The behavioral consequences of norepinephrine (NE) in the basolateral amygdala (BLA) have long been well established. NE increases in the amygdala in response to the presentation of aversive stimuli, presumably due to an activation of locus coeruleus (LC) neurons that send NE efferents to the BLA. The following studies
examine the electrophysiological consequences of alterations of the NE system on neuronal
activity within the BLA.
Single unit recordings of neurons of the BLA were performed, and responses to systemic administration of the anxiogenic agent yohimbine were examined. Yohimbine had both excitatory and inhibitory effects on spontaneous and afferent-evoked neuronal activity of BLA neurons. This was accompanied by a yohimbine-induced increase in NE levels within the BLA, confirmed with microdialysis.
To more precisely examine the effects of NE within the BLA on neuronal activity, we
used iontophoresis combined with single unit recordings of BLA neurons. NE directly applied to
BLA neurons causes predominantly inhibitory effects. Spontaneous activity was inhibited,
presumably via alpha-2 receptor mechanisms, while a smaller subset of neurons were excited via
beta receptor actions. NE also inhibited afferent-evoked activity of BLA neurons. Footshock
and LC stimulation each caused both excitatory and inhibitory effects on BLA neuronal activity;
those effects could be mimicked by NE iontophoresis. Therefore, NE effects are representative of those caused by aversive stimulus presentation (footshock), or by activation of LC neurons.
Chronic stress alters the activity of the NE system, the responsivity of BLA neurons, and
behavioral consequences of NE on targets. Our final studies addressed whether chronic cold
exposure (7 or 14 days, 5C) alters NE modulation of BLA neuronal activity. After 14 days of
v cold exposure, NE caused more excitation of spontaneous and afferent BLA neuron activity, in
contrast to the NE-induced inhibition seen in control rats. Seven days of cold stress caused only moderate changes in NE modulation of evoked activity. These data demonstrate that prolonged
stress alters the way in which NE affects neuronal activity in target regions. We suggest BLA neurons become hyperexcitable, and this pathology may underlie some of the behavioral deficits and symptoms associated with exposure to chronic stress.
| Identifer | oai:union.ndltd.org:PITT/oai:PITTETD:etd-09292006-112125 |
| Date | 30 January 2007 |
| Creators | Buffalari, Deanne Marie |
| Contributors | Alan F. Sved, Susan R. Sesack, Anthony A. Grace, Linda Rinaman, Edda Thiels, Stephen Maren, Bita Moghaddam |
| Publisher | University of Pittsburgh |
| Source Sets | University of Pittsburgh |
| Language | English |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | http://etd.library.pitt.edu/ETD/available/etd-09292006-112125/ |
| Rights | unrestricted, I hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to University of Pittsburgh or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report. |
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