NEW YORK (Reuters Health) — Animal experiments suggest that co-occurring psychiatric illness and drug addiction may stem from a common cause: neurodevelopmental abnormalities in the amygdala, the emotion center of the brain.
As reported in the December issue of Behavioral Neuroscience published by the American Psychological Association, adult rats with amygdala lesions induced during the neonatal period show fearless, novelty-seeking behaviors and are more sensitive to cocaine.
Emerging clinical and basic research suggest that "neurodevelopment abnormalities of temporal-limbic structures may underlie both adult psychiatric syndromes and increased addiction vulnerability, leading to high frequencies of ‘dual diagnosis’ disorders," Dr. R. Andrew Chambers and colleagues of Indiana University School of Medicine, Indianapolis, note in their report.
The amygdala has been implicated in various mental disorders and drug addiction, but no studies have explored the impact of early developmental damage to the amygdala in relation to the co-occurrence of these disorders, they point out.
The researchers put rats with surgically-induced neonatal amygdala lesions and sham-operated control rats through a battery of behavioral tests. They also tested their sensitivity to cocaine.
Compared with control rats, rats with neonatal amygdala defects displayed significantly more novelty-seeking behavior, showed significantly less fear in an elevated maze, and kept socializing even when exposed to the scent of a predator.
They also showed increased sensitivity to cocaine after just one exposure to the drug. After repeated exposure, the amygdala-injured rats showed even stronger sensitivity, suggesting an overall susceptibility to the addictive process, Dr. Chambers and colleagues suggest.
They say further studies using this rat model of amygdala injury may be "useful for understanding addiction vulnerability in the mentally ill or interpreting clinical data suggesting that history of chronic substance use alters neuropsychiatric illness trajectories and treatment responsiveness."
Behav Neurosci 2007;121:1316-1327.
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