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Brain damage linked to addiction

The results of animal experiments suggest that psychiatric illness and drug addiction may stem from a common cause: neuro-developmental abnormalities in the amygdala, the emotion centre of the brain.

Adult rats with amygdala injuries induced during infancy show fearless, novelty-seeking behaviour and are more sensitive to the effects of cocaine, researchers report in the current issue of the journal Behavioral Neuroscience.

Evidence from other research suggests that neuro-development abnormalities may be present in adults with psychiatric disorders and may also increase the vulnerability to addiction, leading to a high rate of "dual diagnoses," report Dr R. Andrew Chambers and colleagues at Indiana University School of Medicine.

The amygdala has been implicated in various mental disorders and in drug addiction, but no studies have explored the impact of early developmental damage to the amygdala on the occurrence of these two conditions, the researchers point out.

Show novelty-seeking behaviour
Chambers and his associates put rats with surgically induced amygdala damage and rats without amygdala damage through a battery of behavioural tests. They also tested their sensitivity to cocaine.

Compared with the undamaged rats, the rats with the amygdala defects displayed significantly more novelty-seeking behaviour, showed significantly less fear in an elevated maze, and kept socialising even after being exposed to the scent of a predator.

The animals 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, Chambers's group suggests.

Based on these findings, the researchers conclude further studies using this experimental 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 neuro-psychiatric illness trajectories and treatment responsiveness." – (Reuters Health)

SOURCE: Behavioral Neuroscience

December 2007

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