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Galanin: A Potentially Significant Neuroendocrine Modulator
Published in Craig A. Johnston, Charles D. Barnes, Brain-Gut Peptides and Reproductive Function, 2020
J.I. Koenig, S.M. Gabriel, L.M. Kaplan
Throughout the CNS, galanin has been found to coexist with numerous other peptides and monoamine neurotransmitters. One of the most striking examples of colocalization occurs in the locus coeruleus between galanin and dopamine β-hydroxylase or tyrosine hydroxylase (Melander et al., 1986c; Levin et al., 1987). Many of these cells are thought to project to the oxytocin-rich regions of the hypothalamic paraventricular nucleus. In addition, neurons of the dorsomedial nucleus containing both galanin and dopamine β-hydroxylase project to the parvocellular regions of the PVN (Melander et al., 1986c). Galanin also is localized in the serotonergic neurons of the brainstem raphe nuclei (Melander et al., 1986c), and with acetylcholine in the nucleus basalis (Melander et al. 1985). Interestingly, galanin appears to modulate the activity of the serotonergic neurons (Sundstrom and Melander, 1988) and selectively decreases the KD of the serotonin 1-A receptors in limbic cortex areas (Fuxe et al., 1988). The relationship between the biological actions of galanin and its coexistence in serotonergic neurons is currently unknown.
Histamine as Neurotransmitter
Published in Divya Vohora, The Third Histamine Receptor, 2008
Oliver Selbach, Helmut L. Haas
Galanin is coexpressed in histaminergic neurons of rodents [70,101,125,126] not in the human TMN [127] and in the GABAergic inputs to them [102]. Galanin inhibits TMN neuron firing [128] and has been shown to act on TMN axon autoreceptors [34]. It may thus contribute to both intrinsic feedback inhibition and extrinsic inhibition from the VLPO. Moreover, galanin exerts orexigenic, antiepileptic, sleep-propensing, and neurotrophic actions.
Applied physiology of nociception
Published in Pamela E Macintyre, Suellen M Walker, David J Rowbotham, Clinical Pain Management, 2008
Galanin is a neuropeptide widely distributed in the nervous system and occurs in a small population of primary sensory neurons and also in spinal interneurons.67 Overwhelming evidence supporting an antinociceptive role for galanin has been obtained from electrophysiological studies in which galanin hyperpolarizes the majority of dorsal horn neurons. Under normal conditions, galanin is released upon C-fiber stimulation and plays an inhibitory role in mediating spinal cord excitability. Studies on the interaction between galanin and morphine support an antinociceptive role for galanin: it is suggested that the spinal effect of morphine is mediated in part by the inhibitory action of galanin.68
Ketogenic diet: overview, types, and possible anti-seizure mechanisms
Published in Nutritional Neuroscience, 2021
Mohammad Barzegar, Mohammadreza Afghan, Vahid Tarmahi, Meysam Behtari, Soroor Rahimi Khamaneh, Sina Raeisi
Noradrenergic neurons in the locus ceruleus contain galanin and neuropeptide Y [68]. These orexigenic neuropeptides are potent endogenous anticonvulsant neuromodulators which can inhibit excessive neuronal excitability[47,53,69]. It has been shown that glucose, insulin, and leptin have suppressive effects on galanin and neuropeptide Y; thus, their expression can be regulated by nutritional status. Galanin expression can also be upregulated by high fat intake. The KD initially mimics the starvation effects. The levels of insulin, glucose, and leptin in the circulation are reduced under this dietary therapy. Therefore, KD may upregulate the expression of neuropeptide Y and galanin by changing the levels of the molecules which maintain energy homeostasis that lead eventually to its anti-seizure effect [53].
The potential effects of anticonvulsant drugs on neuropeptides and neurotrophins in pentylenetetrazol kindled seizures in the rat
Published in International Journal of Neuroscience, 2020
Hasan Tekgul, Erdem Simsek, Mumin Alper Erdoğan, Gürkan Yiğittürk, Oytun Erbaş, Dilek Taşkıran
Galanin and neuropeptide-Y (NPY) have been reported to act as potent endogenous anticonvulsant peptides [5, 6, 11–13]. NPY, a 36-amino acid peptide, is one of the most studied neuropeptides in the epilepsy. NPY is predominantly expressed in GABAergic interneurons in the brain, including the hippocampus. NPY can act through five different receptors Y1–Y5, but mainly shows its effects by binding to Y1, Y2 and Y5 [14]. NPY induces strong, but transient suppression of spikes and seizures, while galanin is more profound in seizure suppression [15]. The neuropeptide galanin and its G protein-coupled receptors (GAL 1–3) are also widely distributed in the nervous system [7, 16]. Galanin exerts its anticonvulsant effect via presynaptic inhibition of excitatory glutamatergic transmission in the hippocampus [17]. Recently, galanin receptors are considered as an interesting target for anticonvulsive therapy.
Emerging drugs for focal epilepsy
Published in Expert Opinion on Emerging Drugs, 2018
Galanin was first identified more than 30 years ago as a neuropeptide acting primarily as a modulator of neurotransmission in the brain and the peripheral nervous system but over time it became evident that galanin and other galanin family peptides have a number of additional non-neuronal actions such as on glia, endocrine cells, energy homeostasis and paracrine effects on bones [31]. A number of studies in animal models of epilepsy have shown that galanin is implicated in epilepsy. In the self-sustaining status epilepticus (SSE) model, hippocampal areas are galanin depleted after stimulation of the perforant path dentate gyrus pathway [32] and the duration of the SSE can be markedly shortened by injection of galanin into the dentate hilus [31–33]. The anticonvulsant effect of galanin seems to be mediated by GalR1 and GalR2 receptors but the use of Galanin itself has been limited by poor metabolic stability and lack of blood-brain penetration [31]. Among different potential galanin receptor agonists, those acting on GalR1 receptors have been rapidly excluded as GalR1 receptors also inhibit the release of insulin leading to poor tolerability and many systemic effects [20,31]. GalR2 receptors seem to be localized just on the CNS and, interestingly, their stimulation seem to reduce glutamate release [34], further suggesting a promising anti-seizure activity for this class of compounds.