Vasoactive intestinal polypeptide excitation of central neurons

Phillis, John W.; Kirkpatrick, J. R.; Said, Sami I.

doi:10.1139/y78-052

Cited by 129 publications

(36 citation statements)

References 2 publications

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“…It is not clear why we observe direct depressant actions of VIP on cortical neurons more frequently than reported (7,8), despite similar conditions of iontophoresis and anesthesia. However, our results suggest that the nature of the direct response to VIP could depend upon the extent of ongoing activation of adrenoceptors by endogenous NE.…”

Section: Resultscontrasting

confidence: 62%

“…Specific binding of labeled VIP in cortex (6) and excitation of some cortical neurons by iontophoretically applied VIP (7,8) suggest the presence of VIP receptors, as does its ability to stimulate cyclic AMP formation (9,10) and glycogenolysis (11) in cortical slices [at lower concentrations than for norepinephrine (NE)]. Although NE-and VIP-containing neurites in cortex show different organizational patterns (12), these axons may converge on a common target neuron, the pyramidal cell (3,13).…”

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confidence: 99%

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Vasoactive intestinal polypeptide acts synergistically with norepinephrine to depress spontaneous discharge rate in cerebral cortical neurons.

Ferron¹,

Siggins²,

Fe³

1985

Proc. Natl. Acad. Sci. U.S.A.

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Vasoactive intestinal polypeptide acts synergistically with norepinephrine to depress spontaneous discharge rate in cerebral cortical neurons (transmitter ABSTRACTCortical neurons are densely innervated by noradrenergic fibers and by intrinsic cortical interneurons containing vasoactive intestinal polypeptide (VIP). Biochemically, VIP and norepinephrine (NE) synergistically interact to stimulate the synthesis of cyclic AMP in cortical slices. Therefore, we sought physiological indices of this peptide-monoamine interaction by applying VIP and NE to single cortical neurons of the rat while recording their spontaneous discharge. VIP applied alone inhibited discharge of 24% and accelerated discharge in 20% of cortical neurons. NE alone had a predominantly depressant effect on the same neurons. However, when VIP was retested during the continuous application of subthreshold currents of NE, VIP exerted predominantly depressant effects. These synergistic inhibitions resulted even in cells previously showing excitations to VIP alone. If VIP alone was depressant, subthreshold NE further enhanced the VIP depression. Subthreshold amounts of phenylephrine, an a-adrenoceptor agonist, also produced comparable interactions, suggesting involvement of an a receptor, as in the biochemical studies. These results support a peptide-monoamine interaction in cortex that could have important ramifiications for neuronal integration.

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Section: Resultscontrasting

confidence: 62%

mentioning

confidence: 99%

Vasoactive intestinal polypeptide acts synergistically with norepinephrine to depress spontaneous discharge rate in cerebral cortical neurons.

Ferron¹,

Siggins²,

Fe³

1985

Proc. Natl. Acad. Sci. U.S.A.

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“…VIP has been reported to depolarize toad motoneurones (Phillis et al 1978), mammalian dorsal horn neurones (Jeftinija et al 1982), rat CA hippocampal neurones (Dodd et al 1979), and opossum oesophageal smooth muscle (Daniel, Helmy-Elkholy, Jager & Kannen, 1983). The VIP depolarization in dorsal horn neurones (Jeftinija et al 1982), hippocampal neurones (Dodd et al 1979) and retinal cells (Lasater, Watling & Dowling, 1983) was associated with a decrease in membrane resistance.…”

Section: Discussionmentioning

confidence: 99%

Vasoactive intestinal polypeptide depolarizations in cat bladder parasympathetic ganglia.

Akasu¹,

Gallagher²,

Hirai³

et al. 1986

The Journal of Physiology

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SUMMARY1. The effect ofvasoactive intestinal polypeptide (VIP) on the neuronal membranes of isolated cat vesical pelvic ganglia and its underlying ionic mechanism were examined by means of intracellular recording and voltage-clamp techniques.2. Application of VIP (0-05-50 #UM) to the neurones by pressure 'puff' ejection through a micropipette placed close to the neurones produced a depolarizing response (2-15 mV) in 83 % of neurones tested; this effect was concentration dependent.3. The VIP-induced depolarization frequently evoked spontaneous action potentials in quiescent neurones and increased the frequency of action potentials in spontaneously firing neurones.4. The VIP depolarization was not blocked in a Ca2+-free, high-Mg2+ solution or in a solution containing hexamethonium (1 mM) and atropine (1 /UM). Tetrodotoxin (TTX; 1 /iM) also did not affect the VIP depolarization.5. The VIP depolarization was associated with an increase in membrane resistance and the slope of a current-voltage relation (I-V curve) was inceased by VIP.6. Conditioning hyperpolarization and depolarization of the membrane increased and decreased the amplitude of the VIP depolarization, respectively. The VIP depolarization reversed polarity around -100 mV.7. The reversal potential shifted about 20 mV to a more positive level in a high-K+ (10 mM) solution in accord with the Nernst equation. Substituting Cl-with isethionate in the superfusate did not affect the reversal potential of the VIP depolarization.8. Closure of M-channels does not underlie VIP action since the VIP depolarization was enhanced by muscarine (10 /UM) and unchanged in the presence of Ba (5 mM), or intracellular or extracellular Cs+, conditions known to block the M-channels (Adams, Brown & Constanti, 1982 a, b). Tetraethylammonium (TEA; 20 mM) also did not affect the VIP depolarization. 9. Voltage-clamp analyses showed that VIP applied by pressure ejection produced an inward current of 80-110 pA associated with a decrease in membrane conductance (from 2-8 to 3-5 nS) at a holding potential of -60 mV.

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“…That VIP in vivo causes neuronal excitation in the brain of mammals [30] and activation of adenylate cyclase [31] has been reported, but the physiological function of VIP in the hen hypothalamus…”

Section: Binding Affinity and Capacitymentioning

confidence: 99%