The CCKB agonist, pentagastrin, has been shown to induce anxiety in human subjects. Similarly, in the cat model, pentagastrin facilitates the expression of hypothalamically activated emotional behavior. Because hypothalamically mediated emotional behavior is also accompanied by increased EMG activity in the jaw muscles, these experiments were designed to examine the combined effects of administration of pentagastrin with activation of hypothalamically mediated emotional behavior upon jaw muscle EMG activity. Electrodes were carefully lowered through previously placed guide tubes overlying the hypothalamus until a behavioral site was identified. Following the establishment of a stable threshold current for eliciting an emotional behavioral response, the skin overlying the ipsilateral masseter muscle was shaved and cleaned with alcohol, and surface electrodes were attached. The EMG was recorded, amplified, digitized, and stored in a microcomputer for analysis. Mean power frequencies (MPF) and latencies for behavior were calculated for baseline prior to infusion of all drugs. Following this, the effects of intravenous administration of pentagastrin and the CCKB antagonist LY288513 on the MPF were determined. The infusion of the CCKB agonist, pentagastrin (0.77, 1.92, and 3.84 μg/kg), decreased MPF in a time-related manner. The effects of pentagastrin 1.92 μg/kg were blocked by the CCKB antagonist, LY288513 (6.54 μg/kg). In addition, the infusion of LY288513 alone increased MPF. These results are surprising in that pentagastrin's anxiogenic properties would appear to make it likely to facilitate motor activity, not suppress it.
All Science Journal Classification (ASJC) codes
- Cholecystokinin agonist
- Defensive rage
- Masseter muscle