Delayed rectifier potassium currents and Kv2.1 mRNA increase in hippocampal neurons of scopolamine-induced memory-deficient rats
To explore the ionic mechanisms of memory deficits induced by cholinergic lesion, whole-cell patch clamp recording techniques in combination with single-cell RT-PCR were used to characterize delayed rectifier potassium currents ( I K) in acutely isolated hippocampal pyramidal neurons of scopolamine-...
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| Veröffentlicht in: | Neuroscience letters 2005-01, Vol.373 (2), p.99-104 |
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| creator | Zhong, Chong-Bo Pan, Ya-Ping Tong, Xiao-Yong Xu, Xiang-Hua Wang, Xiao-Liang |
| description | To explore the ionic mechanisms of memory deficits induced by cholinergic lesion, whole-cell patch clamp recording techniques in combination with single-cell RT-PCR were used to characterize delayed rectifier potassium currents (
I
K) in acutely isolated hippocampal pyramidal neurons of scopolamine-induced cognitive impairment rats. Scopolamine could induce deficits in spatial memory of rats. The peak amplitude and current density of
I
K measured in hippocampal pyramidal neurons were increased from 1.2
±
0.6
nA and 38
±
19
pA/pF of the control group (
n
=
12) to 1.8
±
0.5
nA and 62
±
24
pA/pF (
n
=
48,
P
<
0.01) of the scopolamine-treated group. The steady-state activation curve of
I
K was shifted about 8
mV (
P
<
0.01) in the direction of hyperpolarization in scopolamine-treated rats. The mRNA level of Kv2.1 was increased (
P
<
0.01) in the scopolamine-treated group, but there was no significant change of Kv1.5 mRNA level. The present study demonstrated for the first time that
I
K was enhanced significantly in hippocampal pyramidal neurons of scopolamine-induced cognitive impairment rats. The increase of Kv2.1 mRNA expression in hippocampal pyramidal cells might be responsible for the enhancement of
I
K and could be the ionic basis of the memory deficits induced by scopolamine. |
| doi_str_mv | 10.1016/j.neulet.2004.09.069 |
| format | Article |
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I
K) in acutely isolated hippocampal pyramidal neurons of scopolamine-induced cognitive impairment rats. Scopolamine could induce deficits in spatial memory of rats. The peak amplitude and current density of
I
K measured in hippocampal pyramidal neurons were increased from 1.2
±
0.6
nA and 38
±
19
pA/pF of the control group (
n
=
12) to 1.8
±
0.5
nA and 62
±
24
pA/pF (
n
=
48,
P
<
0.01) of the scopolamine-treated group. The steady-state activation curve of
I
K was shifted about 8
mV (
P
<
0.01) in the direction of hyperpolarization in scopolamine-treated rats. The mRNA level of Kv2.1 was increased (
P
<
0.01) in the scopolamine-treated group, but there was no significant change of Kv1.5 mRNA level. The present study demonstrated for the first time that
I
K was enhanced significantly in hippocampal pyramidal neurons of scopolamine-induced cognitive impairment rats. The increase of Kv2.1 mRNA expression in hippocampal pyramidal cells might be responsible for the enhancement of
I
K and could be the ionic basis of the memory deficits induced by scopolamine.</description><identifier>ISSN: 0304-3940</identifier><identifier>EISSN: 1872-7972</identifier><identifier>DOI: 10.1016/j.neulet.2004.09.069</identifier><identifier>PMID: 15567561</identifier><identifier>CODEN: NELED5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Action Potentials - drug effects ; Action Potentials - physiology ; Animals ; Biological and medical sciences ; Cholinergic dysfunction ; Fundamental and applied biological sciences. Psychology ; Hippocampus - drug effects ; Hippocampus - metabolism ; Kv1.5 Potassium Channel ; Kv2.1 ; Male ; Memory - drug effects ; Memory - physiology ; Muscarinic Antagonists - pharmacology ; Neurons - drug effects ; Neurons - metabolism ; Organ Culture Techniques ; Patch clamp ; Patch-Clamp Techniques ; Potassium - metabolism ; Potassium Channels, Voltage-Gated - physiology ; Potassium current ; Rats ; Rats, Wistar ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - analysis ; Scopolamine ; Scopolamine Hydrobromide - pharmacology ; Shab Potassium Channels ; Single-cell RT-PCR ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuroscience letters, 2005-01, Vol.373 (2), p.99-104</ispartof><rights>2004 Elsevier Ireland Ltd</rights><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c388t-d0eef0a7a8b21cfc101b7b4daf3161b5c2b3e8202407ba328ec0fec34eb3f8543</citedby><cites>FETCH-LOGICAL-c388t-d0eef0a7a8b21cfc101b7b4daf3161b5c2b3e8202407ba328ec0fec34eb3f8543</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neulet.2004.09.069$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16318578$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15567561$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhong, Chong-Bo</creatorcontrib><creatorcontrib>Pan, Ya-Ping</creatorcontrib><creatorcontrib>Tong, Xiao-Yong</creatorcontrib><creatorcontrib>Xu, Xiang-Hua</creatorcontrib><creatorcontrib>Wang, Xiao-Liang</creatorcontrib><title>Delayed rectifier potassium currents and Kv2.1 mRNA increase in hippocampal neurons of scopolamine-induced memory-deficient rats</title><title>Neuroscience letters</title><addtitle>Neurosci Lett</addtitle><description>To explore the ionic mechanisms of memory deficits induced by cholinergic lesion, whole-cell patch clamp recording techniques in combination with single-cell RT-PCR were used to characterize delayed rectifier potassium currents (
I
K) in acutely isolated hippocampal pyramidal neurons of scopolamine-induced cognitive impairment rats. Scopolamine could induce deficits in spatial memory of rats. The peak amplitude and current density of
I
K measured in hippocampal pyramidal neurons were increased from 1.2
±
0.6
nA and 38
±
19
pA/pF of the control group (
n
=
12) to 1.8
±
0.5
nA and 62
±
24
pA/pF (
n
=
48,
P
<
0.01) of the scopolamine-treated group. The steady-state activation curve of
I
K was shifted about 8
mV (
P
<
0.01) in the direction of hyperpolarization in scopolamine-treated rats. The mRNA level of Kv2.1 was increased (
P
<
0.01) in the scopolamine-treated group, but there was no significant change of Kv1.5 mRNA level. The present study demonstrated for the first time that
I
K was enhanced significantly in hippocampal pyramidal neurons of scopolamine-induced cognitive impairment rats. The increase of Kv2.1 mRNA expression in hippocampal pyramidal cells might be responsible for the enhancement of
I
K and could be the ionic basis of the memory deficits induced by scopolamine.</description><subject>Action Potentials - drug effects</subject><subject>Action Potentials - physiology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cholinergic dysfunction</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Kv1.5 Potassium Channel</subject><subject>Kv2.1</subject><subject>Male</subject><subject>Memory - drug effects</subject><subject>Memory - physiology</subject><subject>Muscarinic Antagonists - pharmacology</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Organ Culture Techniques</subject><subject>Patch clamp</subject><subject>Patch-Clamp Techniques</subject><subject>Potassium - metabolism</subject><subject>Potassium Channels, Voltage-Gated - physiology</subject><subject>Potassium current</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - analysis</subject><subject>Scopolamine</subject><subject>Scopolamine Hydrobromide - pharmacology</subject><subject>Shab Potassium Channels</subject><subject>Single-cell RT-PCR</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0304-3940</issn><issn>1872-7972</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1r3DAQhkVpabZp_0EpurQ3uyPJsuRLIaRfISGB0p6FLI-oFttyJTuwt_70atmF3HqaOTzzzvAMIW8Z1AxY-3Ffz7iNuNYcoKmhq6HtnpEd04pXqlP8OdmBgKYSXQMX5FXOewCQTDYvyQWTslWyZTvy9zOO9oADTejW4AMmusTV5hy2ibotJZzXTO080NtHXjM6_bi_omF2CW3G0tDfYVmis9NiR1oOSnHONHqaXVziaKcwYxXmYXNlxYRTTIdqQB9cKLk02TW_Ji-8HTO-OddL8uvrl5_X36u7h28311d3lRNar9UAiB6ssrrnzHlXFPSqbwbrBWtZLx3vBWoOvAHVW8E1OvDoRIO98Fo24pJ8OOUuKf7ZMK9mCtnhONoZ45ZNq7jUWrYFbE6gSzHnhN4sKUw2HQwDczRv9uZk3hzNG-hMMV_G3p3zt37C4WnorLoA78-Azc6OPtnZhfzEtYJpqXThPp04LDYey0NMPtoqAsPxR2aI4f-X_ANhbaae</recordid><startdate>20050110</startdate><enddate>20050110</enddate><creator>Zhong, Chong-Bo</creator><creator>Pan, Ya-Ping</creator><creator>Tong, Xiao-Yong</creator><creator>Xu, Xiang-Hua</creator><creator>Wang, Xiao-Liang</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20050110</creationdate><title>Delayed rectifier potassium currents and Kv2.1 mRNA increase in hippocampal neurons of scopolamine-induced memory-deficient rats</title><author>Zhong, Chong-Bo ; Pan, Ya-Ping ; Tong, Xiao-Yong ; Xu, Xiang-Hua ; Wang, Xiao-Liang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c388t-d0eef0a7a8b21cfc101b7b4daf3161b5c2b3e8202407ba328ec0fec34eb3f8543</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Action Potentials - drug effects</topic><topic>Action Potentials - physiology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cholinergic dysfunction</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - metabolism</topic><topic>Kv1.5 Potassium Channel</topic><topic>Kv2.1</topic><topic>Male</topic><topic>Memory - drug effects</topic><topic>Memory - physiology</topic><topic>Muscarinic Antagonists - pharmacology</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Organ Culture Techniques</topic><topic>Patch clamp</topic><topic>Patch-Clamp Techniques</topic><topic>Potassium - metabolism</topic><topic>Potassium Channels, Voltage-Gated - physiology</topic><topic>Potassium current</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - analysis</topic><topic>Scopolamine</topic><topic>Scopolamine Hydrobromide - pharmacology</topic><topic>Shab Potassium Channels</topic><topic>Single-cell RT-PCR</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhong, Chong-Bo</creatorcontrib><creatorcontrib>Pan, Ya-Ping</creatorcontrib><creatorcontrib>Tong, Xiao-Yong</creatorcontrib><creatorcontrib>Xu, Xiang-Hua</creatorcontrib><creatorcontrib>Wang, Xiao-Liang</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neuroscience letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhong, Chong-Bo</au><au>Pan, Ya-Ping</au><au>Tong, Xiao-Yong</au><au>Xu, Xiang-Hua</au><au>Wang, Xiao-Liang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Delayed rectifier potassium currents and Kv2.1 mRNA increase in hippocampal neurons of scopolamine-induced memory-deficient rats</atitle><jtitle>Neuroscience letters</jtitle><addtitle>Neurosci Lett</addtitle><date>2005-01-10</date><risdate>2005</risdate><volume>373</volume><issue>2</issue><spage>99</spage><epage>104</epage><pages>99-104</pages><issn>0304-3940</issn><eissn>1872-7972</eissn><coden>NELED5</coden><abstract>To explore the ionic mechanisms of memory deficits induced by cholinergic lesion, whole-cell patch clamp recording techniques in combination with single-cell RT-PCR were used to characterize delayed rectifier potassium currents (
I
K) in acutely isolated hippocampal pyramidal neurons of scopolamine-induced cognitive impairment rats. Scopolamine could induce deficits in spatial memory of rats. The peak amplitude and current density of
I
K measured in hippocampal pyramidal neurons were increased from 1.2
±
0.6
nA and 38
±
19
pA/pF of the control group (
n
=
12) to 1.8
±
0.5
nA and 62
±
24
pA/pF (
n
=
48,
P
<
0.01) of the scopolamine-treated group. The steady-state activation curve of
I
K was shifted about 8
mV (
P
<
0.01) in the direction of hyperpolarization in scopolamine-treated rats. The mRNA level of Kv2.1 was increased (
P
<
0.01) in the scopolamine-treated group, but there was no significant change of Kv1.5 mRNA level. The present study demonstrated for the first time that
I
K was enhanced significantly in hippocampal pyramidal neurons of scopolamine-induced cognitive impairment rats. The increase of Kv2.1 mRNA expression in hippocampal pyramidal cells might be responsible for the enhancement of
I
K and could be the ionic basis of the memory deficits induced by scopolamine.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>15567561</pmid><doi>10.1016/j.neulet.2004.09.069</doi><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0304-3940 |
| ispartof | Neuroscience letters, 2005-01, Vol.373 (2), p.99-104 |
| issn | 0304-3940 1872-7972 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Action Potentials - drug effects Action Potentials - physiology Animals Biological and medical sciences Cholinergic dysfunction Fundamental and applied biological sciences. Psychology Hippocampus - drug effects Hippocampus - metabolism Kv1.5 Potassium Channel Kv2.1 Male Memory - drug effects Memory - physiology Muscarinic Antagonists - pharmacology Neurons - drug effects Neurons - metabolism Organ Culture Techniques Patch clamp Patch-Clamp Techniques Potassium - metabolism Potassium Channels, Voltage-Gated - physiology Potassium current Rats Rats, Wistar Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - analysis Scopolamine Scopolamine Hydrobromide - pharmacology Shab Potassium Channels Single-cell RT-PCR Vertebrates: nervous system and sense organs |
| title | Delayed rectifier potassium currents and Kv2.1 mRNA increase in hippocampal neurons of scopolamine-induced memory-deficient rats |
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