Selective suppression of plasticity in amygdala inputs from temporal association cortex by the external capsule
GABAergic neurons in the external capsule (EC) provide feedforward inhibition in the lateral amygdala (LA), but how EC affects synaptic transmission and plasticity in inputs from specific cortical areas remains unknown; this is because axonal fibers from different cortical areas are intermingled in...
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| Veröffentlicht in: | The Journal of neuroscience 2011-01, Vol.31 (1), p.339-345 |
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| creator | Morozov, Alexei Sukato, Daniel Ito, Wataru |
| description | GABAergic neurons in the external capsule (EC) provide feedforward inhibition in the lateral amygdala (LA), but how EC affects synaptic transmission and plasticity in inputs from specific cortical areas remains unknown; this is because axonal fibers from different cortical areas are intermingled in the amygdala and cannot be activated selectively using conventional electrical stimulation. Here, we achieved selective activation of fibers from the temporal association cortex (TeA) or the anterior cingulate cortex (ACC) by using channelrhodopsin-2. Long-term potentiation (LTP) in the TeA-LA pathway, which runs through EC, was enabled by cutting connections between EC and LA or by blocking GABA(A) receptor-mediated transmission. In contrast, LTP in the ACC-LA pathway, which bypasses EC, was GABA(A) receptor independent. The EC transection shifted balance between inhibitory and excitatory responses in the TeA-LA pathway toward excitation, but had no effect on the ACC-LA pathway. Thus, EC provides pathway-specific suppression of amygdala plasticity. |
| doi_str_mv | 10.1523/jneurosci.5537-10.2011 |
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Here, we achieved selective activation of fibers from the temporal association cortex (TeA) or the anterior cingulate cortex (ACC) by using channelrhodopsin-2. Long-term potentiation (LTP) in the TeA-LA pathway, which runs through EC, was enabled by cutting connections between EC and LA or by blocking GABA(A) receptor-mediated transmission. In contrast, LTP in the ACC-LA pathway, which bypasses EC, was GABA(A) receptor independent. The EC transection shifted balance between inhibitory and excitatory responses in the TeA-LA pathway toward excitation, but had no effect on the ACC-LA pathway. 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Here, we achieved selective activation of fibers from the temporal association cortex (TeA) or the anterior cingulate cortex (ACC) by using channelrhodopsin-2. Long-term potentiation (LTP) in the TeA-LA pathway, which runs through EC, was enabled by cutting connections between EC and LA or by blocking GABA(A) receptor-mediated transmission. In contrast, LTP in the ACC-LA pathway, which bypasses EC, was GABA(A) receptor independent. The EC transection shifted balance between inhibitory and excitatory responses in the TeA-LA pathway toward excitation, but had no effect on the ACC-LA pathway. 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Sukato, Daniel ; Ito, Wataru</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c511t-add0a20c4cc3bba985ec5fe85367168be915c5b13847165602c940d764302cb23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>6-Cyano-7-nitroquinoxaline-2,3-dione - pharmacology</topic><topic>Afferent Pathways - drug effects</topic><topic>Afferent Pathways - physiology</topic><topic>Amygdala - cytology</topic><topic>Amygdala - physiology</topic><topic>Animals</topic><topic>Cerebral Cortex - cytology</topic><topic>Cerebral Cortex - physiology</topic><topic>Channelrhodopsins</topic><topic>Dependovirus - genetics</topic><topic>Electric Stimulation - methods</topic><topic>Excitatory Amino Acid Antagonists - pharmacology</topic><topic>Excitatory Postsynaptic Potentials - genetics</topic><topic>Excitatory Postsynaptic Potentials - physiology</topic><topic>GABA Antagonists - pharmacology</topic><topic>Gene Expression Regulation - genetics</topic><topic>Glutamate Decarboxylase - genetics</topic><topic>Green Fluorescent Proteins - genetics</topic><topic>In Vitro Techniques</topic><topic>Luminescent Proteins - genetics</topic><topic>Male</topic><topic>Membrane Potentials - genetics</topic><topic>Membrane Potentials - physiology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Neuronal Plasticity - physiology</topic><topic>Patch-Clamp Techniques - methods</topic><topic>Photic Stimulation - methods</topic><topic>Picrotoxin - pharmacology</topic><topic>Time Factors</topic><topic>Valine - analogs & derivatives</topic><topic>Valine - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Morozov, Alexei</creatorcontrib><creatorcontrib>Sukato, Daniel</creatorcontrib><creatorcontrib>Ito, Wataru</creatorcontrib><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><collection>Neurosciences Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Morozov, Alexei</au><au>Sukato, Daniel</au><au>Ito, Wataru</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Selective suppression of plasticity in amygdala inputs from temporal association cortex by the external capsule</atitle><jtitle>The Journal of neuroscience</jtitle><addtitle>J Neurosci</addtitle><date>2011-01-05</date><risdate>2011</risdate><volume>31</volume><issue>1</issue><spage>339</spage><epage>345</epage><pages>339-345</pages><issn>0270-6474</issn><eissn>1529-2401</eissn><abstract>GABAergic neurons in the external capsule (EC) provide feedforward inhibition in the lateral amygdala (LA), but how EC affects synaptic transmission and plasticity in inputs from specific cortical areas remains unknown; this is because axonal fibers from different cortical areas are intermingled in the amygdala and cannot be activated selectively using conventional electrical stimulation. Here, we achieved selective activation of fibers from the temporal association cortex (TeA) or the anterior cingulate cortex (ACC) by using channelrhodopsin-2. Long-term potentiation (LTP) in the TeA-LA pathway, which runs through EC, was enabled by cutting connections between EC and LA or by blocking GABA(A) receptor-mediated transmission. In contrast, LTP in the ACC-LA pathway, which bypasses EC, was GABA(A) receptor independent. The EC transection shifted balance between inhibitory and excitatory responses in the TeA-LA pathway toward excitation, but had no effect on the ACC-LA pathway. Thus, EC provides pathway-specific suppression of amygdala plasticity.</abstract><cop>United States</cop><pub>Society for Neuroscience</pub><pmid>21209220</pmid><doi>10.1523/jneurosci.5537-10.2011</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 6-Cyano-7-nitroquinoxaline-2,3-dione - pharmacology Afferent Pathways - drug effects Afferent Pathways - physiology Amygdala - cytology Amygdala - physiology Animals Cerebral Cortex - cytology Cerebral Cortex - physiology Channelrhodopsins Dependovirus - genetics Electric Stimulation - methods Excitatory Amino Acid Antagonists - pharmacology Excitatory Postsynaptic Potentials - genetics Excitatory Postsynaptic Potentials - physiology GABA Antagonists - pharmacology Gene Expression Regulation - genetics Glutamate Decarboxylase - genetics Green Fluorescent Proteins - genetics In Vitro Techniques Luminescent Proteins - genetics Male Membrane Potentials - genetics Membrane Potentials - physiology Mice Mice, Inbred C57BL Mice, Transgenic Neuronal Plasticity - physiology Patch-Clamp Techniques - methods Photic Stimulation - methods Picrotoxin - pharmacology Time Factors Valine - analogs & derivatives Valine - pharmacology |
| title | Selective suppression of plasticity in amygdala inputs from temporal association cortex by the external capsule |
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