Regulation of hippocampal synaptic plasticity by cyclic AMP-dependent protein kinases

Nguyen, Peter V.; Woo, Newton H.

doi:10.1016/j.pneurobio.2003.12.003

Cited by 289 publications

(239 citation statements)

References 479 publications

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“…Given our results showing that TSA enhances memory for contextual fear via the transcription factor CREB, we next examined whether HDAC inhibition enhances LTP in hippocampal slices from CREB␣⌬ mutant mice. As mentioned previously, one-train E-LTP has been shown to be independent of CREB function (Pittenger et al, 2002) (for review, see Nguyen and Woo, 2003). Therefore, if disruption of CREB impairs the enhancement of LTP by HDAC inhibition, we can conclude that this is because the action of TSA is dependent on CREB and not because the disruption of CREB affects the underlying electrically induced E-LTP.…”

Section: Figure 2 Tsa Enhances One-train E-ltp Via a Transcription-dmentioning

confidence: 58%

“…Here, we studied the effects of TSA on transient E-LTP induced by a single 1 s, 100 Hz train. Importantly, this form of LTP is independent of transcription or translation, protein kinase A, and CREB (for review, see Pittenger et al, 2002;Nguyen and Woo, 2003). Therefore, this approach allows us to identify genetic and pharmacological manipulations that selectively disrupt the enhancement in LTP attributable to TSA treatment without affecting the underlying E-LTP.…”

Section: Hdac Inhibition Enhances Ltp Induced By One-train Stimulatiomentioning

confidence: 99%

“…To do this, we studied the effects of TSA on hippocampal E-LTP. Because our single 100 Hz train E-LTP induction protocol is independent of transcription and translation (for review, see Nguyen and Woo, 2003), we were able to define the molecular nature of HDAC inhibitor-enhanced LTP. Using this protocol, we found that TSA treatment transformed transient E-LTP into a transcription-dependent, long-lasting form of LTP (Fig.…”

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confidence: 99%

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Histone Deacetylase Inhibitors Enhance Memory and Synaptic Plasticity via CREB: CBP-Dependent Transcriptional Activation

Vecsey¹,

Hawk²,

Lattal³

et al. 2007

Journal of Neuroscience

759

761

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Histone deacetylase (HDAC) inhibitors increase histone acetylation and enhance both memory and synaptic plasticity. The current model for the action of HDAC inhibitors assumes that they alter gene expression globally and thus affect memory processes in a nonspecific manner. Here, we show that the enhancement of hippocampus-dependent memory and hippocampal synaptic plasticity by HDAC inhibitors is mediated by the transcription factor cAMP response element-binding protein (CREB) and the recruitment of the transcriptional coactivator and histone acetyltransferase CREB-binding protein (CBP) via the CREB-binding domain of CBP. Furthermore, we show that the HDAC inhibitor trichostatin A does not globally alter gene expression but instead increases the expression of specific genes during memory consolidation. Our results suggest that HDAC inhibitors enhance memory processes by the activation of key genes regulated by the CREB:CBP transcriptional complex.

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Section: Figure 2 Tsa Enhances One-train E-ltp Via a Transcription-dmentioning

confidence: 58%

Section: Hdac Inhibition Enhances Ltp Induced By One-train Stimulatiomentioning

confidence: 99%

mentioning

confidence: 99%

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Histone Deacetylase Inhibitors Enhance Memory and Synaptic Plasticity via CREB: CBP-Dependent Transcriptional Activation

Vecsey¹,

Hawk²,

Lattal³

et al. 2007

Journal of Neuroscience

759

761

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“…Both of the above actions of theophylline could lead to an increase in cAMP. Elevated levels of cAMP have been shown to be a powerful mediator of synaptic plasticity and memory in the central nervous system (Alberini, 1995;Lee et al 2000;Nguyen and Woo 2003;Inan et al 2006;Tronson et al 2006;Schacher et al 1988;Park et al 2005). Following spinal cord injury, administration of cAMP analogs as well as pharmacological agents capable of elevating cAMP levels in neurons have been shown to promote regeneration and functional recovery (Pearse et al 2004;Nikulina et al 2004;Qiu et al 2002a).…”

Section: Introductionmentioning

confidence: 99%

Administration of phosphodiesterase inhibitors and an adenosine A1 receptor antagonist induces phrenic nerve recovery in high cervical spinal cord injured rats

Satkunendrarajah

Goshgarian

2008

Experimental Neurology

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High cervical spinal cord hemisection interrupts the descending respiratory drive from the medulla to the ipsilateral phrenic motoneurons, consequently leading to the paralysis of the ipsilateral hemidiaphragm. Previous studies have shown that chronic oral administration of theophylline, a phosphodiesterase inhibitor and an adenosine receptor antagonist, can restore function to the quiescent phrenic nerve and hemidiaphragm ipsilateral to hemisection. Both of these actions of theophylline result in an increase in 3′-5′-cyclic adenosine monophosphate (cAMP). Furthermore, the chronic theophylline-mediated respiratory recovery persists long after the animals have been weaned from the drug. To date, the precise cellular mechanisms underlying the recovery induced by theophylline are still not known. Since theophylline has two modes of action, in the present study we tested whether chronic administration of pentoxifylline, a non-selective phosphodiesterase inhibitor, rolipram, a phosphodiesterase-4 specific inhibitor, and 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), an adenosine A1 receptor antagonist, would induce recovery similar to that induced by theophylline in male Sprague Dawley rats following a left C2 spinal cord lesion. Recovery of left phrenic nerve activity was assessed at 5 or 10 days after the last drug administrations to assess the persistent nature of the recovery. Pentoxifylline, rolipram and DPCPX, all capable of modulating 3′, 5′-cyclic monophosphate (cAMP) levels, brought about long-term respiratory recovery in the phrenic nerve ipsilateral to the left C2 lesion at 5 and 10 days after the last drug administration. Therefore, these results suggest that compounds capable of regulating cAMP levels may be therapeutically useful in promoting functional recovery following spinal cord injury.

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“…We show that Pten is ablated in DGCs and pyramidal neurons in the hippocampal CA3 in Pten cKO mice. We find that two PI3K-and protein synthesis-dependent forms of synaptic plasticity, theta burst-induced long-term potentiation (TBS-LTP) (19,20) and metabotropic glutamate receptor-dependent long-term depression (mGluR-LTD) (21), are dysregulated at the postsynaptic side of perforant path-to-DGC synapses of Pten cKO mice before the onset of gross morphological defects. Whereas TBS-LTP is enhanced, mGluR-LTD is impaired.…”

mentioning

confidence: 99%

Dysregulation of synaptic plasticity precedes appearance of morphological defects in a Pten conditional knockout mouse model of autism

Takeuchi

Gertner

Zhou

et al. 2013

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

114

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The phosphoinositide signaling system is a crucial regulator of neural development, cell survival, and plasticity. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) negatively regulates phosphatidylinositol 3-kinase signaling and downstream targets. Nse-Cre Pten conditional knockout mice, in which Pten is ablated in granule cells of the dentate gyrus and pyramidal neurons of the hippocampal CA3, but not CA1, recapitulate many of the symptoms of humans with inactivating PTEN mutations, including progressive hypertrophy of the dentate gyrus and deficits in hippocampus-based social and cognitive behaviors. However, the impact of Pten loss on activity-dependent synaptic plasticity in this clinically relevant mouse model of Pten inactivation remains unclear. Here, we show that two phosphatidylinositol 3-kinase-and protein synthesis-dependent forms of synaptic plasticity, theta burstinduced long-term potentiation and metabotropic glutamate receptor (mGluR)-dependent long-term depression, are dysregulated at medial perforant path-to-dentate gyrus synapses of young NseCre Pten conditional knockout mice before the onset of visible morphological abnormalities. In contrast, long-term potentiation and mGluR-dependent long-term depression are normal at CA3-CA1 pyramidal cell synapses at this age. Our results reveal that deletion of Pten in dentate granule cells dysregulates synaptic plasticity, a defect that may underlie abnormal social and cognitive behaviors observed in humans with Pten inactivating mutations and potentially other autism spectrum disorders.T he discovery of genes associated with autism spectrum disorders (ASDs) has largely depended on gene linkage analyses within lineages of humans with familial ASDs (1-3). A well-established candidate gene is the tumor-suppressor gene, phosphatase and tensin homolog missing on chromosome 10 (PTEN) (4-7). Pten is a lipid and protein phosphatase best known for its role in suppressing tumor formation by inhibiting cellular survival, proliferation, and cellular architecture (8, 9), but which also plays an important role in brain morphology and synaptic function (10, 11). Pten acts via its lipid phosphatase activity to dephosphorylate phosphatidylinositol (3,4,5)-trisphosphate and negatively regulate the PI3K-mammalian target of rapamycin (mTOR) signaling pathway. Although PTEN mutations are present in 5-10% of people with ASDs (12-14), loss-of-function point mutations in this gene give rise to progressive macrocephaly, a hallmark feature that occurs in nearly 20% of humans with ASDs (5, 6). In addition to anatomical abnormalities, humans with inactivating PTEN mutations exhibit spontaneous seizures and deficits in social and cognitive behaviors (10, 11).A conditional Pten knockout mouse (cKO) in which both alleles of the Pten gene contain loxP sites and Cre recombinase (Cre) is expressed under the neuron-specific enolase promoter (Nse-Cre) provides a clinically relevant mouse model for humans with inactivating PTEN mutations (15). In Nse-Cre Pten cKO (hereafter P...

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Regulation of hippocampal synaptic plasticity by cyclic AMP-dependent protein kinases

Cited by 289 publications

References 479 publications

Histone Deacetylase Inhibitors Enhance Memory and Synaptic Plasticity via CREB: CBP-Dependent Transcriptional Activation

Histone Deacetylase Inhibitors Enhance Memory and Synaptic Plasticity via CREB: CBP-Dependent Transcriptional Activation

Administration of phosphodiesterase inhibitors and an adenosine A1 receptor antagonist induces phrenic nerve recovery in high cervical spinal cord injured rats

Dysregulation of synaptic plasticity precedes appearance of morphological defects in a Pten conditional knockout mouse model of autism

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