Previous stress increases in vivo biogenic amine response to swim stress

Jordan, Scott W.; Kramer, Gerald L.; Zukas, Paul K.; Petty, Frederick

doi:10.1007/bf00969000

Cited by 62 publications

(30 citation statements)

References 25 publications

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“…observations in rats and especially in mice that sensory stimulation or a mild stressor increases hippocampal NA and 5-HT release (35)(36)(37)(38). Moreover, our study indicates that the GalOE͞P mice, but much less so the GalOE͞D mice, respond more strongly to swim stress than the corresponding WT mice, as suggested by markedly higher levels of extracellular NA and 5-HT, especially during the second swim stress session.…”

Section: Discussionsupporting

confidence: 58%

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: Discussionsupporting

confidence: 58%

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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“…Previous studies have shown that 5-HT, 5-HIAA, and other transmitters in various brain areas change following forced swimming (Jordan et al 1994;Connor et al 1997Connor et al , 2000. However, the changes were region specific and time dependent, returning to baseline after 15-120 min, depending on the transmitter.…”

Section: Discussionmentioning

confidence: 92%

Increased extracellular serotonin level in rat hippocampus induced by chronic citalopram is augmented by subchronic lithium: neurochemical and behavioural studies in the rat

et al. 2003

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“…The first exposure to swim stress, for instance, while not causing dramatic changes in DA release, may sensitize the MFC to subsequent swim stress. 47 Cross sensitization between different types of stress has also been reported. Tail shock elicits a greater increase in DA efflux with respect to baseline values in rats which have previously been exposed to cold than in naïve rats; once again this increase is observed only in the MFC, and not in the NAc or striatum.…”

Section: Stress Dopamine and Specific Brain Areas (A Clue For Selectmentioning

confidence: 99%

The role of stress in the pathophysiology of the dopaminergic system

2000

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In this review, we will examine the most recent preclinical evidence in support of the fact that both acute and chronic stress may have a detrimental impact on the normal function of the dopaminergic system. In recent decades, the term stress has changed its meaning from that of a 'non-specific body response' to a 'monitoring system of internal and external cues'; that is a modality of reaction of the mammalian central nervous system (CNS) which is critical to the adaptation of the organism to its environment. Compelling results have demonstrated that the dopaminergic system is important not only for hedonic impact or reward learning but also, in a broader sense, for reactivity to perturbation in environmental conditions, for selective information processing, and for general emotional responses, which are essential functions in the ability (or failure) to cope with the external world. In this, stress directly influences several basic behaviors which are mediated by the dopaminergic system such as locomotor activity, sexual activity, appetite, and cross sensitization with drugs of abuse. Studies using rat lines which are genetically different in dopamine (DA) physiology, have shown that even small alterations in the birth procedure or early life stress events may contribute to the pathophysiology of psychiatric disorders-in particular those involving central DA dysfunctionand may cause depression or psychotic derangement in the offspring. Finally, the fact that the dopaminergic system after stress responds, preferentially, in the medial prefrontal cortex (MFC), is thought to serve, in humans, as a protection against positive psychotic symptoms, since the increased DA activity in the MFC suppresses limbic DA transmission. However, excessive MFC dopaminergic activity has a negative impact on the cognitive functions of primates, making them unable to select and process significant environmental stimuli. Thus it appears that a critical range of DA turnover is necessary for optimal cognitive functioning after stress, in the response of the CNS to ever-changing environmental demands. Molecular Psychiatry (2000) 5, 14-21.

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Previous stress increases in vivo biogenic amine response to swim stress

Cited by 62 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

Increased extracellular serotonin level in rat hippocampus induced by chronic citalopram is augmented by subchronic lithium: neurochemical and behavioural studies in the rat

The role of stress in the pathophysiology of the dopaminergic system

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