title: Kalirin-7 is necessary for normal NMDA receptor-dependent synaptic plasticity.
abstract: BACKGROUND
  Dendritic spines represent the postsynaptic component of the vast majority of excitatory synapses present in the mammalian forebrain. The ability of spines to rapidly alter their shape, size, number and receptor content in response to stimulation is considered to be of paramount importance during the development of synaptic plasticity. Indeed, long-term potentiation (LTP), widely believed to be a cellular correlate of learning and memory, has been repeatedly shown to induce both spine enlargement and the formation of new dendritic spines. In our studies, we focus on Kalirin-7 (Kal7), a Rho GDP/GTP exchange factor (Rho-GEF) localized to the postsynaptic density that plays a crucial role in the development and maintenance of dendritic spines both in vitro and in vivo. Previous studies have shown that mice lacking Kal7 (Kal7(KO)) have decreased dendritic spine density in the hippocampus as well as focal hippocampal-dependent learning impairments.
  
  
  RESULTS
  We have performed a detailed electrophysiological characterization of the role of Kal7 in hippocampal synaptic plasticity. We show that loss of Kal7 results in impaired NMDA receptor-dependent LTP and long-term depression, whereas a NMDA receptor-independent form of LTP is shown to be normal in the absence of Kal7.
  
  
  CONCLUSIONS
  These results indicate that Kal7 is an essential and selective modulator of NMDA receptor-dependent synaptic plasticity in the hippocampus.
authors.affiliation: The King Abdullah University of Science and Technology, Thuwal, Kingdom of Saudi Arabia.
authors.forename: Fouad
authors.initials: F
authors.lastname: Lemtiri-Chlieh
authors.forename: Liangfang
authors.initials: L
authors.lastname: Zhao
authors.forename: Drew D
authors.initials: DD
authors.lastname: Kiraly
authors.forename: Betty A
authors.initials: BA
authors.lastname: Eipper
authors.forename: Richard E
authors.initials: RE
authors.lastname: Mains
authors.forename: Eric S
authors.initials: ES
authors.lastname: Levine
mesh_terms: D000818:Animals; D049229:Dendritic Spines / Q000378:metabolism*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D020662:Guanine Nucleotide Exchange Factors / Q000037:antagonists & inhibitors / Q000172:deficiency / Q000502:physiology*; D006624:Hippocampus / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D009924:Organ Culture Techniques; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology*
chemical_list: D004791:Enzyme Inhibitors; D020662:Guanine Nucleotide Exchange Factors; C548820:KALRN protein, mouse; D016194:Receptors, N-Methyl-D-Aspartate