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Alexander M Kleschevnikov

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Frontiers in Genetics|September 29, 2022
Enhanced GIRK2 channel signaling in Down syndrome: A feasible role in the development of abnormal nascent neural circuitsAlexander M Kleschevnikov
The European Journal of Neuroscience|June 26, 2003
Long-term potentiation recruits a trisynaptic excitatory associative network within the mouse dentate gyrusAlexander M Kleschevnikov, Aryeh Routtenberg
Handbook of Clinical Neurology|November 23, 2019
Down syndromeMichael S Rafii, Alexander M Kleschevnikov, Mariko Sawa, et al.
Brain Research Bulletin|January 10, 2026
Chronic suppression of monoacylglycerol lipase restores adult neurogenesis in the septal but not the temporal DG in Ts65Dn mouse model of Down syndromeDonya Fozoonmayeh, Mathangi Sankaran, Jessica Yu, et al.
Experimental Neurology|January 31, 2025
Early postnatal GABAB antagonist treatment normalizes inhibitory/excitatory balance in neonatal Ts65Dn mice, a genetic model of down syndromeJoshua Jin, James Doan, Cassandra Fernandez, et al.
The Journal of Comparative Neurology|April 1, 2011
Three-dimensional synaptic ultrastructure in the dentate gyrus and hippocampal area CA3 in the Ts65Dn mouse model of Down syndromeVictor I Popov, Alexander M Kleschevnikov, Oleg A Klimenko, et al.
The Journal of Comparative Neurology|August 1, 2007
Synaptic and cognitive abnormalities in mouse models of Down syndrome: exploring genotype-phenotype relationshipsPavel V Belichenko, Alexander M Kleschevnikov, Ahmad Salehi, et al.
Neurobiology of Disease|March 19, 2018
Developmental excitatory-to-inhibitory GABA polarity switch is delayed in Ts65Dn mice, a genetic model of Down syndromeLarisa V Lysenko, Jeesun Kim, Francisco Madamba, et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience|May 8, 2009
The "Down syndrome critical region" is sufficient in the mouse model to confer behavioral, neurophysiological, and synaptic phenotypes characteristic of Down syndromeNadia P Belichenko, Pavel V Belichenko, Alexander M Kleschevnikov, et al.
Neurobiology of Disease|March 27, 2017
Evidence that increased Kcnj6 gene dose is necessary for deficits in behavior and dentate gyrus synaptic plasticity in the Ts65Dn mouse model of Down syndromeAlexander M Kleschevnikov, Jessica Yu, Jeesun Kim, et al.
Pageof 3

Showing results (1-10 of 28) with videos related to

Sort By:
Pageof 3
Frontiers in Genetics|September 29, 2022
Enhanced GIRK2 channel signaling in Down syndrome: A feasible role in the development of abnormal nascent neural circuitsAlexander M Kleschevnikov
The European Journal of Neuroscience|June 26, 2003
Long-term potentiation recruits a trisynaptic excitatory associative network within the mouse dentate gyrusAlexander M Kleschevnikov, Aryeh Routtenberg
Handbook of Clinical Neurology|November 23, 2019
Down syndromeMichael S Rafii, Alexander M Kleschevnikov, Mariko Sawa, et al.
Brain Research Bulletin|January 10, 2026
Chronic suppression of monoacylglycerol lipase restores adult neurogenesis in the septal but not the temporal DG in Ts65Dn mouse model of Down syndromeDonya Fozoonmayeh, Mathangi Sankaran, Jessica Yu, et al.
Experimental Neurology|January 31, 2025
Early postnatal GABAB antagonist treatment normalizes inhibitory/excitatory balance in neonatal Ts65Dn mice, a genetic model of down syndromeJoshua Jin, James Doan, Cassandra Fernandez, et al.
The Journal of Comparative Neurology|April 1, 2011
Three-dimensional synaptic ultrastructure in the dentate gyrus and hippocampal area CA3 in the Ts65Dn mouse model of Down syndromeVictor I Popov, Alexander M Kleschevnikov, Oleg A Klimenko, et al.
The Journal of Comparative Neurology|August 1, 2007
Synaptic and cognitive abnormalities in mouse models of Down syndrome: exploring genotype-phenotype relationshipsPavel V Belichenko, Alexander M Kleschevnikov, Ahmad Salehi, et al.
Neurobiology of Disease|March 19, 2018
Developmental excitatory-to-inhibitory GABA polarity switch is delayed in Ts65Dn mice, a genetic model of Down syndromeLarisa V Lysenko, Jeesun Kim, Francisco Madamba, et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience|May 8, 2009
The "Down syndrome critical region" is sufficient in the mouse model to confer behavioral, neurophysiological, and synaptic phenotypes characteristic of Down syndromeNadia P Belichenko, Pavel V Belichenko, Alexander M Kleschevnikov, et al.
Neurobiology of Disease|March 27, 2017
Evidence that increased Kcnj6 gene dose is necessary for deficits in behavior and dentate gyrus synaptic plasticity in the Ts65Dn mouse model of Down syndromeAlexander M Kleschevnikov, Jessica Yu, Jeesun Kim, et al.
Pageof 3