1. 1. The release of vasoactive intestinal polypeptide (VIP) from the surface of the sensorimotor (parietal) cortex of anesthetized cats was measured by radioimmunoassay (RIA) procedures. 2. 2. Two types of anesthetics were examined (chloralose-urethane and halothane). Increasing the dose or concentration of anesthetics produced a suppression of electrocortical activity and resulted in a reduction in the resting of VIP from cerebral cortex. The mean rate of resting release of endogenous VIP in cats anesthetized with chloralose-urethane was 16.8 ± 4.6 fmol/30 min/cm2cortex. 3. 3. Although there were differences in the basal levels of VIP-like immunoreactivity (VIP-LI) among different animals, the baseline levels of VIP-LI varied little during the initial period of 6-7 h period of anesthesia with chloralose-urethane (40 and 300 mg/kg). Examination of representative electrocorticography which corresponded with the superfusion period revealed an association between stable levels and a relatively invariant pattern of electrical activity. All experimental manipulations were carried out during the period of stable release. 4. 4. The rate of release was increase by focal, unilateral stimulation of the cerebral cortex both ipsilateral and contralateral to the side od stimulation (3.2 ± 1.1 and 1.4 ± 0.5 times the resting release, respectively). 5. 5. Bilateral stimulation of the mesencephalic reticular formation (MRF) produced a frequency-dependent increase in cortical VIP release over the range of 60-100 Hz. 6. 6. Bilateral electrical stimulation of sciatic nerves at intensities that recruit Aδ and C fibers failed to consistently increase the release of VIP-LI from the cortex in chloralose-urethane anesthetized cats but did evoke a significant increase of cortical VIP output in cats anesthetized with 1.5 and 1% halothane. 7. 7. Removal of calcium ions from the superfusing fluid and substitution of cobalt (a calcium channel blocker) or EDTA (a calcium chelating agent) for calcium ions did not affect the resting release of endogenous VIP, but attenuated the increase in VIP release normally evoked by electrical stimulation of the cortical surface or MRF. 8. 8. Tetrodotoxin (TTX), which blocks sodium channels and thus blocks the propagation of nerve impulses, did not influence the resting release of VIP. TTX, at concentrations that prevent the increase in VIP release evoked by veratridine, greatly enhanced the surface-stimulated release but abolished the increase in VIP release evoked by MRF stimulation. 9. 9. The present observations indicate that following physiological activation of the cortex by direct stimulation, and indirectly by the stimulation of ascending MRF systems and somatic input, VIP concentrations in cortical superfusate are increased by 1.5-6 fold. Given the characteristics of this stimulated release (calcium dependency, sensitivity of the system to TTX), together with its neuronal localization, receptors and postsynaptic effects, it appears likely that VIP is a transmitter for a population of excitatory intrinsic interneurons in cerebral cortex driven by corticopetal excitatory input. © 1985.
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