Ca-Stimulated Type 8 Adenylyl Cyclase Is Required for Rapid Acquisition of Novel Spatial Information and for Working/Episodic-Like Memory

Zhang, Ming; Moon, Changjong; Chan, Guy C.‐K.; Yang, Lan; Zheng, Fei; Conti, Alana C.; Muglia, Lisa M.; Muglia, Louis J.; Storm, Daniel R.; Wang, Hongbing

doi:10.1523/jneurosci.1177-08.2008

Cited by 59 publications

(56 citation statements)

References 39 publications

(56 reference statements)

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“…Therefore, the association between the dark chamber (the conditioned stimulus) and the aversive footshock (the unconditioned stimulus) was temporally separated by 10 min. Our previous results have demonstrated that animals gradually improve their crossover latency through the multiple trainings, and the task is dependent on the hippocampus (Zhang et al 2008). As shown in Figure 2A, p97FE65 À/À mice displayed significantly slower improvement in crossover latency than WT mice during TDPA training (P < 0.05).…”

Section: Results P97fe65 à/à Mice Show Normal Hippocampus Formationmentioning

confidence: 72%

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The APP-interacting protein FE65 is required for hippocampus-dependent learning and long-term potentiation

Wang¹,

Zhang²,

Moon³

et al. 2009

Learn. Mem.

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FE65 is expressed predominantly in the brain and interacts with the C-terminal domain of b-amyloid precursor protein (APP). We examined hippocampus-dependent memory and in vivo long-term potentiation (LTP) at the CA1 synapses with isoform-specific FE65 knockout (p97FE65 À/À ) mice. When examined using the Morris water maze, p97FE65 À/À mice were impaired for the hidden platform task but showed normal performance in the probe test. To further discriminate the role of FE65 in acquisition and memory consolidation, we examined p97FE65 À/À mice with temporal dissociative passive avoidance (TDPA) and contextual fear conditioning (CFC). p97FE65 À/À mice showed impaired shortterm memory for both TDPA and CFC when tested 10 min after training. After multiple TDPA training sessions, the crossover latency of some p97FE65 À/À mice reached the cutoff value, but it significantly decayed in 8 d. At the Schaffer collateral-CA1 synapses, p97FE65 À/À mice showed defective early-phase LTP (E-LTP). These results demonstrate novel roles of FE65 in synaptic plasticity, acquisition, and retention for certain forms of memory formation.

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Section: Results P97fe65 à/à Mice Show Normal Hippocampus Formationmentioning

confidence: 72%

“…Training and testing for the TDPA paradigm was performed as described (Zhang et al 2008). During training, the mouse was introduced to the lit half of the training chamber (Coulbourn Instruments) and allowed to explore for 1 min before the trap door was opened.…”

Section: Temporal Dissociative Passive Avoidance (Tdpa)mentioning

confidence: 99%

The APP-interacting protein FE65 is required for hippocampus-dependent learning and long-term potentiation

Wang¹,

Zhang²,

Moon³

et al. 2009

Learn. Mem.

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“…Of particular note, some disruptions of cAMP signaling pathways impact ORM but not spatial memory. Knock out of ACVIII inhibits (Zhang et al, 2008) while overexpression of ACI enhances ORM in mice (Garelick et al, 2009), although neither manipulation impacts spatial memory. Broadly increasing AC activity by knocking out the inhibitory G-protein G i␣1 disrupts ORM without affecting spatial memory (Pineda et al, 2004).…”

Section: Discussionmentioning

confidence: 94%

Somatostatin Signaling in Neuronal Cilia Is Criticalfor Object Recognition Memory

Einstein¹,

Patterson²,

Hon³

et al. 2010

J. Neurosci.

107

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Most neurons possess a single, nonmotile cilium that projects out from the cell surface. These microtubule-based organelles are important in brain development and neurogenesis; however, their function in mature neurons is unknown. Cilia express a complement of proteins distinct from other neuronal compartments, one of which is the somatostatin receptor subtype SST 3 . We show here that SST 3 is critical for object recognition memory in mice. sst3 knock-out mice are severely impaired in discriminating novel objects, whereas they retain normal memory for object location. Further, systemic injection of an SST 3 antagonist (ACQ090) disrupts recall of familiar objects in wild-type mice. To examine mechanisms of SST 3 , we tested synaptic plasticity in CA1 hippocampus. Electrically evoked long-term potentiation (LTP) was normal in sst3 knock-out mice, while adenylyl cyclase/cAMP-mediated LTP was impaired. The SST 3 antagonist also disrupted cAMP-mediated LTP. Basal cAMP levels in hippocampal lysate were reduced in sst3 knock-out mice compared with wild-type mice, while the forskolin-induced increase in cAMP levels was normal. The SST 3 antagonist inhibited forskolin-stimulated cAMP increases, whereas the SST 3 agonist L-796,778 increased basal cAMP levels in hippocampal slices but not hippocampal lysate. Our results show that somatostatin signaling in neuronal cilia is critical for recognition memory and suggest that the cAMP pathway is a conserved signaling motif in cilia. Neuronal cilia therefore represent a novel nonsynaptic compartment crucial for signaling involved in a specific form of synaptic plasticity and in novelty detection.

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“…The frequency of NSC division may have a large impact on the number of new neurons. For example, autonomous physical exercise, such as running, can promote NSC division and enhance the production of new neurons (van Praag et al, 2002;Lugert et al, 2010). As the basic process of neuron generation, adult neurogenesis plays a pivotal role in preserving cognitive functions throughout life.…”

Section: Introductionmentioning

confidence: 99%

Ezh2 Regulates Adult Hippocampal Neurogenesis and Memory

et al. 2014

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Adult neurogenesis is thought to be crucial for preserving cognitive functions, which is tightly controlled by various epigenetic regulators. As the methyltransferase of histone H3K27, the role of Ezh2 in neurogenesis of adult mice and its mechanism of action are largely unknown. Here, we show that Ezh2 is expressed in actively dividing neural stem cells (NSCs)/progenitor cells as well as mature neurons, but not in quiescent NSCs in the subgranular zone. The deletion of Ezh2 in NSCs/progenitor cells results in a reduction in progenitor cell proliferation. Furthermore, we found that Ezh2 regulates progenitor cell proliferation by suppressing Pten expression and promoting the activation of Akt-mTOR. Moreover, the loss of Ezh2 in progenitor cells leads to a decrease in the number of neurons, which was observed by long-term tracing. Strikingly, conditional knockout of Ezh2 ultimately results in impairments in spatial learning and memory, contextual fear memory, and pattern separation. Our findings demonstrate the essential role of Ezh2 in the proliferation of progenitor cells, thus providing insight into the molecular mechanisms of adult neurogenesis in preserving cognitive functions.

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Ca-Stimulated Type 8 Adenylyl Cyclase Is Required for Rapid Acquisition of Novel Spatial Information and for Working/Episodic-Like Memory

Cited by 59 publications

References 39 publications

The APP-interacting protein FE65 is required for hippocampus-dependent learning and long-term potentiation

The APP-interacting protein FE65 is required for hippocampus-dependent learning and long-term potentiation

Somatostatin Signaling in Neuronal Cilia Is Criticalfor Object Recognition Memory

Ezh2 Regulates Adult Hippocampal Neurogenesis and Memory

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