A Role of Fos Expression in the CA3 Region of the Hippocampus in Spatial Memory Formation in Rats

He, Jue; Yamada, Kiyofumi; Nabeshima, Toshitaka

doi:10.1016/s0893-133x(01)00332-3

Cited by 115 publications

(103 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Because the molecules that were reduced in the dentate gyrus of FYN/hAPP low mice are critically involved in the formation or consolidation of memories (Molinari et al, 1996;Atkins et al, 1998;Blum et al, 1999;Guzowski et al, 2000;Guzowski, 2002;He et al, 2002), we next assessed the spatial learning and memory of mice in the Morris water maze. NTG, hAPP low , FYN, and FYN/hAPP low mice were able to learn both the cued (platform location visible) and the spatial (platform hidden) components of this task (Fig.…”

Section: Cooperation Of Fyn and Happ/a␤ Impairs Spatial Memory Retentmentioning

confidence: 99%

Fyn Kinase Induces Synaptic and Cognitive Impairments in a Transgenic Mouse Model of Alzheimer's Disease

Chin¹,

Palop²,

Puoliväli³

et al. 2005

J. Neurosci.

294

255

View full text Add to dashboard Cite

Human amyloid precursor protein (hAPP) transgenic mice with high levels of amyloid-␤ (A␤) develop behavioral deficits that correlate with the depletion of synaptic activity-related proteins in the dentate gyrus. The tyrosine kinase Fyn is altered in Alzheimer's disease brains and modulates premature mortality and synaptotoxicity in hAPP mice. To determine whether Fyn also modulates A␤-induced behavioral deficits and depletions of synaptic activity-dependent proteins, we overexpressed Fyn in neurons of hAPP mice with moderate levels of A␤ production. Compared with nontransgenic controls and singly transgenic mice expressing hAPP or FYN alone, doubly transgenic FYN/hAPP mice had striking depletions of calbindin, Fos, and phosphorylated ERK (extracellular signal-regulated kinase), impaired neuronal induction of Arc, and impaired spatial memory retention. These deficits were qualitatively and quantitatively similar to those otherwise seen only in hAPP mice with higher A␤ levels. Surprisingly, levels of active Fyn were lower in high expresser hAPP mice than in NTG controls and lower in FYN/hAPP mice than in FYN mice. Suppression of Fyn activity may result from dephosphorylation by striatal-enriched phosphatase, which was upregulated in FYN/hAPP mice and in hAPP mice with high levels of A␤. Thus, increased Fyn expression is sufficient to trigger prominent neuronal deficits in the context of even relatively moderate A␤ levels, and inhibition of Fyn activity may help counteract A␤-induced impairments.

show abstract

Section: Cooperation Of Fyn and Happ/a␤ Impairs Spatial Memory Retentmentioning

confidence: 99%

Fyn Kinase Induces Synaptic and Cognitive Impairments in a Transgenic Mouse Model of Alzheimer's Disease

Chin¹,

Palop²,

Puoliväli³

et al. 2005

J. Neurosci.

294

255

View full text Add to dashboard Cite

show abstract

“…The training procedure was as described previously. 4,8 Before the actual training began, the animals were shaped for 4 days to run to end of the arms and consume the bait, in groups of four. The bait was initially available throughout the maze, but gradually was restricted to the food cup.…”

Section: Radial Arm Maze Taskmentioning

confidence: 99%

“…[5][6][7] To examine whether spatial learning and memory are associated with activation of BDNF/TrkB signaling, phosphorylated TrkB was measured in the hippocampus of rats trained for the spatial reference and working memory task in a radial arm maze. 4,8 Figure 1a shows the changes in performance produced by daily training (three trials per day). An ANOVA with repeated measures revealed a significant effect of training on reference (F(7,84) ¼ 60.890, Po0.0001) and working memory (F(7,84) ¼ 40.209, Po0.0001), indicating spatial memory formation.…”

mentioning

confidence: 99%

Phosphatidylinositol 3-kinase: a molecule mediating BDNF-dependent spatial memory formation

et al. 2003

Self Cite

View full text Add to dashboard Cite

Brain-derived neurotrophic factor (BDNF) plays a critical role in synaptic plasticity such as long-term potentiation (LTP), a form of synaptic correlate of learning and memory. BDNF is also implicated in learning and memory. We have demonstrated that radial arm maze training in rats for spatial learning and memory results in a significant increase in the BDNF mRNA expression in the hippocampus. Moreover, antisense BDNF oligonucleotide treatment impaired not only acquisition, but also maintenance and/or recall of spatial memory in the maze. Although these results suggest a role of BDNF for spatial memory processes, the signal transduction mechanisms that mediate the actions of BDNF remain unknown. Here we show that phosphorylation of BDNF receptor tyrosine kinase B (TrkB), phosphatidylinositol 3-kinase (PI3-K) and Akt, a target of PI3-K, in the hippocampus increased in parallel with spatial memory formation. Moreover, an activation of translational processes was suggested in the hippocampus after the maze training. When spatial learning was inhibited by antisense BDNF oligodeoxynucleotide, the activation was diminished. Chronic treatment with PI3-K inhibitor wortmannin impaired spatial learning. Our findings suggested that activation of TrkB/PI3-K and protein synthesis signaling pathway by BDNF in the hippocampus is important for spatial memory.

show abstract

“…However, the functional significance of the up-regulation of c-fos gene expression and Fos protein synthesis in these brain sites remains unclear. Several studies have shown that reversible blockage of Fos protein production by the application of a specific antisense oligodeoxynucleotide (AS-ODN) against c-fos mRNA (c-fos AS-ODN) in the brain is useful for studying the function of the c-fos gene and Fos protein (7,(24)(25)(26). Here, we studied the potential roles of Fos protein in the PBN, AMY, and IC in CTA formation using the AS-ODN-mediated disruption of Fos production in vivo.…”

mentioning

confidence: 99%

Acute suppression, but not chronic genetic deficiency, of c- fos gene expression impairs long-term memory in aversive taste learning

Yasoshima

Sako

Senba

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

A Role of Fos Expression in the CA3 Region of the Hippocampus in Spatial Memory Formation in Rats

Abstract: Activity-dependent plastic changes in the strength

Cited by 115 publications

References 35 publications

Fyn Kinase Induces Synaptic and Cognitive Impairments in a Transgenic Mouse Model of Alzheimer's Disease

Fyn Kinase Induces Synaptic and Cognitive Impairments in a Transgenic Mouse Model of Alzheimer's Disease

Phosphatidylinositol 3-kinase: a molecule mediating BDNF-dependent spatial memory formation

Acute suppression, but not chronic genetic deficiency, of c- fos gene expression impairs long-term memory in aversive taste learning

Contact Info

Product

Resources

About