Cholinergic deficit induced memory retrieval deficit and hippocampal CaMKII‐alpha deregulation is counteracted by sub‐chronic agmatine treatment in mice

Background Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative disease characterized by brain cholinergic dysfunction. Evidence suggests the impairment of memory retrieval phase in AD. It has been shown that CaMKII‐α expressing neurons are selectively reduced in the hippocampus i...

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Veröffentlicht in:Alzheimer's & dementia 2023-12, Vol.19 (S13), p.n/a
Hauptverfasser: Ostovan, Vahid Reza, Baberi, Nahid, Farrokhi, Majid Reza, Moezi, Leila, Pirsalami, Fatema, SoukhakLari, Roksana, Moosavi, Maryam
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container_issue S13
container_start_page
container_title Alzheimer's & dementia
container_volume 19
creator Ostovan, Vahid Reza
Baberi, Nahid
Farrokhi, Majid Reza
Moezi, Leila
Pirsalami, Fatema
SoukhakLari, Roksana
Moosavi, Maryam
description Background Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative disease characterized by brain cholinergic dysfunction. Evidence suggests the impairment of memory retrieval phase in AD. It has been shown that CaMKII‐α expressing neurons are selectively reduced in the hippocampus in AD brains. The present study aimed to investigate the effect of scopolamine on the memory retrieval phase and the hippocampal CaMKII‐α signaling. In addition, the effect of sub‐chronic administration of agmatine against scopolamine induced memory and possible hippocampal CaMKII‐α deregulation was investigated in mice. Method Adult male NMRI mice were administered with agmatine at the doses of 5, 10, 20, 30 and 40 mg/kg/i.p. or saline for 11 days. Acquisition and retrieval tests of passive avoidance task were performed on days 10 and 11, respectively (30 Min following agmatine treatment). Scopolamine (1 mg/kg/i.p.) was administered once, 30 Min before retrieval test. Upon completion of the behavioral tasks, the hippocampi were isolated for western blot analysis to detect the phosphorylated and total levels of CaMKII‐α and beta actin proteins. Result The results showed that scopolamine induced memory retrieval deficit and decreased the phosphorylated level of hippocampal CaMKII‐α. Sub‐chronic agmatine treatment at the dose of 40 mg/kg prevented scopolamine induced memory retrieval deficit and restored the level of hippocampal phosphorylated CaMKII‐α. Conclusion This study suggests that hippocampal CaMKII‐α might play a role in scopolamine induced amnesia and sub‐chronic agmatine prevents the impairing effect of scopolamine on the retrieval phase of memory and the phosphorylation of hippocampal CaMKII‐α protein.
doi_str_mv 10.1002/alz.072825
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Evidence suggests the impairment of memory retrieval phase in AD. It has been shown that CaMKII‐α expressing neurons are selectively reduced in the hippocampus in AD brains. The present study aimed to investigate the effect of scopolamine on the memory retrieval phase and the hippocampal CaMKII‐α signaling. In addition, the effect of sub‐chronic administration of agmatine against scopolamine induced memory and possible hippocampal CaMKII‐α deregulation was investigated in mice. Method Adult male NMRI mice were administered with agmatine at the doses of 5, 10, 20, 30 and 40 mg/kg/i.p. or saline for 11 days. Acquisition and retrieval tests of passive avoidance task were performed on days 10 and 11, respectively (30 Min following agmatine treatment). Scopolamine (1 mg/kg/i.p.) was administered once, 30 Min before retrieval test. Upon completion of the behavioral tasks, the hippocampi were isolated for western blot analysis to detect the phosphorylated and total levels of CaMKII‐α and beta actin proteins. Result The results showed that scopolamine induced memory retrieval deficit and decreased the phosphorylated level of hippocampal CaMKII‐α. Sub‐chronic agmatine treatment at the dose of 40 mg/kg prevented scopolamine induced memory retrieval deficit and restored the level of hippocampal phosphorylated CaMKII‐α. Conclusion This study suggests that hippocampal CaMKII‐α might play a role in scopolamine induced amnesia and sub‐chronic agmatine prevents the impairing effect of scopolamine on the retrieval phase of memory and the phosphorylation of hippocampal CaMKII‐α protein.</description><identifier>ISSN: 1552-5260</identifier><identifier>EISSN: 1552-5279</identifier><identifier>DOI: 10.1002/alz.072825</identifier><language>eng</language><ispartof>Alzheimer's &amp; dementia, 2023-12, Vol.19 (S13), p.n/a</ispartof><rights>2023 the Alzheimer's Association.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Falz.072825$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Falz.072825$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids></links><search><creatorcontrib>Ostovan, Vahid Reza</creatorcontrib><creatorcontrib>Baberi, Nahid</creatorcontrib><creatorcontrib>Farrokhi, Majid Reza</creatorcontrib><creatorcontrib>Moezi, Leila</creatorcontrib><creatorcontrib>Pirsalami, Fatema</creatorcontrib><creatorcontrib>SoukhakLari, Roksana</creatorcontrib><creatorcontrib>Moosavi, Maryam</creatorcontrib><title>Cholinergic deficit induced memory retrieval deficit and hippocampal CaMKII‐alpha deregulation is counteracted by sub‐chronic agmatine treatment in mice</title><title>Alzheimer's &amp; dementia</title><description>Background Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative disease characterized by brain cholinergic dysfunction. Evidence suggests the impairment of memory retrieval phase in AD. It has been shown that CaMKII‐α expressing neurons are selectively reduced in the hippocampus in AD brains. The present study aimed to investigate the effect of scopolamine on the memory retrieval phase and the hippocampal CaMKII‐α signaling. In addition, the effect of sub‐chronic administration of agmatine against scopolamine induced memory and possible hippocampal CaMKII‐α deregulation was investigated in mice. Method Adult male NMRI mice were administered with agmatine at the doses of 5, 10, 20, 30 and 40 mg/kg/i.p. or saline for 11 days. Acquisition and retrieval tests of passive avoidance task were performed on days 10 and 11, respectively (30 Min following agmatine treatment). Scopolamine (1 mg/kg/i.p.) was administered once, 30 Min before retrieval test. Upon completion of the behavioral tasks, the hippocampi were isolated for western blot analysis to detect the phosphorylated and total levels of CaMKII‐α and beta actin proteins. Result The results showed that scopolamine induced memory retrieval deficit and decreased the phosphorylated level of hippocampal CaMKII‐α. Sub‐chronic agmatine treatment at the dose of 40 mg/kg prevented scopolamine induced memory retrieval deficit and restored the level of hippocampal phosphorylated CaMKII‐α. Conclusion This study suggests that hippocampal CaMKII‐α might play a role in scopolamine induced amnesia and sub‐chronic agmatine prevents the impairing effect of scopolamine on the retrieval phase of memory and the phosphorylation of hippocampal CaMKII‐α protein.</description><issn>1552-5260</issn><issn>1552-5279</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNp9kM9Og0AQh4nRxFq9-AR7NqHOLizQY0P801jjRS9eyLAMZQ0sZKEaPPkIPoBP55O4TZsePc1k8s1vJp_nXXKYcQBxjfXnDGKRCHnkTbiUwpcinh8f-ghOvbO-fwMIIeFy4v2kVVtrQ3atFSuo1EoPTJtio6hgDTWtHZmlwWp6x_oAoClYpbuuVdh0bp7i48Ny-fv1jXVXocMsrTc1Dro1TPdMtRszkEU1uNB8ZP0md6yqbGvcVVw3jjTEBks4NGS2D7BGKzr3Tkqse7rY16n3cnvznN77q6e7ZbpY-YrzQPoRYpDkFEakRCIRZQEQh2EMQZHwkvJAgoRQ5iRkCUKUiAnn0TwWMsES5kUw9a52ucq2fW-pzDqrG7RjxiHbes2c12zn1cF8B3_omsZ_yGyxet3v_AFuWX_W</recordid><startdate>202312</startdate><enddate>202312</enddate><creator>Ostovan, Vahid Reza</creator><creator>Baberi, Nahid</creator><creator>Farrokhi, Majid Reza</creator><creator>Moezi, Leila</creator><creator>Pirsalami, Fatema</creator><creator>SoukhakLari, Roksana</creator><creator>Moosavi, Maryam</creator><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>202312</creationdate><title>Cholinergic deficit induced memory retrieval deficit and hippocampal CaMKII‐alpha deregulation is counteracted by sub‐chronic agmatine treatment in mice</title><author>Ostovan, Vahid Reza ; Baberi, Nahid ; Farrokhi, Majid Reza ; Moezi, Leila ; Pirsalami, Fatema ; SoukhakLari, Roksana ; Moosavi, Maryam</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1135-6aa38be46ec285aa5d00744703d81feb3505045be25f022faa811697258af09d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ostovan, Vahid Reza</creatorcontrib><creatorcontrib>Baberi, Nahid</creatorcontrib><creatorcontrib>Farrokhi, Majid Reza</creatorcontrib><creatorcontrib>Moezi, Leila</creatorcontrib><creatorcontrib>Pirsalami, Fatema</creatorcontrib><creatorcontrib>SoukhakLari, Roksana</creatorcontrib><creatorcontrib>Moosavi, Maryam</creatorcontrib><collection>CrossRef</collection><jtitle>Alzheimer's &amp; dementia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ostovan, Vahid Reza</au><au>Baberi, Nahid</au><au>Farrokhi, Majid Reza</au><au>Moezi, Leila</au><au>Pirsalami, Fatema</au><au>SoukhakLari, Roksana</au><au>Moosavi, Maryam</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cholinergic deficit induced memory retrieval deficit and hippocampal CaMKII‐alpha deregulation is counteracted by sub‐chronic agmatine treatment in mice</atitle><jtitle>Alzheimer's &amp; dementia</jtitle><date>2023-12</date><risdate>2023</risdate><volume>19</volume><issue>S13</issue><epage>n/a</epage><issn>1552-5260</issn><eissn>1552-5279</eissn><abstract>Background Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative disease characterized by brain cholinergic dysfunction. Evidence suggests the impairment of memory retrieval phase in AD. It has been shown that CaMKII‐α expressing neurons are selectively reduced in the hippocampus in AD brains. The present study aimed to investigate the effect of scopolamine on the memory retrieval phase and the hippocampal CaMKII‐α signaling. In addition, the effect of sub‐chronic administration of agmatine against scopolamine induced memory and possible hippocampal CaMKII‐α deregulation was investigated in mice. Method Adult male NMRI mice were administered with agmatine at the doses of 5, 10, 20, 30 and 40 mg/kg/i.p. or saline for 11 days. Acquisition and retrieval tests of passive avoidance task were performed on days 10 and 11, respectively (30 Min following agmatine treatment). Scopolamine (1 mg/kg/i.p.) was administered once, 30 Min before retrieval test. Upon completion of the behavioral tasks, the hippocampi were isolated for western blot analysis to detect the phosphorylated and total levels of CaMKII‐α and beta actin proteins. Result The results showed that scopolamine induced memory retrieval deficit and decreased the phosphorylated level of hippocampal CaMKII‐α. Sub‐chronic agmatine treatment at the dose of 40 mg/kg prevented scopolamine induced memory retrieval deficit and restored the level of hippocampal phosphorylated CaMKII‐α. Conclusion This study suggests that hippocampal CaMKII‐α might play a role in scopolamine induced amnesia and sub‐chronic agmatine prevents the impairing effect of scopolamine on the retrieval phase of memory and the phosphorylation of hippocampal CaMKII‐α protein.</abstract><doi>10.1002/alz.072825</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record>
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title Cholinergic deficit induced memory retrieval deficit and hippocampal CaMKII‐alpha deregulation is counteracted by sub‐chronic agmatine treatment in mice
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