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Noradrenergic Modulation of the Basolateral Amygdala: Alterations by Stress Exposure

Buffalari, Deanne Marie (2007) Noradrenergic Modulation of the Basolateral Amygdala: Alterations by Stress Exposure. Doctoral Dissertation, University of Pittsburgh. (Unpublished)

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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 studiesexamine the electrophysiological consequences of alterations of the NE system on neuronalactivity 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, weused iontophoresis combined with single unit recordings of BLA neurons. NE directly applied toBLA neurons causes predominantly inhibitory effects. Spontaneous activity was inhibited,presumably via alpha-2 receptor mechanisms, while a smaller subset of neurons were excited viabeta receptor actions. NE also inhibited afferent-evoked activity of BLA neurons. Footshockand 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, andbehavioral consequences of NE on targets. Our final studies addressed whether chronic coldexposure (7 or 14 days, 5C) alters NE modulation of BLA neuronal activity. After 14 days ofv cold exposure, NE caused more excitation of spontaneous and afferent BLA neuron activity, incontrast 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 prolongedstress 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.


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Item Type: University of Pittsburgh ETD
Status: Unpublished
CreatorsEmailPitt UsernameORCID
Buffalari, Deanne Mariedmb115@pitt.eduDMB115
ETD Committee:
TitleMemberEmail AddressPitt UsernameORCID
Committee ChairGrace, Anthony Agrace@bns.pitt.eduGRACEAA
Committee MemberSved, Alan Fsved@bns.pitt.eduSVED
Committee MemberMoghaddam, Bitamoghaddam@bns.pitt.eduBITA
Committee MemberThiels,
Committee MemberRinaman, Lindarinaman@bns.pitt.eduRINAMAN
Committee MemberMaren,
Committee MemberSesack, Susan Rsesack@bns.pitt.eduSESACK
Date: 30 January 2007
Date Type: Completion
Defense Date: 21 September 2006
Approval Date: 30 January 2007
Submission Date: 29 September 2006
Access Restriction: No restriction; Release the ETD for access worldwide immediately.
Institution: University of Pittsburgh
Schools and Programs: Dietrich School of Arts and Sciences > Neuroscience
Degree: PhD - Doctor of Philosophy
Thesis Type: Doctoral Dissertation
Refereed: Yes
Uncontrolled Keywords: alpha-2 receptors; amygdala; beta receptors; electrophysiology; footshock; norepinephrine; stress; yohimbine
Other ID:, etd-09292006-112125
Date Deposited: 10 Nov 2011 20:02
Last Modified: 15 Nov 2016 13:50


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