased Basolateral Amygdala Pyramidal Cell Excitability May Contribute to the Anxiogenic Phenotype Induced by Chronic Early-Life Stress.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Postsynaptic adenosine A2A receptors modulate intrinsic excitability of pyramidal cells in the rat basolateral amygdala.The international journal of neuropsychopharmacology · 2015Article
- Spatio-temporal in vivo recording of dCREB2 dynamics in Drosophila long-term memory processing.Neurobiology of learning and memory · 2015Article
- Age-related deficits in synaptic plasticity rescued by activating PKA or PKC in sensory neurons of Aplysia californica.Frontiers in aging neuroscience · 2015Article
- Transcriptional and epigenetic regulation of Hebbian and non-Hebbian plasticity.Neuropharmacology · 2014Review
- Modulation of BK channels contributes to activity-dependent increase of excitability through MTORC1 activity in CA1 pyramidal cells of mouse hippocampus.Frontiers in cellular neuroscience · 2014Article
- 5-HT7 receptors as modulators of neuronal excitability, synaptic transmission and plasticity: physiological role and possible implications in autism spectrum disorders.Frontiers in cellular neuroscience · 2014Review
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Learning-related reductions of the postburst afterhyperpolarization (AHP) in hippocampal pyramidal neurons have been shown ex vivo, after trace eyeblink conditioning. The AHP is also reduced by many neuromodulators, such as norepinephrine, via activation of protein kinases. Trace eyeblink conditioning, like other hippocampus-dependent tasks, relies on protein synthesis for consolidating the learned memory. Protein kinase A (PKA) has been shown to be a key contributor for protein synthesis via the cAMP-response element-binding pathway. Here, we have explored a potential involvement of PKA and protein kinase C (PKC) in maintaining the learning-related postburst AHP reduction observed in CA1 pyramidal neurons. Bath application of isoproterenol (1 muM), a beta-adrenergic agonist that activates PKA, significantly reduced the AHP in CA1 neurons from control animals, but not from rats that learned. This occlusion suggests that PKA activity is involved in maintaining the AHP reduction measured ex vivo after successful learning. In contrast, bath application of the PKC activator, (-) indolactam V (0.2 muM), significantly reduced the AHP in CA1 neurons from both control and trained rats, indicating that PKC activity is not involved in maintaining the AHP reduction at this point after learning.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.