Location and function of the slow afterhyperpolarization channels in the basolateral amygdala

Power, John M., Bocklisch, Christina, Curby, Peter and Sah, Pankaj (2011) Location and function of the slow afterhyperpolarization channels in the basolateral amygdala. Journal of Neuroscience, 31 2: 526-537. doi:10.1523/JNEUROSCI.1045-10.2011

Attached Files (Some files may be inaccessible until you login with your UQ eSpace credentials)
Name Description MIMEType Size Downloads
UQ230361_OA.pdf Full text (open access) application/pdf 2.12MB 0
UQ230361_SupplementalData_Figures_OA.pdf Full text (open access) application/pdf 1.88MB 0

Author Power, John M.
Bocklisch, Christina
Curby, Peter
Sah, Pankaj
Title Location and function of the slow afterhyperpolarization channels in the basolateral amygdala
Journal name Journal of Neuroscience   Check publisher's open access policy
ISSN 0270-6474
1529-2401
Publication date 2011-01
Sub-type Article (original research)
DOI 10.1523/JNEUROSCI.1045-10.2011
Open Access Status File (Publisher version)
Volume 31
Issue 2
Start page 526
End page 537
Total pages 12
Place of publication Washington, DC, United States
Publisher Society for Neuroscience
Collection year 2012
Language eng
Formatted abstract
The basolateral amygdala (BLA) assigns emotional significance to sensory stimuli. This association results in a change in the output (action potentials) ofBLAprojection neurons in response to the stimulus. Neuronal output is controlled by the intrinsic excitability of the neuron. A major determinant of intrinsic excitability in these neurons is the slow afterhyperpolarization (sAHP) that follows action potential (AP) trains and produces spike-frequency adaptation. The sAHP is mediated by a slow calcium-activated potassium current (sIAHP), but little is known about the channels that underlie this current. Here, using whole-cell patch-clamp recordings and high-speed calcium imaging from rat BLA projection neurons, we examined the location and function of these channels.Wedetermined the location of the sIAHP by applying a hyperpolarizing voltage step during the sIAHP and measuring the time needed for the current to adapt to the new command potential, a function of its electrotonic distance from the somatic recording electrode. Channel location was also probed by focally uncaging calcium using a UV laser. Both methodologies indicated that, in BLA neurons, the sIAHP is primarily located in the dendritic tree. EPSPs recorded at the soma were smaller, decayed faster, and showed less summation during the sAHP. Adrenergic stimulation and buffering calcium reduced the sAHP and the attenuation of the EPSP during the sAHP. The sAHP also modulated the AP in the dendrite, reducing the calcium response evoked by a single AP. Thus, in addition to mediating spike-frequency adaptation, the sIAHP modulates communication between the soma and the dendrite. Copyright © 2011 the authors.
Keyword Ca1 pyramidal neurons
Long-term potentiation
Rat hippocampal-neurons
Excitatory synaptic-transmission
Projection neurons
Activated potassium currents
Lateral amygdala
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Queensland Brain Institute Publications
Official 2012 Collection
 
Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 15 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 15 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Sun, 27 Feb 2011, 00:05:28 EST