Inhibitory effects of group II mGluR-related drugs on memory performance in mice

Sato, Tomoaki; Ohnishi, Yutaka; Teramoto, Toyonori; Irifune, Masahiro; Nishikawa, Takashige

doi:10.1016/j.physbeh.2003.12.010

Cited by 30 publications

(35 citation statements)

References 24 publications

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“…Bonferroni's test after two-way ANOVA. Nagakura Bourtchouladze et al, 2003;Chang et al, 2003;Sato et al, 2004). Recently, it was also shown that low dosage of Rolipram administered for 3 weeks to an Alzheimer mouse model resulted in long-term recovery (2 months after the end of the treatment) of hippocampal CREB phosphorylation and memory, while having no such effects on wild-type animals (Gong et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

“…The consequent increase of cAMP-dependent cellular pathways has antidepressant action and reverses memory deficits caused by antagonists of NMDA receptor and other drugs (Fujimaki et al, 2000;Itho et al, 2004;Imanishi et al, 1997;Zhang et al, , 2004Sato et al, 2004;Vitolo et al, 2002). It also improves memory after ischemia and febrile seizures in a mouse model of Rubinstein-Taybi syndrome (Nagakura et al, 2002;Bourtchouladze et al, 2003;Chang et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

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Subchronic Rolipram Delivery Activates Hippocampal CREB and Arc, Enhances Retention and Slows Down Extinction of Conditioned Fear

Monti

Berteotti

Contestabile

2005

Neuropsychopharmacol

104

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Rolipram, a type IV-specific phosphodiesterase inhibitor, is known to improve memory under various learning tasks. Moreover, Rolipram treatments have been shown to increase expression and phosphorylation of a key factor for hippocampal memory consolidation, the cAMP-dependent response element-binding protein, CREB. However, the exact correlation between hippocampal CREB phosphorylation and memory improvement induced by Rolipram has not yet been determined in a CREB-dependent type of hippocampal-related learning in normogenic, intact rodents. Here, we report that subchronic Rolipram delivery by using osmotic minipumps increased the basal rat hippocampal expression and phosphorylation of CREB, as well as the expression of the cAMPdependent, memory-related protein, Arc. In parallel, the same treatment improved memory consolidation of conditioned fear. Furthermore, the increase of CREB phosphorylation and Arc expression consequent to the learning experience was enhanced in Rolipram-treated rats, compared to controls. By evaluating the time course of memory extinction over 10 days after the initial learning test, we also observed significant slowing down of the memory extinction rate in Rolipram-treated rats. This effect could be attributed to CREB phosphorylation and memory having been initially higher, as osmotic minipumps stopped to release Rolipram the first day after the initial learning test. Our data define the conditions through which the pharmacological manipulation of hippocampal CREB expression and activation result in memory amelioration in normogenic, intact animals. These results are relevant for the study of molecular correlates of memory, and may also be important in view of the efforts to design new pharmacological treatments, targeting the CREB pathway and leading to enhancement of learning and memory, even in the absence of patent neuropathology.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Subchronic Rolipram Delivery Activates Hippocampal CREB and Arc, Enhances Retention and Slows Down Extinction of Conditioned Fear

Monti

Berteotti

Contestabile

2005

Neuropsychopharmacol

104

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“…The arginine-vasopressin fragment [pGlu 4 ,Cyt 6 ] AVP (4)(5)(6)(7)(8)(9) (AVP4-9) has a much more selective and potent effect on avoidance behavior than AVP (1 -3) and may facilitate learning and memory via V 1 receptors coupled with G q/ 11 , resulting in phospholipase C (PLC) / protein kinase C (PKC)-signaling-pathway activation (4,5). At certain doses, AVP fragments facilitate memory performance; however, at an insufficient dose, the effects on learning and memory performance may not be observed.…”

mentioning

confidence: 99%

“…administration of a group II metabotropic glutamate receptor (mGluR2 / 3) agonist (DCG-IV) or antagonist (LY341495) induces memory impairment (7), and we suggested that the relationship between cAMP / PKAsignaling-pathway modulation through the G i protein coupled mGluR2 / 3 and learning and memory facilitation may also be represented by an inverted-U-shaped curve (7,8), and that the increase in activity of the cAMP/ PKA signaling pathway (9) does not always facilitate learning and memory (7).…”

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confidence: 99%

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Ameliorative and Exacerbating Effects of [pGlu4,Cyt6]AVP(4–9) on Impairment of Step-Through Passive Avoidance Task Performance by Group II Metabotropic Glutamate Receptor-Related Drugs in Mice

et al. 2005

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Abstract. To examine the effect of the arginine-vasopressin fragment, [pGlu 4 ,Cyt 6 ]AVP (4-9) (AVP4-9), on group II metabotropic glutamate receptor (mGluR2 / 3) agonist and antagonist induced impairment of passive avoidance (PA) task performance, AVP4-9 or phorbol 12-myristate 13-acetate (PMA) was administered in the presence of mGluR2 / 3-related drugs that induced the impairment of the step-through-type PA task performance. The PA task performance was evaluated in terms of the latency (the time that elapsed prior to entry into the dark compartment) at 24 h after the electrical stimulation. The subcutaneous injection of AVP4-9 at 1 mg / kg had the greatest facilitative effect on the performance, and the facilitative effect of AVP4-9 was inhibited by NPC-15437, a specific protein kinase C (PKC) inhibitor. The injection of AVP4-9 ameliorated PA task performance impairment induced by DCG-IV, an mGluR2 / 3 agonist. Intracisternal injection of PMA, a PKC activator, also ameliorated the DCG-IV-induced impairment. High doses of AVP4-9 exacerbated the PA task performance impairment induced by LY341495 (an mGluR2/ 3 antagonist), and PMA injection (1 m g) also exacerbated the impairment induced by the antagonist. These results suggest that an increase in the activity of the PKCsignaling pathway may not always facilitate PA task performance; therefore, AVP4-9 can either enhance or inhibit memory performance in mice.

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Efficacy of phosphodiesterase‐4 inhibitors in juvenile Batten disease (CLN3)

Aldrich

Bosch

Fallet

et al. 2016

Annals of Neurology

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ObjectiveJuvenile neuronal ceroid lipofuscinosis (JNCL), or juvenile Batten disease, is a pediatric lysosomal storage disease caused by autosomal recessive mutations in CLN3, typified by blindness, seizures, progressive cognitive and motor decline, and premature death. Currently, there is no treatment for JNCL that slows disease progression, which highlights the need to explore novel strategies to extend the survival and quality of life of afflicted children. Cyclic adenosine monophosphate (cAMP) is a second messenger with pleiotropic effects, including regulating neuroinflammation and neuronal survival. Here we investigated whether 3 phosphodiesterase‐4 (PDE4) inhibitors (rolipram, roflumilast, and PF‐06266047) could mitigate behavioral deficits and cell‐specific pathology in the Cln3Δex7/8 mouse model of JNCL.MethodsIn a randomized, blinded study, wild‐type (WT) and Cln3Δex7/8 mice received PDE4 inhibitors daily beginning at 1 or 3 months of age and continuing for 6 to 9 months, with motor deficits assessed by accelerating rotarod testing. The effect of PDE4 inhibitors on cAMP levels, astrocyte and microglial activation (glial fibrillary acidic protein and CD68, respectively), lysosomal pathology (lysosomal‐associated membrane protein 1), and astrocyte glutamate transporter expression (glutamate/aspartate transporter) were also examined in WT and Cln3Δex7/8 animals.ResultscAMP levels were significantly reduced in the Cln3Δex7/8 brain, and were restored by PF‐06266047. PDE4 inhibitors significantly improved motor function in Cln3Δex7/8 mice, attenuated glial activation and lysosomal pathology, and restored glutamate transporter expression to levels observed in WT animals, with no evidence of toxicity as revealed by blood chemistry analysis.InterpretationThese studies reveal neuroprotective effects for PDE4 inhibitors in Cln3Δex7/8 mice and support their therapeutic potential in JNCL patients. Ann Neurol 2016;80:909–923

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Inhibitory effects of group II mGluR-related drugs on memory performance in mice

Cited by 30 publications

References 24 publications

Subchronic Rolipram Delivery Activates Hippocampal CREB and Arc, Enhances Retention and Slows Down Extinction of Conditioned Fear

Subchronic Rolipram Delivery Activates Hippocampal CREB and Arc, Enhances Retention and Slows Down Extinction of Conditioned Fear

Ameliorative and Exacerbating Effects of [pGlu4,Cyt6]AVP(4–9) on Impairment of Step-Through Passive Avoidance Task Performance by Group II Metabotropic Glutamate Receptor-Related Drugs in Mice

Efficacy of phosphodiesterase‐4 inhibitors in juvenile Batten disease (CLN3)

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