Morehead State University

Poster Title

Excitation of the Amygdala Augments the Effects of Amphetamine on Behavior

Institution

Morehead State University

Abstract

The amygdala is an important brain structure, which is involved in emotion, memory, and drug addiction. Dysfunctional amygdala has been implicated in post-traumatic stress disorder (PTDS) in humans. Animal studies indicated that inhibition of the amygdala potentiates behavioral excitation induced by psychostimulants, such as amphetamine and cocaine. In the present study we tested a hypothesis that excitation of the amygdala would produce an opposite effect, the suppression of amphetamine-induced behavior. We compared locomotor activity of rats following stimulation or inhibition of the amygdala, using direct microinfusions of NMDA and lidocaine, respectively. We also examined the effects of permanent damage to the amygdala on behavior. Male Wistar rats were implanted with bilateral cannulae in the amygdala. Another group received excitotoxic or sham lesions. Following recovery, rats were habituated and tested in the open-field. The animal's activity was measured by distance traveled for a 60-min period. Amphetamine markedly enhanced locomotor activity (hyperlocomotion). Stimulation of the amygdala further enhanced hyperlocomotion induced by amphetamine. This effect required for activation of D1 receptors. In contrast to the previous reports, however, neither inhibition nor permanent lesions affected amphetamine-induced hyperlocomotion. Our data suggest that an over-excited amygdala may enhance addictive property of amphetamine, whereas a normal or under-activated amygdala may not. Further investigation of the involvement of amygdala in drug addiction and reward will advance our understanding of the relationship between drug abuse and PTSD.

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Excitation of the Amygdala Augments the Effects of Amphetamine on Behavior

The amygdala is an important brain structure, which is involved in emotion, memory, and drug addiction. Dysfunctional amygdala has been implicated in post-traumatic stress disorder (PTDS) in humans. Animal studies indicated that inhibition of the amygdala potentiates behavioral excitation induced by psychostimulants, such as amphetamine and cocaine. In the present study we tested a hypothesis that excitation of the amygdala would produce an opposite effect, the suppression of amphetamine-induced behavior. We compared locomotor activity of rats following stimulation or inhibition of the amygdala, using direct microinfusions of NMDA and lidocaine, respectively. We also examined the effects of permanent damage to the amygdala on behavior. Male Wistar rats were implanted with bilateral cannulae in the amygdala. Another group received excitotoxic or sham lesions. Following recovery, rats were habituated and tested in the open-field. The animal's activity was measured by distance traveled for a 60-min period. Amphetamine markedly enhanced locomotor activity (hyperlocomotion). Stimulation of the amygdala further enhanced hyperlocomotion induced by amphetamine. This effect required for activation of D1 receptors. In contrast to the previous reports, however, neither inhibition nor permanent lesions affected amphetamine-induced hyperlocomotion. Our data suggest that an over-excited amygdala may enhance addictive property of amphetamine, whereas a normal or under-activated amygdala may not. Further investigation of the involvement of amygdala in drug addiction and reward will advance our understanding of the relationship between drug abuse and PTSD.