| Summary: | Accumulating evidence implicates the amygdala as the main brain region
underlying anxiety and, in a parallel stream of research, suggests that dopamine (DA)
may be a key neuromodulator of experimental anxiety. However, little is currently known
about how the primary output area, the central nucleus, of the amygdala (CeA) and the
mesocorticolimbic D A system interact. Chapter 2 sought to directly assess the role of the
CeA in neurophysiological alterations occurring at the D A cell-body region of the ventral
tegmental area (VTA). The C eA was either activated via pharmacological antagonism of
G A B A A receptors or inactivated via pharmacological agonism of G A B A A / G A B A B
receptors. Subsequently, in vivo electrophysiological measures were used to examine the
modulation of V T A D A neuron (i) population activity, (ii) firing rate, and (iii) bursting.
CeA activation resulted in a significant increase in the population activity and bursting of
V T A D A neurons. Conversely, inactivation of the CeA resulted in a significant reduction
in the population activity of these cells. These are the first electrophysiological data to
demonstrate that the CeA elicits differential regulation of distinct physiological
parameters of V T A D A neurons. To complement these findings, Chapter 3 describes
experiments that investigated the effects of C eA inactivation, in a manner similar to that
used in Chapter 2, utilizing a behavioural approach. This series of experiments employed
a mesocortical DA-dependent conflict paradigm that simultaneously incorporates
appetitive (Reward) and aversive (Conflict) components. CeA inactivation resulted in a
significant reduction of responding during the Reward components and a significant
increase in lever-pressing during the Conflict period of the conflict test (Experiment 1)
and its variant, the extinction of conflict test (Experiment 2). The data from Chapter 3
suggest that the CeA plays dissociable roles in mediating motivational responding under
appetitive conditions and suppressing responding following exposure to aversive,
conflict-inducing, stimuli. Collectively, the results from Chapter 2 and Chapter 3 offer
corroborating evidence from electrophysiological and behavioural perspectives for the
role of the CeA in modulating the mesocorticolimbic D A system. Ultimately, the systems
approach implemented in the current study may offer novel insight into the
neurophysiological mechanisms by which one area of the amygdala mediates
experimental anxiety.
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