Anxiogenic-Like Action of Galanin after Intra-Amygdala Administration in the Rat

Möller, Christian

doi:10.1016/s0893-133x(98)00102-x

Cited by 104 publications

(54 citation statements)

References 25 publications

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“…In vivo microdialysis studies on rats have suggested that galanin plays an important role in modulation of 5-HT (17) and NA (18) neurotransmission, supporting a possible role of galanin in mood control, anxiety, and stress responses, as proposed earlier (19)(20)(21)(22)(23)(24)(25)(26)(27).…”

Section: And 16)supporting

confidence: 57%

Enhanced hippocampal noradrenaline and serotonin release in galanin-overexpressing mice after repeated forced swimming test

Yoshitake

Wang

Kuteeva

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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Basal and forced swimming (FS) stress-induced release of noradrenaline (NA) and serotonin (5-HT) were determined by in vivo microdialysis in the ventral hippocampus of mice overexpressing galanin under the platelet-derived growth factor B promoter (GalOE͞P) or under the dopamine ␤-hydroxylase promoter (GalOE͞D) (only NA). WT mice served as controls. Intraventricular infusion of galanin significantly reduced basal extracellular NA in WT mice and in GalOE͞P mice (albeit less so). Microdialysis sampling during a 10-min FS showed that NA and 5-HT release were elevated to 213% and 156%, respectively, in the GalOE͞P group, whereas in the WT group the increases were only 127% and 119%, respectively. The second (repeated) 10-min FS (RFS) caused a marked enhancement of NA and 5-HT release in the GalOE͞P mice to 344% and 275%, respectively. However, the RFS caused only a 192% increase of extracellular NA levels in the GalOE͞D mice. Pretreatment with the putative peptidergic galanin receptor antagonist M35 almost completely blocked the elevation of NA and 5-HT levels in the GalOE͞P after RFS. These results suggest that the NA and 5-HT hippocampal afferents in GalOE͞P mice are hypersensitive to both conditioned and unconditioned stressful stimuli, such as FS, and that this effect is mediated by galanin receptors. The present findings support a role of galanin in the regulation of release of NA and 5-HT, two neurotransmitters involved in mood control.microdialysis ͉ 5-hydroxytryptamine ͉ transgenic mice ͉ hippocampus ͉ affective disorders G alanin, a 29-aa (30 in human) neuropeptide (1), is widely distributed throughout the central nervous system (2, 3), where it coexists with several classic neurotransmitters (4). A similarly widespread distribution of galanin-like immunoreactivity (LI) in neurons and fibers was observed in the brain of the mouse (5). Three galanin receptor subtypes (GalR1-GalR3) have been cloned (see refs. 6 and 7), all belonging to the 7-transmembrane, G protein-coupled receptor superfamily. Both the noradrenaline (NA) neurons of locus coeruleus (LC) and the 5-hydroxytryptamine (5-HT) neurons of the dorsal raphe nucleus (DRN) (8) can synthesize galanin (4, 9-11). In the rat brain, galanin-LI can be observed in the terminal ramifications of the NA nerve terminals in cortical͞hippocampal areas (11). However, it has been more difficult to demonstrate galanin-LI in 5-HT terminals, suggesting a higher galanin expression in the NA than in the 5-HT system.Recently, mice with a targeted disruption of the galanin gene (12), or overexpressing galanin under the dopamine ␤-hydroxylase (D␤H) promoter (GalOE͞D) (13, † †) or the plateletderived growth factor B promoter (GalOE͞P) (14, ‡ ‡), have been generated and characterized with regard to several functional parameters (see refs. 15 and 16).In vivo microdialysis studies on rats have suggested that galanin plays an important role in modulation of 5-HT (17) and NA (18) neurotransmission, supporting a possible role of galanin in mood control, anxiety, and stress response...

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Section: And 16)supporting

confidence: 57%

Enhanced hippocampal noradrenaline and serotonin release in galanin-overexpressing mice after repeated forced swimming test

Yoshitake

Wang

Kuteeva

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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“…These observations may be important in reconciling the seemingly inconsistent results generated in previous investigations of the effects of exogenous galanin on anxiety-like behaviors (Bing et al 1993;Moller et al 1999). One study showed that i.c.v.…”

Section: Discussionmentioning

confidence: 65%

“…Furthermore, systemic IL-␤ administration activates distinct subsets of neurons in the BSTL and CeA, suggesting that there may be neurochemically distinct subpopulations of cells in the BSTL and CeA that are activated selectively by different stressful stimuli, and that may have different functional effects (Day et al 1999). Thus, depending on the context and the specific nature of the initiating stimulus, a modulatory neurotransmitter such as galanin, acting in the CeA or BSTL, could have a variety of effects on behavioral and neuroendocrine reactivity.These observations may be important in reconciling the seemingly inconsistent results generated in previous investigations of the effects of exogenous galanin on anxiety-like behaviors (Bing et al 1993;Moller et al 1999). One study showed that i.c.v.…”

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confidence: 65%

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Modulatory Effects of Galanin in the Lateral Bed Nucleus of the Stria Terminalis on Behavioral and Neuroendocrine Responses to Acute Stress

Khoshbouei

Cecchi

Morilak

2002

Neuropsychopharmacology

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The neuropeptide galanin has been identified as a possible neurotransmitter/neuromodulator within the central nervous system. In the present study, a potential role for galanin in the lateral bed nucleus of the stria terminalis (BSTL) in modulating behavioral and neuroendocrine responses to an acute stress was investigated. In the first experiment, acute immobilization stress induced anxietylike behavioral responses in ratsSince its discovery (Tatemoto et al. 1983), the peptide neurotransmitter galanin has been implicated in numerous autonomic and physiologic regulatory processes, including feeding (Crawley 1999), cardiovascular control (Shih et al. 1996), learning and memory (McDonald et al. 1998), and the response to stress (Holmes et al. 1995; Khoshbouei et al. 2000;Sweerts et al. 1999Sweerts et al. , 2000. Furthermore, it has been hypothesized that galanin may also be involved in disease states such as depression (Seutin et al. 1989), feeding disorders (Crawley et al. 1990(Crawley et al. , 1993, and Alzheimer's disease (Bartfai et al. 1992;Mufson et al. 1993Mufson et al. , 1998Mufson et al. , 2000.Limbic forebrain structures important for the expression of fear and anxiety, such as the central nucleus of the amygdala and the bed nucleus of the stria terminalis (BST), show a rich expression of galanin and galanin receptors (Bartfai et al. 1992; Gustafson et al. 1996; Melander et al. 1986a,b). Within the BST, there is extensive overlap between galanin-immunoreactive terminals and galanin receptors (Gray and Magnuson 1987b; . 1993b, 1997). The BST is a component of the "extended amygdala", which plays a critical role in the integration of autonomic and behavioral responses to stress (Davis and Shi 1999; Davis et al. 1997a; Herman and Cullinan 1997). The lateral BST (BSTL) in particular has been implicated in modulation of behavioral-affective responses (Cecchi et al. 2001; Davis and Shi 1999). Lesions of the BST blocked the enhancement of acoustic startle induced by i.c.v. infusion of CRH (Davis et al. 1997b). Similarly, blockade of glutamate receptors in BSTL antagonized the unconditioned potentiation of startle induced by exposure to bright light (reviewed by (Davis and Shi 1999)).In addition to playing a potential role in modulating the behavioral response to stress, the BSTL also exerts an extrahypothalamic modulatory influence on stressinduced hypothalamic-pituitary-adrenal (HPA) activation (Cecchi et al. 2001; Herman and Cullinan 1997; Herman et al. 1996). While some investigators have suggested that the BST has an inhibitory influence on HPA activation (Herman and Cullinan 1997), others have suggested a facilitatory role. A small cluster of CRF-immunoreactive neurons in ventrolateral BST project to mid-parvocellular PVN (Moga and Saper 1994). Lesions of BST attenuated the increase in plasma ACTH and corticosterone induced by reintroduction of rats into a context in which they had previously been exposed to foot shock (Gray et al. 1993), and specific lesioning of anterolateral BST cause a decrease ...

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“…Following the completion of the conflict procedure, shock thresholds were tested as described previously (Möller et al 1999). …”

Section: Punished Drinking Testmentioning

confidence: 99%

Local 5,7-Dihydroxytryptamine Lesions of Rat Amygdala Release of Punished Drinking, Unaffected Plus-Maze Behavior and Ethanol Consumption

Sommer

2001

Neuropsychopharmacology

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Accumulating data indicate that serotonin uptake inhibitors are clinically effective for most if not all anxiety disorders (Perse et al. 1987;Den Boer and Westenberg 1988;Katzelnick et al. 1995;Rocca et al. 1997;Ballenger et al. 1998). While this provides renewed evidence for an involvement of 5-HT transmission in mechanisms of fear and anxiety, the role of serotonergic transmission in this context is not well understood. Experimental findings in animal studies aimed at elucidating serotonergic mechanisms in fear and anxiety have been inconsistent, possibly due to the diversity of central 5-HT systems.Thus, a 'classical hypothesis' states that increased 5-HT transmission is anxiogenic and reduction is anxiolytic. This is supported by data from animal models based on fear-induced response inhibition, such as conflict tests, for example. However, in animal models which rely on suppression of exploratory behavior by an innate fear stimulus, such as the elevated plus-maze,

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Anxiogenic-Like Action of Galanin after Intra-Amygdala Administration in the Rat

Cited by 104 publications

References 25 publications

Enhanced hippocampal noradrenaline and serotonin release in galanin-overexpressing mice after repeated forced swimming test

Enhanced hippocampal noradrenaline and serotonin release in galanin-overexpressing mice after repeated forced swimming test

Modulatory Effects of Galanin in the Lateral Bed Nucleus of the Stria Terminalis on Behavioral and Neuroendocrine Responses to Acute Stress

Local 5,7-Dihydroxytryptamine Lesions of Rat Amygdala Release of Punished Drinking, Unaffected Plus-Maze Behavior and Ethanol Consumption

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