Dynorphin expression is increased during periods of dehydration

and so continues to provide a feedback inhibition even while spike frequency is increased to counter dehydration effects by increasing vasopressin release (Scott et al., 2009). Dynorphin also reduces transmitter release from presynaptic glutamate axons (Iremonger and Bains, 2009). The dual effect of direct inhibition of release from the parent cell or its similar neighbors, and presynaptic reduction in excitatory transmitter stimulation, serve a similar role allowing dynorphin to depress activity by multiple converging mechanisms. Actions of dynorphin in attenuating hippocampal mossy fiber glutamate release are discussed above. Kisspeptin is synthesized by cells of the medial hypothalamus, and the peptide modulates the activity of GnRH neurons and regulates PD0325901 reproduction and onset of puberty (Kauffman et al., 2007; Han et al., 2005). Mutations of the GPR54, the kisspeptin receptor, block puberty and cause infertility in rodents and humans (Dungan et al., 2006; Smith and Clarke, 2007). Dynorphin and neurokinin B colocalize with kisspeptin in many mammals (Goodman et al., 2007); dynorphin is proposed to act back on the releasing kisspeptin neurons to synchronize and shape

pulsatile release patterns of kisspeptin (Navarro et al., 2009; Wakabayashi et al., 2010). Although we generally VX-770 chemical structure think of neuroactive peptides as being synthesized by and exerting effects on neurons, the focus of this review, glial cells may also employ neuropeptide signaling and express receptors for neuromodulators in the CNS (Azmitia et al., 1996; Kimelberg, 1988; Tasker et al., 2012). For instance, one class of olfactory ensheathing glia that accompanies

the olfactory nerve from the olfactory mucosa into the olfactory bulb shows very high levels of NPY expression (Ubink et al., 1994; Ubink and Hökfelt, 2000); NPY may act here as a trophic factor to promote olfactory receptor neuron maturation and survival (Doyle et al., 2012). Schwann cell precursors also express NPY, and this expression Rutecarpine is lost during postnatal development (Ubink and Hökfelt, 2000). NPY may also be released by astrocytes. Ramamoorthy and Whim (2008) employed NPY-bound red fluorescent protein to show glutamate-agonist mediated NPY secretion from cortical astrocytes. Astrocytes in many brain regions express functionally active vasopressin receptors (Brinton et al., 1998; Jurzak et al., 1995; Kozniewska and Romaniuk, 2008). Peptide-responsive astrocytes can show fairly rapid activity-dependent structural plasticity which may allow a further dimension of modulation of neuropeptide actions and diffusion (Miyata et al., 2001; Theodosis et al., 2008), including potential selective restriction of peptide diffusion from a release site.