Muscarinic depolarization of layer II neurons of the parasubiculum.
The parasubiculum (PaS) is a component of the hippocampal formation that sends its major output to layer II of the entorhinal cortex. The PaS receives strong cholinergic innervation from the basal forebrain that is likely to modulate neuronal excitability and contribute to theta-frequency network ac...
| Main Authors: | , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2013-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC3592838?pdf=render |
| _version_ | 1811278771648462848 |
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| author | Stephen D Glasgow C Andrew Chapman |
| author_facet | Stephen D Glasgow C Andrew Chapman |
| author_sort | Stephen D Glasgow |
| collection | DOAJ |
| description | The parasubiculum (PaS) is a component of the hippocampal formation that sends its major output to layer II of the entorhinal cortex. The PaS receives strong cholinergic innervation from the basal forebrain that is likely to modulate neuronal excitability and contribute to theta-frequency network activity. The present study used whole cell current- and voltage-clamp recordings to determine the effects of cholinergic receptor activation on layer II PaS neurons. Bath application of carbachol (CCh; 10-50 µM) resulted in a dose-dependent depolarization of morphologically-identified layer II stellate and pyramidal cells that was not prevented by blockade of excitatory and inhibitory synaptic inputs. Bath application of the M1 receptor antagonist pirenzepine (1 µM), but not the M2-preferring antagonist methoctramine (1 µM), blocked the depolarization, suggesting that it is dependent on M1 receptors. Voltage-clamp experiments using ramped voltage commands showed that CCh resulted in the gradual development of an inward current that was partially blocked by concurrent application of the selective Kv7.2/3 channel antagonist XE-991, which inhibits the muscarine-dependent K(+) current I M. The remaining inward current also reversed near EK and was inhibited by the K(+) channel blocker Ba(2+), suggesting that M1 receptor activation attenuates both I M as well as an additional K(+) current. The additional K(+) current showed rectification at depolarized voltages, similar to K(+) conductances mediated by Kir 2.3 channels. The cholinergic depolarization of layer II PaS neurons therefore appears to occur through M1-mediated effects on I M as well as an additional K(+) conductance. |
| first_indexed | 2024-04-13T00:43:00Z |
| format | Article |
| id | doaj.art-271d2645acc54da987753f64557ff836 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-04-13T00:43:00Z |
| publishDate | 2013-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-271d2645acc54da987753f64557ff8362022-12-22T03:10:06ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-0183e5890110.1371/journal.pone.0058901Muscarinic depolarization of layer II neurons of the parasubiculum.Stephen D GlasgowC Andrew ChapmanThe parasubiculum (PaS) is a component of the hippocampal formation that sends its major output to layer II of the entorhinal cortex. The PaS receives strong cholinergic innervation from the basal forebrain that is likely to modulate neuronal excitability and contribute to theta-frequency network activity. The present study used whole cell current- and voltage-clamp recordings to determine the effects of cholinergic receptor activation on layer II PaS neurons. Bath application of carbachol (CCh; 10-50 µM) resulted in a dose-dependent depolarization of morphologically-identified layer II stellate and pyramidal cells that was not prevented by blockade of excitatory and inhibitory synaptic inputs. Bath application of the M1 receptor antagonist pirenzepine (1 µM), but not the M2-preferring antagonist methoctramine (1 µM), blocked the depolarization, suggesting that it is dependent on M1 receptors. Voltage-clamp experiments using ramped voltage commands showed that CCh resulted in the gradual development of an inward current that was partially blocked by concurrent application of the selective Kv7.2/3 channel antagonist XE-991, which inhibits the muscarine-dependent K(+) current I M. The remaining inward current also reversed near EK and was inhibited by the K(+) channel blocker Ba(2+), suggesting that M1 receptor activation attenuates both I M as well as an additional K(+) current. The additional K(+) current showed rectification at depolarized voltages, similar to K(+) conductances mediated by Kir 2.3 channels. The cholinergic depolarization of layer II PaS neurons therefore appears to occur through M1-mediated effects on I M as well as an additional K(+) conductance.http://europepmc.org/articles/PMC3592838?pdf=render |
| spellingShingle | Stephen D Glasgow C Andrew Chapman Muscarinic depolarization of layer II neurons of the parasubiculum. PLoS ONE |
| title | Muscarinic depolarization of layer II neurons of the parasubiculum. |
| title_full | Muscarinic depolarization of layer II neurons of the parasubiculum. |
| title_fullStr | Muscarinic depolarization of layer II neurons of the parasubiculum. |
| title_full_unstemmed | Muscarinic depolarization of layer II neurons of the parasubiculum. |
| title_short | Muscarinic depolarization of layer II neurons of the parasubiculum. |
| title_sort | muscarinic depolarization of layer ii neurons of the parasubiculum |
| url | http://europepmc.org/articles/PMC3592838?pdf=render |
| work_keys_str_mv | AT stephendglasgow muscarinicdepolarizationoflayeriineuronsoftheparasubiculum AT candrewchapman muscarinicdepolarizationoflayeriineuronsoftheparasubiculum |