Medial septal galanin and acetylcholine: influence on hippocampal acetylcholine and spatial learning

Elvander, E.; Ögren, Sven Ove

doi:10.1016/j.npep.2004.12.018

Cited by 13 publications

(9 citation statements)

References 22 publications

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“…GAL also increased the excitability of these cells under current-clamp conditions [97]. These results complement in vivo studies showing that chronic infusion of 1 -3 nanomolar GAL into the rat medial septum/diagonal band region resulted in increased ACh release in the ventral hippocampus and improved spatial memory performance on the water maze [98]. This finding from awake, freely moving animals stands in contrast to the inhibitory effects of GAL on ACh release described in rat hippocampal slices (see above) and suggests that a putative neuroprotective role for GAL may involve the survival and/or regulation of the tone of CBF neurons.…”

Section: Galanin Plasticity As a Neuroprotective Factor In Adsupporting

confidence: 77%

Galanin – 25 years with a multitalented neuropeptide

Counts

Perez

Mufson

2008

Cell. Mol. Life Sci.

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Galanin (GAL) and GAL receptors (GALRs) are overexpressed in degenerating brain regions associated with cognitive decline in Alzheimer's disease (AD). The functional consequences of GAL plasticity in AD are unclear. GAL inhibits cholinergic transmission in the hippocampus and impairs spatial memory in rodent models, suggesting GAL overexpression exacerbates cognitive impairment in AD. By contrast, gene expression profiling of individual cholinergic basal forebrain (CBF) neurons aspirated from AD tissue revealed that GAL hyperinnervation positively regulates mRNAs that promote CBF neuronal function and survival. GAL also exerts neuroprotective effects in rodent models of neurotoxicity. These data support the growing concept that GAL overexpression preserves CBF neuron function which in turn may slow the onset of AD symptoms. Further elucidation of GAL activity in selectively vulnerable brain regions will help gauge the therapeutic potential of GALR ligands for the treatment of AD.

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Section: Galanin Plasticity As a Neuroprotective Factor In Adsupporting

confidence: 77%

Galanin – 25 years with a multitalented neuropeptide

Counts

Perez

Mufson

2008

Cell. Mol. Life Sci.

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“…In addition, it has been shown that antagonism of hippocampal nicotinic receptors and ablation of prefrontal cortical noradrenergic afferents inhibits morphine CPP (Rezayof et al, 2006; Ventura et al, 2005). Since galanin can modulate both acetylcholine and noradrenergic release in the hippocampus, it is possible that galanin differentially modulates the effects of drugs of abuse dependent on function of these neurotransmitters (Kehr et al 2001; Elvander and Ogren 2005). …”

Section: Discussionmentioning

confidence: 99%

Mice lacking the galanin gene show decreased sensitivity to nicotine conditioned place preference

Neugebauer

Henehan

Hales

et al. 2011

Pharmacology Biochemistry and Behavior

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Previous work has indicated that the neuropeptide galanin decreases sensitivity to the rewarding effects of morphine and cocaine, but increases alcohol drinking. The aim of the current study was to examine the role of galanin signaling in nicotine reward by testing the effects of nicotine in mice lacking galanin peptide (Gal −/−) as compared to wild-type (Gal +/+) controls. Using an unbiased, three-chamber conditioned place preference (CPP) paradigm the dose-response function for nicotine CPP was tested in Gal −/− and Gal +/+ mice. Since activation of extracellular signal-related kinase (ERK2) is involved in the rewarding effects of several classes of drugs of abuse, we then measured the level of ERK2 phosphorylation in the nucleus accumbens shell (NACsh) and core (NACco) of Gal −/− and Gal +/+ mice following re-exposure to the CPP chamber previously paired with nicotine as a marker of mesolimbic system activation. Finally, we examined whether acute nicotine administration affects ERK2 activity in Gal −/− and Gal +/+ mice. Gal −/− mice required a higher dose of nicotine to induce a significant CPP compared to Gal +/+ mice. Upon re-exposure to the CPP apparatus, only Gal +/+ mice showed activation of ERK2 in the NACsh after training with the optimal dose for nicotine CPP, suggesting that the CPP observed following training with a higher dose of nicotine in Gal −/− mice resulted in differential recruitment of ERK signaling in the NACsh. In addition, no activation of ERK2 was observed following acute nicotine administration in either genotype. These data, along with prior results, suggest that galanin alters sensitivity to drugs of abuse differentially, with morphine, cocaine and amphetamine place preference suppressed, and nicotine and alcohol preference increased, by galanin signaling.

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“…Differences among primates have been reported for the localization of galanin relative to cholinergic neurons in the basal forebrain (Kordower and Mufson,1990; Benzing et al,1993). Galanin is an inhibitory modulator of acetylcholine in rats (Laplante et al,2004; Elvander and Ögren,2005) and galanin‐ir fibers are hypertrophied in Alzheimer's disease, with increased expression of galanin receptors within the nucleus basalis corresponding to late‐stage Alzheimer's disease (Mufson et al,2000). Galanin hyperfunction is associated with the cholinergic hypofunction and likely contributes to the associated learning and memory deficits characteristic of Alzheimer's patients (Chan‐Palay,1988).…”

Section: Discussionmentioning

confidence: 99%

Cholinergic innervation of the frontal cortex: Differences among humans, chimpanzees, and macaque monkeys

Raghanti

Stimpson

Marcinkiewicz

et al. 2007

J of Comparative Neurology

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Cholinergic innervation of the frontal cortex is important in higher cognitive functions and may have been altered in humans relative to other species to support human-specific intellectual capacities. To evaluate this hypothesis we conducted quantitative comparative analyses of choline acetyltransferase-immunoreactive axons in cortical areas 9, 32, and 4 among humans, chimpanzees, and macaque monkeys. Area 9 of the dorsolateral prefrontal cortex is involved in inductive reasoning and specific components of working memory processes, while area 32 of the medial prefrontal cortex has been implicated in theory of mind. Area 4 (primary motor cortex) was also evaluated because it is not directly associated with higher cognitive functions. The findings revealed no quantitative species differences in the three cortical areas examined, indicating that human cognitive specializations are not related to a quantitative increase in cortical cholinergic input. However, species-specific morphological specializations were observed. Clusters of cholinergic fibers that may be indicative of cortical plasticity events were present in chimpanzees and humans, but not in macaques. The other significant morphology noted was the common and distinctive oval or ovoid perisomatic staining in macaque cortices. This feature was also sporadically observed in chimpanzee cortex. Our findings suggest a potential alteration of cortical cholinergic afferents within the prefrontal cortex of humans and chimpanzees, to the exclusion of macaque monkeys.

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Medial septal galanin and acetylcholine: influence on hippocampal acetylcholine and spatial learning

Cited by 13 publications

References 22 publications

Galanin – 25 years with a multitalented neuropeptide

Galanin – 25 years with a multitalented neuropeptide

Mice lacking the galanin gene show decreased sensitivity to nicotine conditioned place preference

Cholinergic innervation of the frontal cortex: Differences among humans, chimpanzees, and macaque monkeys

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