Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Galanin”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMed1993

Galanin receptors from human pituitary tumors assayed with human galanin as ligand.

Galanin (i.v.) elevates circulating growth hormone levels in humans, and human growth hormone producing tumors show galanin-like immunoreactivity. We have therefore investigated the presence of galanin receptors in sixteen human pituitary tumors. Specific binding of [125I]monoiodo-[Tyr26]-porcine galanin was found in membranes from four clinically inactive and three growth hormone producing tumors. The affinity of human, rat and porcine galanin to these receptor sites was identical (Kd = 0.9 nM). The rank order of potency of galanin receptor ligands was the same in the human pituitary tissue as in the rat and porcine pituitary, hypothalamus, pancreas and hippocampus. GTP (1 mM) or GMPP(NH)P (0.5 mM) lowered the apparent specific binding of [125I]galanin (0.2 nM), suggesting that the human pituitary galanin receptor is coupled via a G-protein similarly to galanin receptors in mouse, rat and pig. The possible significance of galanin receptors in pituitary tumors is discussed.

Adult↗
PubMed2002

Galanin and galanin receptor expression in neuroblastic tumours: correlation with their differentiation status.

Neuroblastoma and its benign differentiated counterpart, ganglioneuroma, are paediatric neuroblastic tumours arising in the sympathetic nervous system. Their broad spectrum of clinical virulence is mainly related to heterogeneous biologic background and tumour differentiation. Neuroblastic tumours synthesize various neuropeptides acting as neuromodulators. Previous studies suggested that galanin plays a role in sympathetic tissue where it could be involved in differentiation and development. We investigated the expression and distribution of galanin and its three known receptors (Gal-R1, Gal-R2, Gal-R3) in 19 samples of neuroblastic tumours tissue by immunohistochemistry, in situ hybridization and fluorescent-ligand binding. This study provides clear evidence for galanin and galanin receptor expression in human neuroblastic tumours. The messengers coding for galanin, Gal-R1 and -R3 were highly expressed in neuroblastoma and their amount dramatically decreased in ganglioneuroma. In contrast, Gal-R2 levels remained unchanged. Double labelling studies showed that galanin was mainly co-expressed with its receptors whatever the differentiation stage. In neuroblastic tumours, galanin might promote cell-survival or counteract neuronal differentiation through the different signalling pathways mediated by galanin receptors. Finally, our results suggest that galanin influences neuroblastoma growth and development as an autocrine/paracrine modulator. These findings suggest potential critical implications for galanin in neuroblastic tumours development.

Cell Differentiation↗
PubMed1995

Intracerebroventricular galanin and N-terminal galanin fragment enhance the morphine-induced analgesia in the rat.

Behavioral effect of galanin and its fragments, galanin1-15 and galanin16-29 (200 ng, 1 and 5 micrograms), after intracerebroventricular (i.c.v.) administration was studied in rats. The number of crossings and pippings and the time of locomotion (an open field test) showed a similar sedative action of galanin and galanin16-29, with no significant effect of galanin1-15. Galanin and its fragments, injected in doses of 200 ng, 1 and 5 micrograms, did not affect nociception, as measured by a tail-flick and paw pressure test. Galanin and galanin1-15, but not galanin16-29 (5 micrograms i.c.v.), injected together with morphine (2.5 micrograms i.c.v.), significantly potentiated the analgetic effect of morphine assessed by a paw pressure test; a similar tendency was also observed in a tail-flick test. Galanin and its two fragments injected in doses of 200 ng, 1 and 5 micrograms, did not change the effect of morphine given in a dose of 1 microgram. These data suggest that galanin, having no effect when given alone, potentiate the analgetic effect of morphine. The fact that the N-terminal fragment of galanin acts like a natural peptide suggests a receptor mediated action. In conclusion, the analgesic effect of morphine was potentiated by galanin and its N-terminal fragment galanin1-15. On the other hand, behavioral study showed a similar sedative action of galanin and C-terminal fragment galanin16-29. This suggests that the N- and C-terminal fragments of galanin are differentially involved in behavioral effects of the peptide.

Analgesics, Opioid↗
PubMed1995

Vasoconstrictor effects of galanin and distribution of galanin containing fibres in three species of elasmobranch fish.

Galanin is found in perivascular sympathetic neurons in a wide range of vertebrate species. In placental mammals, galanin has either no effect on blood pressure, or weak depressor effects, but in other vertebrates it has been shown to be a potent pressor agent. To investigate how extensive the vasoconstrictor effects of galanin may be in the vertebrates, the vascular effects of galanin were tested in two species of shark, Heterodontus portusjacksoni, and Hemiscyllium ocellatum, and a ray, Rhinobatos typus. Nerve fibres showing immunoreactivity to galanin were located surrounding gut blood vessels, but were absent from branchial efferent arteries in all three species. Intravenous injection of galanin caused a significant rise in caudal arterial blood pressure in H. portusjacksoni and H. ocellatum, but no change in R. typus. Contraction of segments of pancreatico-mesenteric artery were measured in an organ bath also. Galanin (10(-6) M) caused 21-38% of the maximum K+ induced contraction in all species, but no response in efferent branchial arteries from R. typus. In conclusion, in three elasmobranchs, a galanin-like peptide is present in perivascular nerve fibres, and galanin causes differential vasoconstriction in vascular beds. These data extend the number of vertebrate groups in which galanin has been shown to be a vasoconstrictor peptide.

Animals↗
PubMed1998

Developmental changes in galanin receptors in the quail oviduct and the effect of ovarian sex steroids on galanin receptor induction.

We have recently isolated an oviposition-inducing peptide from mature quail oviducts identified as avian galanin. This peptide evoked vigorous contractions of the uterine oviduct through binding to receptors located in the uterus. The questions arising from these findings are: what changes occur in galanin receptors in the uterus during maturation, and what is the hormonal factor(s) that induces uterine galanin receptors? Therefore, the present study examined changes in uterine galanin receptors with age and the effect of administration of ovarian sex steroids on galanin receptors in the quail. Immature females reared under long day (LD) photoperiods from 4 weeks of age demonstrated a progressive increase in specific galanin binding per both unit uterine weight and per whole uterus concurrent with uterine development during 4-13 weeks. Scatchard plot analyses of the binding to the uterine preparation showed that the equilibrium dissociation constant (Kd) was about 0.30-0.34 nM regardless of age, and the change in galanin binding during uterine development was due to a change in the number of binding sites. Plasma 17beta-estradiol and progesterone concentrations were almost constant between 4-6 weeks and tended to increase thereafter. Administration of 17beta-estradiol to immature females for 1 week increased not only uterine weight but also specific galanin binding per unit uterine weight, whereas progesterone increased only the binding per unit uterine weight. Both sex steroids also induced an increase in total binding per uterus. Combined administration of 17beta-estradiol and progesterone induced marked increases in the galanin binding, and the effect was not additive but, rather, was synergistic. Scatchard plot analysis showed that the number of binding sites, but not the Kd, was increased by steroid treatment. Administration of 17beta-estradiol or progesterone increased each circulating steroid level to that relatively similar to the maximal levels observed in females exposed to LD. Thus, ovarian sex steroids may contribute at least in part as hormonal factors to galanin receptor induction, which takes place in the uterine oviduct during development.

Age Factors↗
PubMed2004

Galanin and galanin receptors in epilepsy.

The shift in the balance between the inhibition and the excitation in favor of the latter is a major mechanism of the evolvement of epileptic seizures. On the neurotransmitter level two major players contribute to such misbalance: an inhibitory transmitter gamma-aminobutyric acid, and an excitatory amino acid glutamate. Neuropeptides are powerful modulators of classical neurotransmitters, and thus represent an intriguing tool for restoring the balance between the inhibition and the excitation, through either blocking or activating peptide receptors depending on whether a peptide is pro- or anticonvulsant. Galanin, a 29-amino acid residues neuropeptide which inhibits glutamate release in the hippocampus, is a likely member of the anticonvulsant peptide family. During the past decade growing evidence has been suggesting that galanin is in fact a powerful inhibitor of seizure activity. This review summarizes the state of research of galanin in epilepsy, beginning with the first simple experiments which showed that central injection of galanin agonists inhibited seizures, and that seizures themselves affected galanin signaling in the hippocampus; exploring the impact of active manipulation with the expression of galanin and galanin receptors on seizures, using transgenic animals, antisense and peptide-expressing vector approaches; and concluding with the recent advances in pharmacology, which led to the synthesis of non-peptide galanin receptor agonists with anticonvulsant properties. We also address recently established functions of galanin in seizure-associated neuronal degeneration and neuronal plasticity.

Animals↗
PubMed1998

NMR study of the conformation and localization of porcine galanin in SDS micelles. Comparison with an inactive analog and a galanin receptor antagonist.

Galanin is a 29/30-residue neuro-endocrine peptide which performs its many important physiological functions via a membrane-bound receptor. By using two-dimensional proton NMR spectroscopy, complete relaxation matrix analysis, and simulated annealing, the conformation of porcine galanin was determined in a membrane-mimicking solvent containing sodium dodecyl sulfate (SDS) micelles. The final family of calculated structures displays three well-defined beta- or gamma-turn regions, comprising residues 1-5, 7-10, and 24-27, but has otherwise a random conformation. The receptor-interacting N-terminal part, residues 1-5, was found to be best defined with a backbone RMSD value of 0.12 A. The mode of association between galanin and the SDS micelle was determined by observing the broadening effect on proton resonances, when spin-labeled 5- and 12-doxyl stearate molecules were added. It was concluded that galanin is located close to the surface of the micelle with two regions, residues 6-9 and 24-29, as well as two single residues, 18 and 21, reaching out into the aqueous solvent. Additional NMR studies were carried out on an inactive analogue, Ala2-galanin, and an antagonist M40. The results show that the proton resonances of galanin and M40 have identical chemical shifts in the N-terminal receptor-interacting region, indicating similar solution structures in this region. For Ala2-galanin, the same region displays a spectral heterogeneity with chemical shifts clearly different from the other two peptides, indicative of different secondary structures. These results may provide a structural background for the antagonist activity of M40 and the hormonal inactivity of Ala2-galanin, as compared to galanin.

Alanine↗
PubMed2003

Differential galanin receptor-1 and galanin expression by 5-HT neurons in dorsal raphé nucleus of rat and mouse: evidence for species-dependent modulation of serotonin transmission.

Galanin and galanin receptors are widely expressed by neurons in rat brain that either synthesize/release and/or are responsive to, classical transmitters such as gamma-aminobutyric acid, acetylcholine, noradrenaline, histamine, dopamine and serotonin (5-hydroxytryptamine, 5-HT). The dorsal raphé nucleus (DRN) contains approximately 50% of the 5-HT neurons in the rat brain and a high percentage of these cells coexpress galanin and are responsive to exogenous galanin in vitro. However, the precise identity of the galanin receptor(s) present on these 5-HT neurons has not been previously established. Thus, the current study used a polyclonal antibody for the galanin receptor-1 (GalR1) to examine the possible expression of this receptor within the DRN of the rat and for comparative purposes also in the mouse. In the rat, intense GalR1-immunoreactivity (IR) was detected in a substantial population of 5-HT-immunoreactive neurons in the DRN, with prominent receptor immunostaining associated with soma and proximal dendrites. GalR1-IR was also observed in many cells within the adjacent median raphé nucleus. In mouse DRN, neurons exhibited similar levels and distribution of 5-HT-IR to that in the rat, but GalR1-IR was undetectable. Consistent with this, galanin and GalR1 mRNA were also undetectable in mouse DRN by in situ hybridization histochemistry, despite the detection of GalR1 mRNA (and GalR1-IR) in adjacent cells in the periaqueductal grey and other midbrain areas. 5-HT neuron activity in the DRN is primarily regulated via 5-HT1A autoreceptors, via inhibition of adenylate cyclase and activation of inward-rectifying K+ channels. Notably, the GalR1 receptor subtype signals via identical mechanisms and our findings establish that galanin modulates 5-HT neuron activity in the DRN of the rat via GalR1 (auto)receptors. However, these studies also identify important species differences in the relationship between midbrain galanin and 5-HT systems, which should prompt further investigations in relation to comparative human neurochemistry and which have implications for studies of animal models of relevant neurological conditions such as stress, anxiety and depression.

Animals↗
PubMed2003

Differential patterns of Fos induction in the hypothalamus of the rat following central injections of galanin-like peptide and galanin.

Galanin and its newly discovered relative galanin-like peptide (GALP) are neuropeptides that are implicated in the neuroendocrine regulation of body weight and reproduction. GALP has been shown to bind in vitro to galanin receptor subtypes 1 and 2, but whether it has its own specific receptor(s) is unknown. We reasoned that if GALP acts through a receptor that is distinct from galanin receptors, then GALP should activate central pathways that are different from those activated by galanin. The purpose of this study was to determine whether galanin and GALP produce different patterns of neuronal activation within the hypothalamus. Quantitative analysis of Fos immunoreactivity showed that galanin induced a significantly greater number of Fos-positive nuclei in the paraventricular nucleus compared with GALP (P < 0.001); however, compared with galanin, GALP induced significantly more Fos-positive cells in the horizontal limb of the diagonal band of Broca, caudal preoptic area, arcuate nucleus, and median eminence (P < 0.05). These observations suggest that GALP and galanin act through different receptor-mediated pathways to exert their effects on the regulation of body weight and reproduction and identify target cells for GALP's specific actions in the hypothalamus, including the preoptic area, paraventricular and arcuate nuclei, and the median eminence.

Animals↗
PubMed1985

Distribution of galanin immunoreactivity in the central nervous system and the responses of galanin-containing neuronal pathways to injury.

Radioimmunoassay and immunocytochemistry were used to study the distribution of galanin, a novel 29 amino acid porcine intestinal peptide, in the central nervous system of the rat and pig. The pattern of distribution was similar in the two species, with the highest concentrations of galanin-like immunoreactivity found in the neurohypophysis, hypothalamus and sacral spinal cord. Immunocytochemical studies of these regions localized galanin-like immunoreactivity to cell bodies in the paraventricular and supraoptic nuclei of the hypothalamus, to fibres in the pars nervosa and to numerous cell bodies and fibres in the dorsal horn of the spinal cord. On both gel and high pressure liquid chromatography, galanin-like immunoreactivity in rat and pig nervous tissue eluted as a single peak in a position similar to purified procine intestinal galanin standard. Surgical and pharmacological manipulations in the rat suggest the presence of galanin in afferent fibres. An increase of galanin-like immunoreactivity was observed in the sacral spinal cord of the rat following thoracic spinal cord transection. Thus galanin-like immunoreactivity in the brain is mainly localized in the hypothalamopituitary region. The decrease of galanin-like immunoreactivity in the dorsal horn of the spinal cord, following dorsal rhizotomy and pre-treatment of rats with capsaicin, indicates that many of the fibres, which are of small diameter, may well be derived from spinal sensory neurones.

Animals↗
PubMed2004

Selective reduction in ventral hippocampal acetylcholine release in awake galanin-treated rats and galanin-overexpressing transgenic mice.

The neuropeptide galanin is an inhibitory modulator of hippocampal acetylcholine (ACh) release and cognitive functions. Anatomical evidence demonstrated some differences between the dorsal and ventral hippocampi notably in the expression of galanin receptor subtypes, and the neuronal population on which galanin-like immunoreactivity is expressed. This is suggestive of a differential role for this peptide in these two areas of the hippocampal formation. Using in vivo microdialysis, we investigated the role of galanin on ACh release in the dorsal and ventral hippocampi. Two models were studied: galanin-administered rats and transgenic mice over-expressing galanin (GAL-tg). In rats, galanin (2.0 and 10.0 microM) infused locally through the dialysis probe induced a significant decrease in ACh release in the ventral hippocampus, confirming previous findings, while no effect was seen in the dorsal hippocampus. Using the no net flux method, a significant reduction in ACh levels was noted only in the ventral hippocampus of GAL-tg compared to wild-type littermates. These results suggest that excess endogenous galanin can suppress basal ACh release, with anatomical specificity, to the ventral hippocampus. These results are of interest in the context of galanin receptor subtypes in the dorsal and ventral hippocampus, and the differential alterations of hippocampal subregions in neurological diseases such as Alzheimer's dementia.

Acetylcholine↗
PubMed2002

Galanin peptide levels in hippocampus and cortex of galanin-overexpressing transgenic mice evaluated for cognitive performance.

Galanin-overexpressing transgenic mice (GAL-tg) generated on a dopamine beta-hydroxylase promoter were previously shown to express high levels of galanin mRNA in the locus coeruleus, and to perform poorly on challenging cognitive tasks. The present study employed radioimmunoassay to quantitate the level of galanin peptide overexpression in two brain regions relevant to learning and memory, the hippocampus and cerebral cortex. Approximately 4-fold higher levels of galanin were detected in the hippocampus of GAL-tg as compared to WT. Approximately 10-fold higher levels of galanin were detected in the frontal cortex of GAL-tg as compared to WT. A second cohort of GAL-tg and WT again showed high levels of galanin overexpression in GAL-tg as compared to WT in both brain regions. Correlation analyses were conducted between galanin peptide concentrations and behavioral scores on four learning and memory tasks: the Morris water maze, social transmission of food preference, standard delay fear conditioning, and trace fear conditioning. While some significant correlations were detected, neither hippocampal nor cortical galanin levels in the two cohorts of GAL-tg consistently correlated with performance across these diverse cognitive tasks. Several interpretations of these findings are discussed, including the possibility that a threshold level of galanin overexpression is sufficient to impair performance on learning and memory tasks in mice.

Animals↗
PubMed1996

The effect of galanin and galanin fragments on blood pressure in the Cane toad, Bufo marinus.

Galanin has previously been shown to have a slight vasodepressor or no effect on blood pressure in placental mammals, but causes potent increases in blood pressure in several other vertebrate species. In this paper, the part of the galanin molecule responsible for the pressor activity was investigated in the Cane road, Bufo marinus by administration of fragments of galanin into anaesthetised toads and isolated arterial segments in an organ bath. In anaesthetised toads, the order of efficacy was human galanin > porcine galanin > Gal 1-16 > Gal 1-15 > Gal 3-15 > Gal 21-29 = 0. In isolated vessels, the first three peptides were equally effective. When four fragments of human galanin were tested in anaesthetised toads, the order of efficacy was human galanin > Gal 1-15 > Gal 5-20 > Gal 10-25 > Gal 15-30. The substitution of alanine for tryptophan at position 2 or for tyrosine at position 9 abolished the pressor response to the human galanin fragment 1-18 in anaesthetised toads. These results suggest that vascular activity in the toad is retained within the N-terminus and that positions 2 (tryptophan) and 9 (tyrosine) are key amino acids in retention of the vascular activity of galanin.

Amino Acid Sequence↗
PubMed2004

Analysis of the contribution of galanin receptors 1 and 2 to the central actions of galanin-like peptide.

Galanin-like peptide (GALP) shares partial sequence identity with galanin and exhibits agonistic activity at two of the galanin receptor subtypes (GALR1 and GALR2) in vitro. The goal of these experiments was to determine whether galanin receptors mediate the effects of central GALP administration on food intake, body weight, and luteinizing hormone (LH) secretion in the mouse. We first evaluated the effects of intracerebroventricular injections of GALP or its vehicle alone in GALR1 knockout mice, GALR2 knockout mice, and their respective wild-type controls. GALP reduced food intake and body weight after 24 h to a similar degree in wild-type, GALR1 knockout, and GALR2 knockout mice. The wild-type, GALR1 knockout, and GALR2 knockout mice also exhibited significant increases in serum levels of LH following the GALP injections. To help delineate the biologically active moiety of the GALP molecule, we injected wild-type mice with shorter fragments of the full-length GALP peptide. Neither GALP((1-21)) (the fragment containing the galanin-homologous sequence) nor GALP((22-60)) (the C-terminal portion of the GALP molecule lacking sequence identity with galanin) had any discernable effect on food intake, body weight or circulating LH. These observations demonstrate that neither GALR1 nor GALR2 are essential for mediating the effects of GALP on feeding, body weight or LH secretion. Furthermore, the galanin-homologous region of the GALP molecule is not sufficient to mimic the effects of full-length GALP. Together, these findings argue against the hypothesis that GALP signals solely through galanin receptors in vivoand suggest the existence of a yet-to-be-identified GALP-specific receptor.

Analysis of Variance↗
PubMed1992

Galanin and galanin antagonists: molecular and biochemical perspectives.

The neuropeptide galanin potently inhibits insulin release, hippocampal acetylcholine release and firing of locus coeruleus cells, and stimulates feeding and release of growth hormone. Galanin regulates K+ channels, adenylyl cyclase and phospholipase C by acting at Gi/Go protein-coupled high-affinity receptors. Galanin receptor agonists such as the N-terminal fragment galanin1-16 act synergistically with morphine in the somatosensory system and have potential analgetic application. Galanin antagonists may be useful therapeutic agents in endocrinology, neurology and psychiatry. The enhancing effect of such agents on hippocampal cholinergic function would be useful in treatment of Alzheimer's disease. Recent synthesis of a series of high-affinity galanin antagonists, reviewed, along with galanin's actions, by Tamas Bartfai and colleagues, opens the possibility of examining the functions of endogenous galanin and test the pharmacological usefulness of antagonism of galanin function in the endocrine, somatosensory and central nervous systems.

Acetylcholine↗
PubMed1990

Galanin receptors in the post-mortem human brain. Regional distribution of 125I-galanin binding sites using the method of in vitro receptor autoradiography.

The distribution of putative receptors for the peptide galanin was studied in the normal post-mortem human brain by using 125I-galanin (0.5 nM) in combination with in vitro receptor autoradiography. Specific binding of 125I-galanin was found in a large number of brain areas throughout the neuraxis. Highest binding densities occurred in the basal forebrain and hypothalamus, while the basal ganglia, major parts of the thalamus and the tectum were found to be poor in binding sites. All cortical areas harboured 125I-galanin binding, and in the visual cortex a laminated pattern was present. In the hippocampus, 125I-galanin binding occurred in layer 2 of the entorhinal cortex, in the uncus and in the hippocampal-amygdala area. In the brain-stem, 125I-galanin binding was found in serotoninergic noradrenergic cell groups as well as in the reticular formation and in the parabrachial nuclei. Galanin receptors may, thus, mediate the response of galanin in numerous structures in the human brain.

Aged↗
PubMed2004

Galanin- but not galanin-like peptide-containing axon terminals innervate hypophysiotropic TRH-synthesizing neurons in the hypothalamic paraventricular nucleus.

Galanin and galanin-like peptide (GALP) are both orexigenic peptides involved in the regulation of food intake and energy metabolism. To determine whether these peptides may directly influence the hypophysiotropic thyrotropin-releasing hormone (TRH)-synthesizing neurons, double-labeling immunocytochemistry was performed at light and electron microscopic levels using antisera against proTRH, galanin and GALP. Galanin-IR axons densely innervated all of the major parvocellular subdivisions of the PVN where proTRH neurons were identified. The periventricular and anterior parvocellular subdivisions exhibited a prominent network of galaninergic nerve fibers, while the density of fibers was less intense in the medial parvocellular subdivision. Galanin-immunoreactive (IR) axon varicosities were juxtaposed to the majority of TRH-synthesizing neurons in the anterior, medial and periventricular subdivisions of the PVN. Ultrastucturally, galanin-IR nerve terminals established symmetric type synapses with the perikarya of proTRH-IR neurons, suggesting an inhibitory nature of these contacts. In contrast, GALP immunoreactive fibers and nerve terminals concentrated primarily in the anterior parvocellular subdivision of the PVN and were found in association with only few proTRH-IR neurons in the periventricular and medial parvocellular subdivisions. In conclusion, the dense innervation of TRH neurons in all subdivisions of the PVN by galanin-IR axons indicates that galanin may be involved in the central regulation of the hypothalamic-pituitary-thyroid axis. In contrast, the relative paucity of GALP-containing axons in juxtapsoition to TRH neurons in the medial and periventricular parvocellular subdivisions of the PVN, the origin of hypophysiotropic TRH neurons, makes it unlikely that GALP similarly exerts direct regulatory effects on hypophysiotropic TRH neurons.

Animals↗
PubMed1996

Galanin receptor antagonist M40 blocks galanin-induced choice accuracy deficits on a delayed-nonmatching-to-position task.

Galanin is a 29-amino acid neuropeptide that coexists with acetylcholine in the medial septum/diagonal band in the rat and impairs choice accuracy on an operant delayed-nonmatching-to-position (DNMTP) working-memory task. M40, a peptidergic galanin antagonist, has previously been shown to block several physiological actions of galanin. The present experiments tested the ability of M40 to block the effects of galanin on DNMTP performance. M40 completely blocked choice-accuracy deficits induced by galanin administration in both the lateral ventricle and ventral hippocampus, at doses of M40 approximately 5-fold the molar dose of galanin. M40 appears to be an effective galanin antagonist in a rodent memory paradigm, indicating that this compound may prove useful in investigating the role of endogenous galanin in learning and memory.

Animals↗