author_facet Tu, Bin
Gu, Zhenglin
Shen, Jian-xin
Lamb, Patricia W.
Yakel, Jerrel L.
Tu, Bin
Gu, Zhenglin
Shen, Jian-xin
Lamb, Patricia W.
Yakel, Jerrel L.
author Tu, Bin
Gu, Zhenglin
Shen, Jian-xin
Lamb, Patricia W.
Yakel, Jerrel L.
spellingShingle Tu, Bin
Gu, Zhenglin
Shen, Jian-xin
Lamb, Patricia W.
Yakel, Jerrel L.
The Journal of Neuroscience
Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex
General Neuroscience
author_sort tu, bin
spelling Tu, Bin Gu, Zhenglin Shen, Jian-xin Lamb, Patricia W. Yakel, Jerrel L. 0270-6474 1529-2401 Society for Neuroscience General Neuroscience http://dx.doi.org/10.1523/jneurosci.2580-09.2009 <jats:p>The entorhinal cortex (EC) is a part of the hippocampal complex that is essential to learning and memory, and nicotine affects memory by activating nicotinic acetylcholine receptors (nAChRs) in the hippocampal complex. However, it is not clear what types of neurons in the EC are sensitive to nicotine and whether they play a role in nicotine-induced memory functions. Here, we have used voltage-sensitive dye imaging methods to locate the neuronal populations responsive to nicotine in entorhino-hippocampal slices and to clarify which nAChR subtypes are involved. In combination with patch-clamp methods, we found that a concentration of nicotine comparable to exposure during smoking depolarized neurons in layer VI of the EC (ECVI) by acting through the non-α7 subtype of nAChRs. Neurons in the subiculum (Sb; close to the deep EC layers) also contain nicotine-sensitive neurons, and it is known that Sb neurons project to the ECVI. When we recorded evoked EPSCs (eEPSCs) from ECVI neurons while stimulating the Sb near the CA1 region, a low dose of nicotine not only enhanced synaptic transmission (by increasing eEPSC amplitude) but also enhanced plasticity by converting tetanus stimulation-induced short-term potentiation to long-term potentiation; nicotine enhanced synaptic transmission and plasticity of ECVI synapses by acting on both the α7 and non-α7 subtypes of nAChRs. Our data suggest that ECVI neurons are important regulators of hippocampal function and plasticity during smoking.</jats:p> Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex The Journal of Neuroscience
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title Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex
title_unstemmed Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex
title_full Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex
title_fullStr Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex
title_full_unstemmed Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex
title_short Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex
title_sort characterization of a nicotine-sensitive neuronal population in rat entorhinal cortex
topic General Neuroscience
url http://dx.doi.org/10.1523/jneurosci.2580-09.2009
publishDate 2009
physical 10436-10448
description <jats:p>The entorhinal cortex (EC) is a part of the hippocampal complex that is essential to learning and memory, and nicotine affects memory by activating nicotinic acetylcholine receptors (nAChRs) in the hippocampal complex. However, it is not clear what types of neurons in the EC are sensitive to nicotine and whether they play a role in nicotine-induced memory functions. Here, we have used voltage-sensitive dye imaging methods to locate the neuronal populations responsive to nicotine in entorhino-hippocampal slices and to clarify which nAChR subtypes are involved. In combination with patch-clamp methods, we found that a concentration of nicotine comparable to exposure during smoking depolarized neurons in layer VI of the EC (ECVI) by acting through the non-α7 subtype of nAChRs. Neurons in the subiculum (Sb; close to the deep EC layers) also contain nicotine-sensitive neurons, and it is known that Sb neurons project to the ECVI. When we recorded evoked EPSCs (eEPSCs) from ECVI neurons while stimulating the Sb near the CA1 region, a low dose of nicotine not only enhanced synaptic transmission (by increasing eEPSC amplitude) but also enhanced plasticity by converting tetanus stimulation-induced short-term potentiation to long-term potentiation; nicotine enhanced synaptic transmission and plasticity of ECVI synapses by acting on both the α7 and non-α7 subtypes of nAChRs. Our data suggest that ECVI neurons are important regulators of hippocampal function and plasticity during smoking.</jats:p>
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author Tu, Bin, Gu, Zhenglin, Shen, Jian-xin, Lamb, Patricia W., Yakel, Jerrel L.
author_facet Tu, Bin, Gu, Zhenglin, Shen, Jian-xin, Lamb, Patricia W., Yakel, Jerrel L., Tu, Bin, Gu, Zhenglin, Shen, Jian-xin, Lamb, Patricia W., Yakel, Jerrel L.
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container_issue 33
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container_title The Journal of Neuroscience
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description <jats:p>The entorhinal cortex (EC) is a part of the hippocampal complex that is essential to learning and memory, and nicotine affects memory by activating nicotinic acetylcholine receptors (nAChRs) in the hippocampal complex. However, it is not clear what types of neurons in the EC are sensitive to nicotine and whether they play a role in nicotine-induced memory functions. Here, we have used voltage-sensitive dye imaging methods to locate the neuronal populations responsive to nicotine in entorhino-hippocampal slices and to clarify which nAChR subtypes are involved. In combination with patch-clamp methods, we found that a concentration of nicotine comparable to exposure during smoking depolarized neurons in layer VI of the EC (ECVI) by acting through the non-α7 subtype of nAChRs. Neurons in the subiculum (Sb; close to the deep EC layers) also contain nicotine-sensitive neurons, and it is known that Sb neurons project to the ECVI. When we recorded evoked EPSCs (eEPSCs) from ECVI neurons while stimulating the Sb near the CA1 region, a low dose of nicotine not only enhanced synaptic transmission (by increasing eEPSC amplitude) but also enhanced plasticity by converting tetanus stimulation-induced short-term potentiation to long-term potentiation; nicotine enhanced synaptic transmission and plasticity of ECVI synapses by acting on both the α7 and non-α7 subtypes of nAChRs. Our data suggest that ECVI neurons are important regulators of hippocampal function and plasticity during smoking.</jats:p>
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spelling Tu, Bin Gu, Zhenglin Shen, Jian-xin Lamb, Patricia W. Yakel, Jerrel L. 0270-6474 1529-2401 Society for Neuroscience General Neuroscience http://dx.doi.org/10.1523/jneurosci.2580-09.2009 <jats:p>The entorhinal cortex (EC) is a part of the hippocampal complex that is essential to learning and memory, and nicotine affects memory by activating nicotinic acetylcholine receptors (nAChRs) in the hippocampal complex. However, it is not clear what types of neurons in the EC are sensitive to nicotine and whether they play a role in nicotine-induced memory functions. Here, we have used voltage-sensitive dye imaging methods to locate the neuronal populations responsive to nicotine in entorhino-hippocampal slices and to clarify which nAChR subtypes are involved. In combination with patch-clamp methods, we found that a concentration of nicotine comparable to exposure during smoking depolarized neurons in layer VI of the EC (ECVI) by acting through the non-α7 subtype of nAChRs. Neurons in the subiculum (Sb; close to the deep EC layers) also contain nicotine-sensitive neurons, and it is known that Sb neurons project to the ECVI. When we recorded evoked EPSCs (eEPSCs) from ECVI neurons while stimulating the Sb near the CA1 region, a low dose of nicotine not only enhanced synaptic transmission (by increasing eEPSC amplitude) but also enhanced plasticity by converting tetanus stimulation-induced short-term potentiation to long-term potentiation; nicotine enhanced synaptic transmission and plasticity of ECVI synapses by acting on both the α7 and non-α7 subtypes of nAChRs. Our data suggest that ECVI neurons are important regulators of hippocampal function and plasticity during smoking.</jats:p> Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex The Journal of Neuroscience
spellingShingle Tu, Bin, Gu, Zhenglin, Shen, Jian-xin, Lamb, Patricia W., Yakel, Jerrel L., The Journal of Neuroscience, Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex, General Neuroscience
title Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex
title_full Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex
title_fullStr Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex
title_full_unstemmed Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex
title_short Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex
title_sort characterization of a nicotine-sensitive neuronal population in rat entorhinal cortex
title_unstemmed Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex
topic General Neuroscience
url http://dx.doi.org/10.1523/jneurosci.2580-09.2009