Eniko A. Kramar, Ph.D.

Affiliations: 
Washington State University, Pullman, WA, United States 
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"Eniko Kramar"
Mean distance: 22.83 (cluster 6)
 

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John Wright grad student 2000 WSU
 (Characterization of long-term potentiation induced by AT4 receptor activation in area CA1 of the hippocampus.)
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Publications

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White AO, Kramár EA, López AJ, et al. (2016) BDNF rescues BAF53b-dependent synaptic plasticity and cocaine-associated memory in the nucleus accumbens. Nature Communications. 7: 11725
López AJ, Kramár E, Matheos DP, et al. (2016) Promoter-Specific Effects of DREADD Modulation on Hippocampal Synaptic Plasticity and Memory Formation. The Journal of Neuroscience : the Official Journal of the Society For Neuroscience. 36: 3588-99
Trieu BH, Kramár EA, Cox CD, et al. (2015) Pronounced differences in signal processing and synaptic plasticity between piriform-hippocampal network stages: a prominent role for adenosine. The Journal of Physiology. 593: 2889-907
Lynch G, Kramár EA, Gall CM. (2014) Protein synthesis and consolidation of memory-related synaptic changes. Brain Research
Ozkan ED, Creson TK, Kramár EA, et al. (2014) Reduced cognition in Syngap1 mutants is caused by isolated damage within developing forebrain excitatory neurons. Neuron. 82: 1317-33
Babayan AH, Kramár EA. (2013) Rapid effects of oestrogen on synaptic plasticity: interactions with actin and its signalling proteins. Journal of Neuroendocrinology. 25: 1163-72
Vogel-Ciernia A, Matheos DP, Barrett RM, et al. (2013) The neuron-specific chromatin regulatory subunit BAF53b is necessary for synaptic plasticity and memory. Nature Neuroscience. 16: 552-61
Scharfman HE, Kramár EA, Luine V, et al. (2013) Introduction to 'steroid hormone actions in the CNS: the role of brain-derived neurotrophic factor (BDNF)'. Neuroscience. 239: 1-2
Kramár EA, Babayan AH, Gall CM, et al. (2013) Estrogen promotes learning-related plasticity by modifying the synaptic cytoskeleton. Neuroscience. 239: 3-16
Chen Y, Kramár EA, Chen LY, et al. (2013) Impairment of synaptic plasticity by the stress mediator CRH involves selective destruction of thin dendritic spines via RhoA signaling. Molecular Psychiatry. 18: 485-96
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