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299 results on '"Heinemann, Stephen F."'

1. Astrocytes contribute to gamma oscillations and recognition memory

Author

Lee, Hosuk Sean, Ghetti, Andrea, Pinto-Duarte, António, Wang, Xin, Dziewczapolski, Gustavo, Galimi, Francesco, Huitron-Resendiz, Salvador, Piña-Crespo, Juan C, Roberts, Amanda J, Verma, Inder M, Sejnowski, Terrence J, and Heinemann, Stephen F

Subjects
Biomedical and Clinical Sciences, Biological Psychology, Medical Physiology, Neurosciences, Psychology, Mental Health, Behavioral and Social Science, Brain Disorders, Basic Behavioral and Social Science, Aetiology, 2.1 Biological and endogenous factors, Underpinning research, 1.1 Normal biological development and functioning, Mental health, Neurological, Animals, Astrocytes, Brain Waves, Calcium Signaling, Carbachol, Electroencephalography, Gene Expression, Glutamic Acid, Hippocampus, Metalloendopeptidases, Mice, Mice, Inbred C57BL, Mice, Transgenic, Models, Neurological, Nerve Net, Recognition, Psychology, Recombinant Proteins, Synaptic Transmission, Tetanus Toxin, Tissue Culture Techniques, alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid, glia, electroencephalogram, network oscillation, gliotransmitter, glial fibrillary acidic protein
Abstract

Glial cells are an integral part of functional communication in the brain. Here we show that astrocytes contribute to the fast dynamics of neural circuits that underlie normal cognitive behaviors. In particular, we found that the selective expression of tetanus neurotoxin (TeNT) in astrocytes significantly reduced the duration of carbachol-induced gamma oscillations in hippocampal slices. These data prompted us to develop a novel transgenic mouse model, specifically with inducible tetanus toxin expression in astrocytes. In this in vivo model, we found evidence of a marked decrease in electroencephalographic (EEG) power in the gamma frequency range in awake-behaving mice, whereas neuronal synaptic activity remained intact. The reduction in cortical gamma oscillations was accompanied by impaired behavioral performance in the novel object recognition test, whereas other forms of memory, including working memory and fear conditioning, remained unchanged. These results support a key role for gamma oscillations in recognition memory. Both EEG alterations and behavioral deficits in novel object recognition were reversed by suppression of tetanus toxin expression. These data reveal an unexpected role for astrocytes as essential contributors to information processing and cognitive behavior.

Published
2014

4. A role for calcium-permeable AMPA receptors in synaptic plasticity and learning.

Author

Wiltgen, Brian J, Royle, Gordon A, Gray, Erin E, Abdipranoto, Andrea, Thangthaeng, Nopporn, Jacobs, Nate, Saab, Faysal, Tonegawa, Susumu, Heinemann, Stephen F, O'Dell, Thomas J, Fanselow, Michael S, and Vissel, Bryce

Subjects
Hippocampus, Synapses, Animals, Mice, Knockout, Mice, Calcium, Receptors, AMPA, Receptors, N-Methyl-D-Aspartate, Learning, Neuronal Plasticity, Long-Term Potentiation, Female, Male, Knockout, Receptors, AMPA, N-Methyl-D-Aspartate, General Science & Technology
Abstract

A central concept in the field of learning and memory is that NMDARs are essential for synaptic plasticity and memory formation. Surprisingly then, multiple studies have found that behavioral experience can reduce or eliminate the contribution of these receptors to learning. The cellular mechanisms that mediate learning in the absence of NMDAR activation are currently unknown. To address this issue, we examined the contribution of Ca(2+)-permeable AMPARs to learning and plasticity in the hippocampus. Mutant mice were engineered with a conditional genetic deletion of GluR2 in the CA1 region of the hippocampus (GluR2-cKO mice). Electrophysiology experiments in these animals revealed a novel form of long-term potentiation (LTP) that was independent of NMDARs and mediated by GluR2-lacking Ca(2+)-permeable AMPARs. Behavioral analyses found that GluR2-cKO mice were impaired on multiple hippocampus-dependent learning tasks that required NMDAR activation. This suggests that AMPAR-mediated LTP interferes with NMDAR-dependent plasticity. In contrast, NMDAR-independent learning was normal in knockout mice and required the activation of Ca(2+)-permeable AMPARs. These results suggest that GluR2-lacking AMPARs play a functional and previously unidentified role in learning; they appear to mediate changes in synaptic strength that occur after plasticity has been established by NMDARs.

Published
2010

6. Mice lacking doublecortin and doublecortin-like kinase 2 display altered hippocampal neuronal maturation and spontaneous seizures

Author

Kerjan, Géraldine, Koizumi, Hiroyuki, Han, Edward B, Dubé, Celine M, Djakovic, Stevan N, Patrick, Gentry N, Baram, Tallie Z, Heinemann, Stephen F, and Gleeson, Joseph G

Subjects
Epilepsy, Brain Disorders, Neurosciences, Neurodegenerative, 2.1 Biological and endogenous factors, Aetiology, Neurological, Animals, Cell Differentiation, Cell Polarity, Dendrites, Doublecortin Domain Proteins, Doublecortin Protein, Hippocampus, Interneurons, Mice, Mice, Knockout, Microtubule-Associated Proteins, Neurons, Neuropeptides, Protein Serine-Threonine Kinases, Proto-Oncogene Proteins c-fos, Pyramidal Cells, Seizures, Somatostatin, Survival Analysis, Synapses, Weaning, gamma-Aminobutyric Acid, epilepsy, receptive field, pyramidal neuron, dendrites, delamination
Abstract

Mutations in doublecortin (DCX) are associated with intractable epilepsy in humans, due to a severe disorganization of the neocortex and hippocampus known as classical lissencephaly. However, the basis of the epilepsy in lissencephaly remains unclear. To address potential functional redundancy with murin Dcx, we targeted one of the closest homologues, doublecortin-like kinase 2 (Dclk2). Here, we report that Dcx; Dclk2-null mice display frequent spontaneous seizures that originate in the hippocampus, with most animals dying in the first few months of life. Elevated hippocampal expression of c-fos and loss of somatostatin-positive interneurons were identified, both known to correlate with epilepsy. Dcx and Dclk2 are coexpressed in developing hippocampus, and, in their absence, there is dosage-dependent disrupted hippocampal lamination associated with a cell-autonomous simplification of pyramidal dendritic arborizations leading to reduced inhibitory synaptic tone. These data suggest that hippocampal dysmaturation and insufficient receptive field for inhibitory input may underlie the epilepsy in lissencephaly, and suggest potential therapeutic strategies for controlling epilepsy in these patients.

Published
2009

12. Ionotropic glutamate receptors in GtoPdb v.2023.1

Author

Bettler, Bernhard, primary, Collingridge, Graham L., primary, Dingledine, Ray, primary, Heinemann, Stephen F., primary, Hollmann, Michael, primary, Lerma, Juan, primary, Lodge, David, primary, Mayer, Mark, primary, Mishina, Masayoshi, primary, Mulle, Christophe, primary, Nakanishi, Shigetada, primary, Olsen, Richard, primary, Peineau, Stephane, primary, Peters, John A., primary, Seeburg, Peter, primary, Spedding, Michael, primary, and Watkins, Jeffrey C., primary

Published
2023
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13. Workshop on Schizophrenia

Author

Barondes, Samuel H., Alberts, Bruce M., Andreasen, Nancy C., Bargmann, Cornelia, Benes, Francine, Goldman-Rakic, Patricia, Gottesman, Irving, Heinemann, Stephen F., Jones, Edward G., Kirschner, Marc, Lewis, David, Raff, Martin, Roses, Allen, Rubenstein, John, Snyder, Solomon, Watson, Stanley J., Weinberger, Daniel R., and Yolken, Robert H.

Published
1997

14. Correction for Aβ induces astrocytic glutamate release, extrasynaptic NMDA receptor activation, and synaptic loss

Author

Talantova, Maria, Sanz-Blasco, Sara, Zhang, Xiaofei, Xia, Peng, Akhtar, Mohd Waseem, Okamoto, Shu-ichi, Dziewczapolski, Gustavo, Nakamura, Tomohiro, Cao, Gang, Pratt, Alexander E., Kang, Yeon-Joo, Tu, Shichun, Molokanova, Elena, McKercher, Scott R., Hires, Samuel Andrew, Sason, Hagit, Stouffer, David G., Buczynski, Matthew W., Solomon, James P., Michael, Sarah, Powers, Evan T., Kelly, Jeffery W., Roberts, Amanda, Tong, Gary, Fang-Newmeyer, Traci, Parker, James, Holland, Emily A., Zhang, Dongxian, Nakanishi, Nobuki, Chen, H.-S. Vincent, Wolosker, Herman, Wang, Yuqiang, Parsons, Loren H., Ambasudhan, Rajesh, Masliah, Eliezer, Heinemann, Stephen F., Piña-Crespo, Juan C., and Lipton, Stuart A.

Published
2013

15. Aβ induces astrocytic glutamate release, extrasynaptic NMDA receptor activation, and synaptic loss

Author

Talantova, Maria, Sanz-Blasco, Sara, Zhang, Xiaofei, Xia, Peng, Akhtar, Mohd Waseem, Okamoto, Shu-ichi, Dziewczapolski, Gustavo, Nakamura, Tomohiro, Cao, Gang, Pratt, Alexander E., Kang, Yeon-Joo, Tu, Shichun, Molokanova, Elena, McKercher, Scott R., Hires, Samuel Andrew, Sason, Hagit, Stouffer, David G., Buczynski, Matthew W., Solomon, James P., Michael, Sarah, Powers, Evan T., Kelly, Jeffery W., Roberts, Amanda, Tong, Gary, Fang-Newmeyer, Traci, Parker, James, Holland, Emily A., Zhang, Dongxian, Nakanishi, Nobuki, Chen, H.-S. Vincent, Wolosker, Herman, Wang, Yuqiang, Parsons, Loren H., Ambasudhan, Rajesh, Masliah, Eliezer, Heinemann, Stephen F., Piña-Crespo, Juan C., and Lipton, Stuart A.

Published
2013

34. Ionotropic glutamate receptors in GtoPdb v.2021.3

Author

Bettler, Bernhard, primary, Collingridge, Graham L., primary, Dingledine, Ray, primary, Heinemann, Stephen F., primary, Hollmann, Michael, primary, Lerma, Juan, primary, Lodge, David, primary, Mayer, Mark, primary, Mishina, Masayoshi, primary, Mulle, Christophe, primary, Nakanishi, Shigetada, primary, Olsen, Richard, primary, Peineau, Stephane, primary, Peters, John A., primary, Seeburg, Peter, primary, Spedding, Michael, primary, and Watkins, Jeffrey C., primary

Published
2021
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37. Altered synaptic physiology and reduced susceptibility to kainate-induced seizures in GluR6-deficient mice

Author

Mulle, Christophe, Sailer, Andreas, Perez-Otano, Isabel, Dickinson-Anson, Heather, Castillo, Pablo E., Bureau, Ingrid, Maron, Cornelia, Gage, Fred H., Mann, Jeffrey R., Bettler, Bernhard, and Heinemann, Stephen F.

Subjects
Neural receptors -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Kainate receptors assembled with the GluR6 subunit are significant for both the sensitivity of CA3 neurons to kainate and for synaptic transmission at the mossy fibre-CA3 synapse, according to research using mutant mice lacking the kainate-receptor subunit GluR6. It was established that GluR6-deficient mice are less susceptible to systemic administration of kainate. This research indicates a vital role for kainate receptors, rather than alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors, in kainate-induced seizures and excitoxic neuronal death in the hippocampus.

Published
1998

41. Ca2+ permeability of unedited and edited versions of the kainate selective glutamate receptor GluR6

Author

Egebjerg, Jan and Heinemann, Stephen F.

Subjects
Calcium ions -- Physiological aspects, Neural transmission -- Regulation, Neurotransmitter receptors -- Physiological aspects, Science and technology
Abstract

The kainate selective glutamate receptor GluR6 undergoes editing at a level of 70% of its mRNA transcripts. The edited versioncontains a glutamine residue at position 621, while the unedited version contains an arginine at the same postion. The Ca2+ permeability of the edited and unedited versions of the GluR6 receptor was investigated. The results showed that the edited version of the receptor exhibits lower Ca2+ permeability. The level of permeability was dependent on the level of editing, which in turn, may regulate synaptic activity.

Published
1993

42. Identification of a subunit-specific antagonist of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate/kainate receptor channels

Author

Keller, Bernhard U., Blaschke, Martina, Rivosecchi, Roberta, Hollmann, Michael, Heinemann, Stephen F., and Konnerth, Arthur

Subjects
Neural transmission -- Research, Neurotransmitter receptors -- Research, Neuropharmacology -- Research, Science and technology
Abstract

The alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate/kainate (AMPA/KA) receptortype of glutamete receptors are the primary mediators of excitatory synaptic transmission in the mammalian central nervous system. A pharmacological distinction between AMPA/KA receptor subtypes was determined using the biphenylderivative of 1,3-naphthalene disulfonic acid, Evans blue, which acted as an antagonist for some receptor subtypes, but did not affect other subtypes. The structure of Evans blue could be used as a starting point for the development of substances to reduce excitatory activity of specific brain regions.

Published
1993

44. Ionotropic glutamate receptors (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database

Author

Bettler, Bernhard, primary, Collingridge, Graham L., primary, Dingledine, Ray, primary, Heinemann, Stephen F., primary, Hollmann, Michael, primary, Lerma, Juan, primary, Lodge, David, primary, Mayer, Mark, primary, Mishina, Masayoshi, primary, Mulle, Christophe, primary, Nakanishi, Shigetada, primary, Olsen, Richard, primary, Peineau, Stephane, primary, Peters, John A., primary, Seeburg, Peter, primary, Spedding, Michael, primary, and Watkins, Jeffrey C., primary

Published
2019
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