Assessing the Neural Mechanisms of Anxiety

A "Lesser Wrong" Model of Assessing the Neural Mechanisms of Anxiety

The objective of our class and the neuroscientific community is to understand the complex neural pathways of the brain. The neural mechanisms of anxiety have long puzzled researchers. Thus far, the belief is that two structures of the limbic system known as the lateral septum and the amygdala regulate anxiety. The present paper will examine the role of the lateral septum and the amygdala in propagating anxiety (supporting the brain = behavior paradigm), discuss the neural connection that exist between the Am and LS, consider the effects that benzodiazepine anxiolytics have on this neural connection, as well as introduce findings from my current research that supports the "lesser wrong" model of anxiety.

Amygdala and Anxiogenesis

The amygdala (hereafter cited as Am) is a known anxiety producing or anxiogenic structure (1). Anxiety is assessed through a number of animal studies that examine fear and stress responses in the presence of aversive stimuli such as a shock. Fear and stress responses in animals are good measures of anxiety because they correlate well with the symptoms observed in people with generalized anxiety disorder. For instance, studies that assess anxiety in animal paradigms report increased stress induced ulceration, increased heart beat, and increased galvanic skin conductance. Similarly, individuals diagnosed with generalized anxiety disorder show upset stomach, increased hear rate, and increased sweating. Hence, anxiety, fear, and stress responses are closely related.

Fear responses are behavioral changes that occur in the presence of aversive stimuli. The most common behavioral response (in rats) to aversive stimuli is behavioral arrest also referred to as "freezing". Behavioral arrest occurs when the animal "freezes following a cue for the aversive stimulus. Davis (1992) describes the freezing behavior as the animal's apprehensive expectation that something bad is about to happen.

Stress responses are physiological changes that occur in response to aversive stimuli. Stress responses in animal and human studies include pupil dilation, increased heart beat, decreased salivation (or dry mouth), increase galvanic skin conductance (or increased sweating) and frequent defecation (or diarrhea). Studies have shown that during the presentation of a tone that forewarns the animal of a shock, the animal show a multitude of stress responses including the ones listed above.

Similarly, in a fMRI scan study, human subjects showed Am activation in instructed fear or anticipatory anxiety task. In this task, subjects are manipulated into believing that they will receive a shock when a threatening stimulus is presented.