How VIP Induces Rems A Hypothesis

Several studies have demonstrated that injection of VIP in areas of the brain related with REMS generation induced REMS for several days (Bourgin et al. 1997). The most remarkable result is that VIP, possibly in association with cholinergic mechanisms, plays a critical role in the long-term regulation of REMS. Furthermore, the coexistence of VIP with acetylcholine (ACh) has been reported (Whittaker 1989; Magistretti 1990).

It has been suggested that the oral pontine reticular nucleus (PnO) could be a common target for the induction of REMS by VIP, and that the interaction between VIP-ACh at the PnO level is responsible for REMS induction. This hypothesis is supported by the observation that the injection the VIP into PnO in combination with atropine, a cholinergic muscarinic antagonist, prevented REMS increase (Bourgin, Ahnaou, Laporte, Hamon, and Adrien 1990). Also, it has been reported that injection of VIP into medial pontine reticular formation (mPRF) of rats induced REMS and neuronal depolarization (Kohlmeier and Reiner 1999). In addition, the microinjection of a cholinergic agonists into the mPRF also produces a state that is behaviorally indistinguishable from naturally occurring REMS (Baghdoyan, Spotts, and Snyder 1993). Together these results support that VIP plays an important role in the induction and maintenance of the REMS via its interaction with ACh. The mechanisms could be prolonged depolarization of mPRF cells during REMS period; however, more studies are necessary to elucidate this hypothesis.

On the other hand, there are other studies that suggest that the effect of VIP on REMS is independent of cholinergic mechanisms. For instance, VIP administered in combination with atropine in PCPA-treated cats insomnia induced an increase in total time REMS (Prospero-García, Jimenez-Anguiano, and Drucker-Colín 1993). Additionally, it has been observed that the administration of PRL-antiserum blocked the increase in circulating levels of PRL and prevented VIP-enhanced REMS (Obál, Payne, Kacsoh, Opp, Kapas, Grosvenor, and Krueger 1994). VIP injections stimulate PRL secretion in plasma and i.c.v. injection of VIP also increase mRNA PRL levels in the hypothalamus of the rat (Bredow et al. 1994; Abe, Engler, Molitch, Bollinguer-Gruber, and Reinchlin 1985). According to these results it is possible to suggest that the REMS-promoting activity of VIP may be mediated by endogenous PRL.

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