Wang J Y, Yaksh T L, Harty G J, Go V L
Am J Physiol. 1986 Jan;250(1 Pt 2):R104-11. doi: 10.1152/ajpregu.1986.250.1.R104.
The cortical release of vasoactive intestinal polypeptide-like immunoreactivity (VIP-LI) in vivo was examined by superfusion of the pial surface of the cerebral cortex of the cat. The modulation of cortical VIP release by several neurotransmitters [gamma-aminobutyric acid (GABA), opioids, norepinephrine, acetylcholine, and glutamate] normally present in the cerebral cortex was studied by administering respective agonists and antagonists for their receptors. Although GABA and opiate agonists did not influence the resting release of VIP-LI, GABA antagonists (picrotoxin and bicuculline) and opiate antagonists (naloxone and naltrexone) significantly elevated the resting release. The evoked release from cortex of VIP-LI (by electrical stimulation of the cortex or mesencephalic reticular formation) was suppressed by GABA and mu- but not delta-, kappa-, or sigma-opioid receptor agonists. Glutamate and kainic acid increased the resting release of VIP-LI from the cerebral cortex. Noradrenergic (alpha 2 but not alpha 1) displayed an inhibitory effect on the evoked release of cortical VIP-LI release. Resting VIP-LI release was enhanced by cholinergic agents (carbachol). The facilitatory effects of mesencephalic reticular formation stimulation on VIP-LI release were demonstrated by atropine. These observations suggest characteristic interactions reflecting the circuitry modulating the activity of cortical VIP-releasing neurons.
