GABAA-mediated IPSCs in piriform cortex have fast and slow components with different properties and locations on pyramidal cells. Kapur, A., Pearce, R., Lytton, W., & Haberly, L. J. Neurophysiol., 78:2531--2545, Nov, 1997. abstract bibtex GABAA-mediated IPSCs in piriform cortex have fast and slow components with different properties and locations on pyramidal cells. J. Neurophysiol. 78: 2531-2545, 1997. A recent study in piriform (olfactory) cortex provided evidence that, as in hippocampus and neocortex, gamma-aminobutyric acid-A (GABAA)-mediated inhibition is generated in dendrites of pyramidal cells, not just in the somatic region as previously believed. This study examines selected properties of GABAA inhibitory postsynaptic currents (IPSCs) in dendritic and somatic regions that could provide insight into their functional roles. Pharmacologically isolated GABAA-mediated IPSCs were studied by whole cell patch recording in slices. To compare properties of IPSCs in distal dendritic and somatic regions, local stimulation was carried out with tungsten microelectrodes, and spatially restricted blockade of GABAA-mediated inhibition was achieved by pressure-ejection of bicuculline from micropipettes. The results revealed that largely independent circuits generate GABAA inhibition in distal apical dendritic and somatic regions. With such independence, a selective decrease in dendritic-region inhibition could enhance integrative or plastic processes in dendrites while allowing feedback inhibition in the somatic region to restrain system excitability. This could allow modulatory fiber systems from the basal forebrain or brain stem, for example, to change the functional state of the cortex by altering the excitability of interneurons that mediate dendritic inhibition without increasing the propensity for regenerative bursting in this highly epileptogenic system. As in hippocampus, GABAA-mediated IPSCs were found to have fast and slow components with time constants of decay on the order of 10 and 40 ms, respectively, at 29 degrees C. Modeling analysis supported physiological evidence that the slow time constant represents a true IPSC component rather than an artifactual slowing of the fast component from voltage clamp of a dendritic current. The results indicated that, whereas both dendritic and somatic-region IPSCs have both fast and slow GABAA components, there is a greater proportion of the slow component in dendrites. In a companion paper, the hypothesis is explored that the resulting slower time course of the dendritic IPSC increases its capacity to regulate the N-methyl--aspartate component of EPSPs. Finally, evidence is presented that the slow GABAA-mediated IPSC component is regulated by presynaptic GABAB inhibition whereas the fast is not. Based on the requirement for presynaptic GABAB-mediated block of inhibition for expression of long-term potentiation, this finding is consistent with participation of the slow GABAA component in regulation of synaptic plasticity. The lack of susceptibility of the fast GABAA component to the long-lasting, activity-induced suppression mediated by presynaptic GABAB receptors is consistent with a protective role for this process in preventing seizure activity.
@article{ Kapur_etal97,
author = {Kapur, A. and Pearce, R.A. and Lytton, W.W. and Haberly, L.B.},
title = {{{G}{A}{B}{A}{A}-mediated {I}{P}{S}{C}s in piriform cortex have fast
and slow components with different properties and locations on pyramidal
cells}},
journal = {J. Neurophysiol.},
year = {1997},
volume = {78},
pages = {2531--2545},
month = {Nov},
abstract = {GABAA-mediated IPSCs in piriform cortex have fast and slow components
with different properties and locations on pyramidal cells. J. Neurophysiol.
78: 2531-2545, 1997. A recent study in piriform (olfactory) cortex
provided evidence that, as in hippocampus and neocortex, gamma-aminobutyric
acid-A (GABAA)-mediated inhibition is generated in dendrites of pyramidal
cells, not just in the somatic region as previously believed. This
study examines selected properties of GABAA inhibitory postsynaptic
currents (IPSCs) in dendritic and somatic regions that could provide
insight into their functional roles. Pharmacologically isolated GABAA-mediated
IPSCs were studied by whole cell patch recording in slices. To compare
properties of IPSCs in distal dendritic and somatic regions, local
stimulation was carried out with tungsten microelectrodes, and spatially
restricted blockade of GABAA-mediated inhibition was achieved by
pressure-ejection of bicuculline from micropipettes. The results
revealed that largely independent circuits generate GABAA inhibition
in distal apical dendritic and somatic regions. With such independence,
a selective decrease in dendritic-region inhibition could enhance
integrative or plastic processes in dendrites while allowing feedback
inhibition in the somatic region to restrain system excitability.
This could allow modulatory fiber systems from the basal forebrain
or brain stem, for example, to change the functional state of the
cortex by altering the excitability of interneurons that mediate
dendritic inhibition without increasing the propensity for regenerative
bursting in this highly epileptogenic system. As in hippocampus,
GABAA-mediated IPSCs were found to have fast and slow components
with time constants of decay on the order of 10 and 40 ms, respectively,
at 29 degrees C. Modeling analysis supported physiological evidence
that the slow time constant represents a true IPSC component rather
than an artifactual slowing of the fast component from voltage clamp
of a dendritic current. The results indicated that, whereas both
dendritic and somatic-region IPSCs have both fast and slow GABAA
components, there is a greater proportion of the slow component in
dendrites. In a companion paper, the hypothesis is explored that
the resulting slower time course of the dendritic IPSC increases
its capacity to regulate the N-methyl--aspartate component of EPSPs.
Finally, evidence is presented that the slow GABAA-mediated IPSC
component is regulated by presynaptic GABAB inhibition whereas the
fast is not. Based on the requirement for presynaptic GABAB-mediated
block of inhibition for expression of long-term potentiation, this
finding is consistent with participation of the slow GABAA component
in regulation of synaptic plasticity. The lack of susceptibility
of the fast GABAA component to the long-lasting, activity-induced
suppression mediated by presynaptic GABAB receptors is consistent
with a protective role for this process in preventing seizure activity.}
}
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{"_id":"XddsWt3JTWyaEpgJX","bibbaseid":"kapur-pearce-lytton-haberly-gabaamediatedipscsinpiriformcortexhavefastandslowcomponentswithdifferentpropertiesandlocationsonpyramidalcells-1997","downloads":0,"creationDate":"2015-02-08T05:14:47.669Z","title":"GABAA-mediated IPSCs in piriform cortex have fast and slow components with different properties and locations on pyramidal cells","author_short":["Kapur, A.","Pearce, R.","Lytton, W.","Haberly, L."],"year":1997,"bibtype":"article","biburl":"http://cnslab.mb.jhu.edu/niebase.bib","bibdata":{"abstract":"GABAA-mediated IPSCs in piriform cortex have fast and slow components with different properties and locations on pyramidal cells. J. Neurophysiol. 78: 2531-2545, 1997. A recent study in piriform (olfactory) cortex provided evidence that, as in hippocampus and neocortex, gamma-aminobutyric acid-A (GABAA)-mediated inhibition is generated in dendrites of pyramidal cells, not just in the somatic region as previously believed. This study examines selected properties of GABAA inhibitory postsynaptic currents (IPSCs) in dendritic and somatic regions that could provide insight into their functional roles. Pharmacologically isolated GABAA-mediated IPSCs were studied by whole cell patch recording in slices. To compare properties of IPSCs in distal dendritic and somatic regions, local stimulation was carried out with tungsten microelectrodes, and spatially restricted blockade of GABAA-mediated inhibition was achieved by pressure-ejection of bicuculline from micropipettes. The results revealed that largely independent circuits generate GABAA inhibition in distal apical dendritic and somatic regions. With such independence, a selective decrease in dendritic-region inhibition could enhance integrative or plastic processes in dendrites while allowing feedback inhibition in the somatic region to restrain system excitability. This could allow modulatory fiber systems from the basal forebrain or brain stem, for example, to change the functional state of the cortex by altering the excitability of interneurons that mediate dendritic inhibition without increasing the propensity for regenerative bursting in this highly epileptogenic system. As in hippocampus, GABAA-mediated IPSCs were found to have fast and slow components with time constants of decay on the order of 10 and 40 ms, respectively, at 29 degrees C. Modeling analysis supported physiological evidence that the slow time constant represents a true IPSC component rather than an artifactual slowing of the fast component from voltage clamp of a dendritic current. The results indicated that, whereas both dendritic and somatic-region IPSCs have both fast and slow GABAA components, there is a greater proportion of the slow component in dendrites. In a companion paper, the hypothesis is explored that the resulting slower time course of the dendritic IPSC increases its capacity to regulate the N-methyl--aspartate component of EPSPs. Finally, evidence is presented that the slow GABAA-mediated IPSC component is regulated by presynaptic GABAB inhibition whereas the fast is not. Based on the requirement for presynaptic GABAB-mediated block of inhibition for expression of long-term potentiation, this finding is consistent with participation of the slow GABAA component in regulation of synaptic plasticity. The lack of susceptibility of the fast GABAA component to the long-lasting, activity-induced suppression mediated by presynaptic GABAB receptors is consistent with a protective role for this process in preventing seizure activity.","author":["Kapur, A.","Pearce, R.A.","Lytton, W.W.","Haberly, L.B."],"author_short":["Kapur, A.","Pearce, R.","Lytton, W.","Haberly, L."],"bibtex":"@article{ Kapur_etal97,\n author = {Kapur, A. and Pearce, R.A. and Lytton, W.W. and Haberly, L.B.},\n title = {{{G}{A}{B}{A}{A}-mediated {I}{P}{S}{C}s in piriform cortex have fast\n\tand slow components with different properties and locations on pyramidal\n\tcells}},\n journal = {J. Neurophysiol.},\n year = {1997},\n volume = {78},\n pages = {2531--2545},\n month = {Nov},\n abstract = {GABAA-mediated IPSCs in piriform cortex have fast and slow components\n\twith different properties and locations on pyramidal cells. J. Neurophysiol.\n\t78: 2531-2545, 1997. A recent study in piriform (olfactory) cortex\n\tprovided evidence that, as in hippocampus and neocortex, gamma-aminobutyric\n\tacid-A (GABAA)-mediated inhibition is generated in dendrites of pyramidal\n\tcells, not just in the somatic region as previously believed. This\n\tstudy examines selected properties of GABAA inhibitory postsynaptic\n\tcurrents (IPSCs) in dendritic and somatic regions that could provide\n\tinsight into their functional roles. Pharmacologically isolated GABAA-mediated\n\tIPSCs were studied by whole cell patch recording in slices. To compare\n\tproperties of IPSCs in distal dendritic and somatic regions, local\n\tstimulation was carried out with tungsten microelectrodes, and spatially\n\trestricted blockade of GABAA-mediated inhibition was achieved by\n\tpressure-ejection of bicuculline from micropipettes. The results\n\trevealed that largely independent circuits generate GABAA inhibition\n\tin distal apical dendritic and somatic regions. With such independence,\n\ta selective decrease in dendritic-region inhibition could enhance\n\tintegrative or plastic processes in dendrites while allowing feedback\n\tinhibition in the somatic region to restrain system excitability.\n\tThis could allow modulatory fiber systems from the basal forebrain\n\tor brain stem, for example, to change the functional state of the\n\tcortex by altering the excitability of interneurons that mediate\n\tdendritic inhibition without increasing the propensity for regenerative\n\tbursting in this highly epileptogenic system. As in hippocampus,\n\tGABAA-mediated IPSCs were found to have fast and slow components\n\twith time constants of decay on the order of 10 and 40 ms, respectively,\n\tat 29 degrees C. Modeling analysis supported physiological evidence\n\tthat the slow time constant represents a true IPSC component rather\n\tthan an artifactual slowing of the fast component from voltage clamp\n\tof a dendritic current. The results indicated that, whereas both\n\tdendritic and somatic-region IPSCs have both fast and slow GABAA\n\tcomponents, there is a greater proportion of the slow component in\n\tdendrites. In a companion paper, the hypothesis is explored that\n\tthe resulting slower time course of the dendritic IPSC increases\n\tits capacity to regulate the N-methyl--aspartate component of EPSPs.\n\tFinally, evidence is presented that the slow GABAA-mediated IPSC\n\tcomponent is regulated by presynaptic GABAB inhibition whereas the\n\tfast is not. Based on the requirement for presynaptic GABAB-mediated\n\tblock of inhibition for expression of long-term potentiation, this\n\tfinding is consistent with participation of the slow GABAA component\n\tin regulation of synaptic plasticity. The lack of susceptibility\n\tof the fast GABAA component to the long-lasting, activity-induced\n\tsuppression mediated by presynaptic GABAB receptors is consistent\n\twith a protective role for this process in preventing seizure activity.}\n}","bibtype":"article","id":"Kapur_etal97","journal":"J. 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