The Role of the Amygdala Gaba Receptors and Benzodiazepines in Anxiety

Topics: Neurotransmitter, Benzodiazepine, Receptor antagonist Pages: 10 (2754 words) Published: June 28, 2008
Abstract
Discussed is some of the research that has been conducted on the role of the amygdala in anxiety, as well as the role of GABA and benzodiazepines in anxiety. Research has indicated through amygdala lesions and stimulation that the amygdala does indeed play a major role in the expression of anxiety. Research has also indicated, through drug infusions to the amygdala, that benzodiazepines cause anxiolysis (by increasing GABA transmission), and that benzodiazepine antagonists increase anxiety (by decreasing GABA transmission). Also discussed are some limitations and problems found with benzodiazepine use.

On the Role of the Amygdala in Anxiety and How Treatment is Effective
The functional anatomy of anxiety involves amygdala-based neurocircuits with critical reciprocal connections to the medial prefrontal cortex (i.e. Mailizia, 1999). An understanding of the functional anatomy of anxiety allows for a new perspective on the various anxiety disorders. The neurotransmitters involved in these circuits are reviewed for their relevance to the pharmacologic choices in the treatment of anxiety (i.e. Kang, Wilson & Wilson, 2000). Much research has been conducted on gamma-aminobutyric acid (GABA) as it is the major inhibitory neurotransmitter in the mammalian Central Nervous System (CNS) (i.e. Vekovischeva, Haapalinna & Sarviharju, 1999). GABA participates in the regulation of neuronal excitability through specific membrane proteins (the GABAA receptors). The binding of GABA to these postsynaptic receptor results in an opening of chloride channel integrated in the receptor, which allows the entry of Cl-. As a consequence, this leads to the hyperpolarization of the recipient cell, which is allosterically modulated by a wide variety of chemical entities that interact with distinct binding sites at the GABAA receptor complex. One of the most thoroughly investigated modulatory sites is the benzodiazepine-binding site. The purpose of this paper is to examine some of the research that has been conducted on the relationship between the amygdala and anxiety. As well, the paper examines how benzodiazepines interact with GABAA receptors in the amygdala and the resulting effects on anxiety. The Amygdala and Its Role in Anxiety

Anxiety is a fundamental emotion that is characterized by an increase in autonomic activity, motor tension, vigilance, and apprehension in response to a present danger or impending threat (Wolkowitz & Paul, 1985). While there is no complete theory of the biological basis of anxiety, there is considerable evidence that anxiety may be primarily modulated by limbic sysem structures (i.e. Davis & Shi, 1999), including the septum and the amygdala. The amygdala's contribution to emotional processes--particularly to the recognition of emotional events and the production of appropriate responses--is the most extensively investigated and best understood function of this part of the brain.

The amygdala is a critical part of the circuitry involved in fear in rats, as well as in nonhuman primates (i.e. Hode, Ratomponirina, & Gobailles, 2000). Unfortunately, it has been difficult to study the involvement of the amygdala to anxiety in humans, due to ethical considerations and and due to the lack of a sufficient population of patients with brain damage restricted to the amygdala. However there is some evidence for the existence of similar mechanisms in humans (i.e. Mailiza, 1999).

Recent reviews strongly support the working conclusion that the amygdaloid complex is a major brain site at which fear-inducing conditional associations can be acquired and can educe a physiological expression of fear (i.e. Pitkanen, Savander, & LeDoux, 1997). Evidence supporting the above claim can be seen in studies exploring the effects of electrical stimulation of the central nucleus of the amygdala which show a production of fear behaviour (i.e. Petrovitch & Swanson, 1997); as well as studies conducted on the...

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