The effects of periaqueductally injected transmitter antagonists on forebrain-elicited vocalization in the squirrel monkey.

In 15 squirrel monkeys, vocalization-eliciting electrodes were implanted into the following forebrain structures: anterior cingulate cortex, genu of the internal capsule, amygdala, bed nucleus of the stria terminalis, hypothalamus, midline thalamus, inferior thalamic peduncle and periventricular grey. Then, injections of 29 transmitter antagonists were made into the midbrain periaqueductal grey (PAG) and their effects tested on the elicitability of vocalization from the forebrain. Vocalization could be blocked completely with glutamate antagonists. NMDA receptor antagonists as well as kainate/quisqualate receptor antagonists were effective. Facilitatory effects, i.e. a decrease in threshold of forebrain-elicited vocalization, was obtained with GABA-A receptor, glycine and opioid antagonists. The facilitatory effect of the opioid antagonist naloxone was limited to vocalizations expressing aversive emotional states. GABA-A receptor antagonists not only facilitated forebrain-induced vocalization but also produced vocalization themselves, i.e. without concomitant forebrain stimulation. No effects were obtained with antagonists of muscarinic and nicotinic receptors, with the GABA-B receptor antagonist phaclofen and antagonists of the monoamines dopamine, noradrenaline, adrenaline, serotonin and histamine. It is concluded that the PAG represents a crucial relay station of the vocalization-controlling system. In this station, transmission of vocalization-relevant information depends upon the activation of glutamatergic synapses. Inhibitory control is exerted by GABA, glycine and endogenous opioids. Acetylcholine, dopamine, noradrenaline, adrenaline, serotonin and histamine may play a transient modulatory role; forebrain-induced vocalization, however, does not depend upon the cholinergic or monoaminergic activation of PAG neurons.