The CCKB agonist, pentagastrin, has been shown to induce anxiety in human s
ubjects. Similarly, in the cat model, pentagastrin facilitates the expressi
on of hypothalamically activated emotional behavior. Because hypothalamical
ly mediated emotional behavior is also accompanied by increased EMG activit
y in the jaw muscles, these experiments were designed to examine the combin
ed effects of administration of pentagastrin with activation of hypothalami
cally 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 establis
hment of a stable threshold current for eliciting an emotional behavioral r
esponse, the skin overlying the ipsilateral masseter muscle was shaved and
cleaned with alcohol, and surface electrodes were attached. The EMG was rec
orded, amplified, digitized, and stored in a microcomputer for analysis. Me
an power frequencies (MPF) and latencies for behavior were calculated for b
aseline prior to infusion of all drugs. Following this, the effects of intr
avenous administration of pentagastrin and the CCKB antagonist LY288513 on
the MPF were determined. The infusion of the CCKB agonist, entagastrin (0.7
7, 1.92, and 3.84 mug/kg), decreased MPF in a time-related manner. The effe
cts of pentagastrin 1.92 mug/kg were blocked by the CCKB antagonist, LY2885
13 (6.54 mug/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.