Inhibition of the dopamine system in rat amygdala attenuates the picrotoxin-induced locomoter hyperactivity and hypertension

1. The aim of the present study was to investigate whether picrotoxin-induced locomotor hyperactivity and hypertension can be inhibited by dopaminergic inhibition in rat amygdala. 2. Locomotor activity was detected using a modularized infrared light matrix system in freely moving rats. In anaesthetized rats, blood pressure was measured while dopamine release was detected using in vivo voltammetry with carbon fibre electrodes. 3. Systemic administration of picrotoxin (1-4 mg/kg) increased both locomotor activity (including horizontal motion, vertical motion and total distance travelled) and the number of turnings (both clockwise and anticlockwise), but inhibited postural freezing. The locomotor hyperactivity induced by systemic administration of picrotoxin was mimicked by direct injection of a small dose (1-3 mug in 1.0 muL) of picrotoxin into the amygdala. 4. In vivo voltammetry data revealed that systemic administration of picrotoxin increased the release of dopamine in the amygdala of rat brain accompanied by hypertension. 5. Local injection of kainic acid into the paramedian reticular nucleus (PRN) of the medulla oblongata decreased both the spontaneous release of dopamine in the amygdala and spontaneous levels of locomotor activity in rats. 6. Furthermore, the picrotoxin-induced locomotor hyperactivity, hypertension and increased amygdaloid dopamine release were all suppressed following chemical stimulation of the PRN with kainic acid. 7. Blockade of dopamine receptors with systemic or intra-amygdaloid injection of haloperidol (a dopamine receptor antagonist) significantly attenuated the picrotoxin-induced locomotor hyperactivity and hypertension. 8. These results demonstrate that picrotoxin-induced hyperactivity and hypertension involve an increase in amygdaloid dopamine transmission that can be modulated by ascending projections from the PRN in the medulla oblongata.