22 COGNITIVE THEORY AND RESEARCH ON ANXIETY
ing the function of other neurotransmitters (Noyes & Hoehn-Saric, 1998; Sinha et al.,
2004).
A subgroup of the inhibitory transmitter GABA contains benzodiazepine receptors
that enhance the inhibitory effects of GABA when benzodiazepine molecules bind to
these receptor sites (Gardner, Tully, & Hedgecock, 1993). Evidence that generalized
anxiety may be due to a suppressed benzodiazepine-GABA system comes from the anxi-
olytic effects of benzodiazepine drugs (e.g., lorazepam [Ativan], alprazolam [Xanax]),
which appear to have their clinical effectiveness by enhancing benzodiazepine-GABA
inhibition (Barlow, 2002).
Corticotropin- releasing hormone (CRH) is a neurotransmitter that is primar-
ily stored in the hypothalamic paraventricular nuclei (PVN). Stressful or threatening
stimuli can activate certain brain regions like the locus ceruleus, amygdala, hippocam-
pus, and prefrontal cortex, which then releases CRH. CRH then stimulates secretion
of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland and other
pituitary– adrenal activity that results in increased production and release of cortisol
(Barlow, 2002; Noyes & Hoehn-Saric, 1998). The CRH, then, not only mediates endo-
crine responses to stress but also other broad brain and behavioral responses that play
a role in the expression of stress, anxiety, and depression (Barlow, 2002). Overall, then,
abnormalities at the neurotransmitter level appear to have anxiogenic or anxiolytic
effects that play an important contributory role in heightened physiological states that
characterize fear and anxiety. However, the exact nature of these abnormalities is still
unknown. Table 1.4 provides a summary of the biological aspects of anxiety that might
underlie the cognitive features of these disorders discussed later in this volume.
Clinician Guideline 1.11
Discuss the neural basis of anxiety when educating the client about the cognitive model of
anxiety. The rationale for cognitive therapy should include a discussion of how the higher
order cortical centers of the brain involved in memory, reasoning, and judgment can “over-
ride” or inhibit subcortical emotional brain structures, thereby reducing the subjective
experience of anxiety.table 1.4. biological Concomitants of Cognition in anxiety
Biological factors Cognitive sequelae
••Elevated tonic autonomic activation ••Increased salience of threat-related stimuli
••Slower habituation rate ••Sustained attention to threat
••Diminished autonomic flexibility ••Reduced ability to shift attention
••Genetic predisposition for negative emotionality ••Hypervalent schemas of threat and danger
••Subcortical fear potentiation ••Preconscious fear stimulus identification and
immediate physiological arousal
••Extensive cortical afferent and efferent pathways
to subcortical emotion-relevant circuitry••Cognitive appraisal and memory influence fear
perception and modulates fear expression and
action