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  • In summary this study demonstrated the cDNA cloning and char

    2021-11-29

    In summary, this study demonstrated the cDNA cloning and characterization of the galanin type II receptor (GalR2) and a novel GalR2-like receptor (GalR2-L) in chickens, in which these two receptors are possibly originated from a gene STF-62247 event that occurred in the early vertebrate lineage. Results from the present study showed that both cGalR2 and cGalR2-L are widely expressed in the adult chicken tissues, and are potentially coupled to the Gs and Gq protein signaling pathways. Moreover, the functional assays also revealed that the previously identified cGalR1 and cGalR1-L are coupled to the Gi/o proteins solely, whilst the chicken galanin (cGal 1–29) is much more potent than human galanin-like peptide (hGALP 1–60) in activating all the four identified chicken galanin receptors.
    Introduction Since its discovery (Tatemoto et al., 1983), a variety of biological effects of neuropeptide galanin have been described. In the central nervous system galanin regulates learning and memory, nociception, mood, feeding behavior, as well as associated pathologies (for reviews see Hokfelt et al., 1998a, Hokfelt et al., 1998b). In 1992 the first brief report (Mazarati et al., 1992) indicated that galanin inhibited seizures in kindling model of epilepsy. Soon after that Zini et al. (1993b) showed that bath application of galanin receptor (GalR) agonists inhibited depolarization-induced glutamate release from rat hippocampal slices, thus suggesting, that galanin presynaptically inhibited excitatory glutamatergic neurotransmission. Since then growing evidence coming from various research groups and employing different methodologies have been confirming that galanin is indeed a powerful endogenous anticonvulsant factor.
    Physiological properties and neuroanatomical localization of galanin suggest its anticonvulsant effects Hippocampus is a key structure in the initiation and progression of seizures. Dentate gyrus is particularly important, as it represents a major gateway in the propagation of seizure activity (Heinemann et al., 1992). Dentate gyrus receives abundant galaninergic innervation from two major sources: catecholaminergic input from locus coeruleus (Hokfelt et al., 1998a, Hokfelt et al., 1998b, Xu et al., 1998), and cholinergic projection from septum/diagonal band complex (Consolo et al., 1994, Lamour et al., 1988, Melander et al., 1986, Fig. 1(a)). The highest density of galanin-immunoreactive fibers is found in the dentate granule cell layer (Fig. 1(b)). Dentate granule cells, in turn, receive excitatory glutamatergic input from entorhinal cortex (Heinemann et al., 2000, Fig. 1(b)). Seizures can be easily evoked in both rats and mice by brief electrical stimulation of entorhinal cortex-dentate gyrus projection, perforant path (Mazarati et al., 2000, Pereira de Vasconcelos et al., 1999). Neuroanatomical localization of galanin and its inhibitory effects on glutamatergic transmission suggest that the shift in the balance between glutamatergic excitation and galaninergic inhibition in the dentate gyrus in favor of the former may contribute to the progression of seizures. Conversely, inhibition of seizures originating from the hippocampus may be achieved through the activation of GalR. GalR belong to G-protein coupled receptor superfamily. Activation of GalR triggers multiple intracellular cascades which ultimately affect neuronal excitability. Thus, activation of GalR inhibits cAMP; opens STF-62247 ATP-sensitive K+ channels and inwardly rectifying K+ channels, particularly, GIRK1; inhibits L-type and N-type Ca++ channels; stimulates inositol phospholipids turnover; stimulates or inhibits Ca++ mobilization; stimulates phospholipase A; activates MAP kinase (for review see Branchek et al., 1998, Branchek et al., 2000). Galanin has been long known as a universal neurotransmitter-inhibiting peptide, as it inhibited the release of acetylcholine, dopamine, norepinephrine, glutamate, serotonin (Ibid.). Thus, intracellular events coupled to GalR may be both pro- and anticonvulsant. The first plausible scenario explaining why and how galanin might inhibit seizures was proposed by Zini et al., 1993a, Zini et al., 1993b, who showed that galanin inhibited depolarization-induced glutamate release from hippocampal slices, and that this effect was prevented by co-application of glybenclamide, a blocker of ATP-dependent K+ channels. These results implied that in the hippocampus galanin opens ATP-dependent K+ channels, which in turn leads to membrane hyperpolarization and ultimately to the inhibition of glutamate release from presynaptic terminals. Furthermore, galanin was shown to directly close voltage-gated Ca++ channels (Palazzi et al., 1991), which would also hyperpolarize presynaptic membrane and impede glutamate release. More recent data, however, suggested, that galanin may also inhibit excitatory neurotransmission postsynaptically (see below).