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Alpha-2 adrenergic modulation of prefrontal cortical neuronal activity related to a visual discrimination task with
Abstract:
The effects of clonidine (a selective agonist for alpha-2 receptor) and B-HT920 (an agonist for both alpha-2 and D2 receptors) were examined iontophoretically on neurons in the prefrontal cortex of three monkeys performing a visual discrimination task with GO and NO-GO responses. A total of 212 task-related neurons were sampled, of which 120 neurons were related to the visual signals (visually-related neurons; 32 neurons were related to the warning signal, 45 to the GO signal and 43 to the NO-GO signal), 34 neurons were related to both the GO signal and GO response ('intermediate'-related neurons), and 58 neurons were related to GO response (movement-related neurons). Clonidine and B-HT920 were tested in 137 and 115 neurons, respectively, and showed mainly a facilitatory effect on the neurons. Clonidine enhanced the visually-related activity in 83.0% of modulated neurons, the intermediate-related activity in 81.0% neurons and the movement-related activity in 85.0% neurons. Similarly, B-HT920 enhanced the visually-related activity in 80.0% of modulated neurons, the intermediate-related activity in 77.8% neurons and the movement-related activity in 81.0% neurons. The facilitatory effect of clonidine or B-HT920 on the visually-related activity was stronger than that on the movement-related activity. In 22 visually-related neurons enhanced by clonidine and-or B-HT920 (6 WS-, 7 GS- and 9 NS-related neurons), the alpha-2 antagonist yohimbine suppressed the visually-related activities. In 13 neurons enhanced by B-HT920, the facilitatory effect of B-HT920 was blocked by yohimbine, but not by the D2 antagonist sulpiride. The present results suggest that alpha-2 adrenoceptors in the monkey prefrontal cortex are involved in neural processing related to visual discrimination and selection of GO and NO-GO responses, and that the facilitatory effect of B-HT920 may be mediated vis alpha-2 adrenoceptors instead of D2-receptors.