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Nitric oxide releases acetylcholine in the basal forebrain

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Abstract

In conscious rats, the basal forebrain was superfused through a push-pull cannula and the release of acetylcholine was determined in the superfusate. Superfusion with the nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine, diminished the release of acetylcholine. Subsequent superfusion with the NO donor, 3-morpholino-sydnonimine, enhanced the release of the neurotransmitter. It is concluded that endogenous NO enhances the release of acetylcholine from its neurons.

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    These cholinergic projections provide a substrate for cognitive processes, particularly those involved in attention, learning and memory (Ma and Luo, 2012; Craig et al., 2011). It has been shown that NO contributes to the control of the basal and modulated release of neurotransmitters and neurohormones acting in the hypothalamus (Affleck et al., 2012; Martins-Pinge et al., 2013; Prast and Philippu, 1992; Stern, 2004). Expectedly, many physiological and pathological conditions that alter the function of the hypothalamus also change the expression of NOS in particular hypothalamic areas (Gadek-Michalska et al., 2012; Heesch et al., 2009; Ueta et al., 1995a, 1995b; Whitaker and Molina, 2013).

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    One is that the neuronal release of endogenous opioid peptide is NO-dependent, as suggested by the antagonism of release of spinal cord methionine-enkephalin by NOS-inhibitor (Hara et al., 1995) and that cyclic GMP and PKG are components of this presynaptic signaling pathway that regulates opioid peptide release. The feasibility of this concept is strong as NO has been implicated as a modulator in the neuronal release of several different neurotransmitters (Lonart et al., 1992; Prast and Philippu, 1992; Tanioka et al., 2002; Kodama and Koyama, 2006) and endocrine hormones (Uretsky et al., 2003; Rubinek et al., 2005). The other possible explanation is that the signaling pathway activated by the κ opioid receptor may itself involve NO–cyclic GMP–PKG.

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