Effects of a phosphodiesterase IV inhibitor rolipram on microsphere embolism‐induced defects in memory function and cerebral cyclic AMP signal transduction system in rats

The effects of treatment with rolipram, a specific phosphodiesterase IV inhibitor, on learning and memory function and on the cyclic AMP/PKA/CREB signal transduction system were examined in rats with microsphere embolism (ME)‐induced cerebral ischaemia. Sustained cerebral ischaemia was induced by th...

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Veröffentlicht in:British journal of pharmacology 2002-04, Vol.135 (7), p.1783-1793
Hauptverfasser: Nagakura, Akira, Niimura, Makiko, Takeo, Satoshi
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creator Nagakura, Akira
Niimura, Makiko
Takeo, Satoshi
description The effects of treatment with rolipram, a specific phosphodiesterase IV inhibitor, on learning and memory function and on the cyclic AMP/PKA/CREB signal transduction system were examined in rats with microsphere embolism (ME)‐induced cerebral ischaemia. Sustained cerebral ischaemia was induced by the injection of 900 microspheres (48 μm in diameter) into the right hemisphere of the rat brain. The animals were treated once daily with 3 mg kg−1 rolipram i.p. from 6 h after the onset of the operation for consecutive 10 days. Microsphere‐embolized rats showed prolongation of the escape latency in the water maze task starting from day 7 after the operation and lasting for 3 consecutive days. Treatment with rolipram reduced the escape latency. ME decreased the cyclic AMP content, cytosolic PKA Cβ level, and nuclear PKA Cα and Cβ levels, as well as reduced the pCREB level and the DNA‐binding activity of CREB in the cerebral cortex and hippocampus on day 10 after the operation. These alterations were attenuated by treatment with rolipram. These results suggest that ME‐induced failure in learning and memory function may be mediated by dysfunction of the cyclic AMP/PKA/CREB signal transduction system, that rolipram may ameliorate ME‐induced impairment of learning and memory function, and that the drug effect may be partly attributed to activation of the cyclic AMP/PKA/CREB signal transduction system. British Journal of Pharmacology (2002) 135, 1783–1793; doi:10.1038/sj.bjp.0704629
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Sustained cerebral ischaemia was induced by the injection of 900 microspheres (48 μm in diameter) into the right hemisphere of the rat brain. The animals were treated once daily with 3 mg kg−1 rolipram i.p. from 6 h after the onset of the operation for consecutive 10 days. Microsphere‐embolized rats showed prolongation of the escape latency in the water maze task starting from day 7 after the operation and lasting for 3 consecutive days. Treatment with rolipram reduced the escape latency. ME decreased the cyclic AMP content, cytosolic PKA Cβ level, and nuclear PKA Cα and Cβ levels, as well as reduced the pCREB level and the DNA‐binding activity of CREB in the cerebral cortex and hippocampus on day 10 after the operation. These alterations were attenuated by treatment with rolipram. These results suggest that ME‐induced failure in learning and memory function may be mediated by dysfunction of the cyclic AMP/PKA/CREB signal transduction system, that rolipram may ameliorate ME‐induced impairment of learning and memory function, and that the drug effect may be partly attributed to activation of the cyclic AMP/PKA/CREB signal transduction system. 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Sustained cerebral ischaemia was induced by the injection of 900 microspheres (48 μm in diameter) into the right hemisphere of the rat brain. The animals were treated once daily with 3 mg kg−1 rolipram i.p. from 6 h after the onset of the operation for consecutive 10 days. Microsphere‐embolized rats showed prolongation of the escape latency in the water maze task starting from day 7 after the operation and lasting for 3 consecutive days. Treatment with rolipram reduced the escape latency. ME decreased the cyclic AMP content, cytosolic PKA Cβ level, and nuclear PKA Cα and Cβ levels, as well as reduced the pCREB level and the DNA‐binding activity of CREB in the cerebral cortex and hippocampus on day 10 after the operation. These alterations were attenuated by treatment with rolipram. These results suggest that ME‐induced failure in learning and memory function may be mediated by dysfunction of the cyclic AMP/PKA/CREB signal transduction system, that rolipram may ameliorate ME‐induced impairment of learning and memory function, and that the drug effect may be partly attributed to activation of the cyclic AMP/PKA/CREB signal transduction system. British Journal of Pharmacology (2002) 135, 1783–1793; doi:10.1038/sj.bjp.0704629</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>11934820</pmid><doi>10.1038/sj.bjp.0704629</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record>
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subjects 3',5'-Cyclic-AMP Phosphodiesterases - drug effects
3',5'-Cyclic-AMP Phosphodiesterases - metabolism
Animals
Binding Sites
Biological and medical sciences
Brain Ischemia - etiology
Brain Ischemia - metabolism
Brain Ischemia - prevention & control
Cell Nucleus - drug effects
Cell Nucleus - metabolism
Cyclic AMP - metabolism
Cyclic AMP Response Element-Binding Protein - drug effects
Cyclic AMP Response Element-Binding Protein - metabolism
Cyclic AMP-Dependent Protein Kinases - metabolism
cyclic AMP/PKA/CREB signal transduction system
Cyclic Nucleotide Phosphodiesterases, Type 4
Cytosol - drug effects
Cytosol - metabolism
Embolism - complications
learning and memory
Male
Medical sciences
Memory - drug effects
microsphere embolism
Microspheres
Phosphodiesterase Inhibitors - pharmacology
Phosphodiesterase Inhibitors - therapeutic use
Protein Subunits
Rats
Rats, Wistar
Rolipram
Rolipram - pharmacology
Rolipram - therapeutic use
Signal Transduction - drug effects
title Effects of a phosphodiesterase IV inhibitor rolipram on microsphere embolism‐induced defects in memory function and cerebral cyclic AMP signal transduction system in rats
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