Brief reportsLocomotor hyperactivity induced by blockade of prefrontal cortical α2-adrenoceptors in monkeys
Section snippets
Subjects
Two young monkeys (Macaca mulatta, female, 2 years old) were used. They were housed individually in custom-made cages (80 cm × 80 cm × 90 cm, length × width × height) and maintained on a 12 hr-light/12 hr-dark cycle at a temperature of 25 ± 2°C. Food and water were available ad libitum. The monkeys were cared for in accordance with the Guiding Principles for the Care and the Use of Laboratory Animals issued by the National Institutes of Health in 1996. This study was approved and monitored by
Results
A total of 6 bilateral, symmetric infusions with yohimbine were carried out in the dlPFC, 3 infusions in each monkey. The cortical area and reconstructed sites for infusion are shown in the inset of Figure 1. All of the 6 infusions were effective for induction of locomotor hyperactivity (Figure 1A and B). Each monkey showed a dramatic increase in daily locomotion during the 8-day administration of yohimbine (Figure 1B; p < .01 for during infusion vs. before infusion, Mann-Whitney U-test).
Discussion
The neurobiological base for hyperactivity seen in ADHD is still unknown. Locomotor hyperactivity could have multiple neural origins. Many studies indicate that hyperactivity in ADHD involves dopaminergic mechanisms in the striatum and the prefrontal cortex (for review, see Levy and Swanson 2001). The present study provides the first evidence that α2-ARs in the monkey’s dlPFC may be involved in neural mechanisms regulating locomotor activity and offers a hypothesis that down-regulation or
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2020, Neurobiology of Learning and MemoryCitation Excerpt :Guanfacine infusions into the aged rat mPFC also improve working memory, and are reversed by local activation of cAMP-PKA signaling (Ramos, Stark, Verduzco, van Dyck, & Arnsten, 2006). Conversely, infusion of the α2-AR antagonist, yohimbine, into the monkey dlPFC impaired working memory (Li & Mei, 1994), impulse control (Ma, Qi, Peng, & Li, 2003) and regulation of locomotor activity (Ma, Arnsten, & Li, 2005), producing an “ADHD-like” phenotype. Guanfacine and yohimbine also produce markedly opposing effects on the neuronal firing of dlPFC Delay cells in monkeys performing the ODR working memory task.
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