Noradrenergic facilitation of shock-probe defensive burying in lateral septum of rats, and modulation by chronic treatment with desipramine

Bondi, Corina O.; Barrera, Gabriel; Lapiz, M.D.S.; Bédard, Tania; Mahan, Amy; Morilak, David A.

doi:10.1016/j.pnpbp.2006.11.015

Cited by 46 publications

(56 citation statements)

References 76 publications

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“…Notably, previous tracing studies have shown that the SP innervation of the LS derives from both extrinsic as well as intrinsic sources (Sakanaka et al, 1982;Szeidemann et al, 1995). The present study provides the first evidence that a stressful, emotionally challenging situation such as forced swimming triggers local SP release within the LS, a key area of the limbic stress circuitry important for affective regulation (Sheehan et al, 2004;Burgdorf and Panksepp, 2006;Bondi et al, 2007).…”

Section: Stressor-induced Release Of Spsupporting

confidence: 56%

Neurokinin 1 Receptor Antagonism Promotes Active Stress Coping Via Enhanced Septal 5-HT Transmission

Ebner

Singewald

Whittle

et al. 2007

Neuropsychopharmacol

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Antagonists of the substance P (SP) preferring neurokinin 1 receptor (NK1R) represent a promising novel class of drugs for the treatment of stress-related disorders such as depression and anxiety disorders; however, the involved neuronal pathways releasing SP in response to stressors are ill defined. By using in vivo microdialysis in combination with a highly sensitive and selective radioimmunoassay we found that exposure to forced swim stress increased SP release in the rat lateral septum (LS), a key area in processing emotions and stress responses. Acute administration of the selective NK1R antagonist L-822429 injected either systemically or locally into the LS reduced passive and facilitated active stress-coping strategies in the forced swim test. This effect seems to be mediated by enhanced intraseptal serotonergic transmission via serotonin (5-HT)1A receptors since NK1R blockade reversed the swim stress-induced decrease to an increase in extracellular 5-HT efflux, and furthermore the behavioral effects of L-822429 were blocked by intraseptal 5-HT1A receptor antagonism. A direct heterosynaptic regulation by NK1R on 5-HT release from serotonergic fibers was ruled out by immunocytochemistry at the light and electron microscopic level indicating involvement of GABAergic interneuron(s) in this interaction. Taken together, our data identify the LS as a critical brain area for the involvement of SP transmission in the modulation of stress responses and demonstrate that NK1R blockade can elicit a functionally significant facilitatory effect on 5-HT transmission, which does not necessarily involve the previously proposed interaction with neuronal firing at the cell body level of raphe neurons.

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Section: Stressor-induced Release Of Spsupporting

confidence: 56%

Neurokinin 1 Receptor Antagonism Promotes Active Stress Coping Via Enhanced Septal 5-HT Transmission

Ebner

Singewald

Whittle

et al. 2007

Neuropsychopharmacol

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“…Stress-induced hyperactivity of the LC neurons and increased release of NA have been proposed to contribute to development of human depression (Nestler et al, 1990; see Mongeau et al, 1997;Grant and Weiss, 2001;Morilak and Frazer, 2004). Importantly, chronic treatment with NA reuptake inhibitors was shown to reduce activation of the LC and exaggerated NA release in response to acute stress, but to increase synaptic levels of NA under basal conditions (Valentino and Curtis, 1991;Morilak and Frazer, 2004;Bondi et al, 2007).…”

Section: Integrative Mechanism Of Galanininergic Regulation Of Depresmentioning

confidence: 99%

Differential Role of Galanin Receptors in the Regulation of Depression-Like Behavior and Monoamine/Stress-Related Genes at the Cell Body Level

Kuteeva

Wardi

Lundström

et al. 2008

Neuropsychopharmacol

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The present study on rat examined the role of galanin receptor subtypes in regulation of depression-like behavior as well as potential molecular mechanisms involved in the locus coeruleus (LC) and dorsal raphe (DR). The effect of intracerebroventricular (i.c.v.) infusion of galanin or galanin receptor GalR1-and GalR2-selective ligands was studied in the forced swim test, followed by quantitative in situ hybridization studies. Naive control, non-treated (swim control), saline-and fluoxetine-treated rats were used as controls in the behavioral and in situ hybridization studies. Subchronic treatment with fluoxetine reduced immobility and climbing time. Intracerebroventricular infusion of galanin, the GalR1 agonist M617 or the GalR2 antagonist M871 increased, while the GalR2(R3) agonist AR-M1896 decreased, immobility time compared to the aCSF-treated animals. Galanin also decreased the time of climbing. Galanin mRNA levels were upregulated by the combination of injection + swim stress in the saline-and the fluoxetine-treated groups in the LC, but not in the DR. Also tyrosine hydroxylase levels in the LC were increased following injection + swim stress in the saline-and fluoxetine-treated rats. Tryptophan hydroxylase 2 and serotonin transporter mRNAs were not significantly affected by any treatment. 5-HT 1A mRNA levels were downregulated following i.c.v. galanin, M617 or AR-M1896 infusion. These results indicate a differential role of galanin receptor subtypes in depression-like behavior in rodents: GalR1 subtype may mediate 'prodepressive' and GalR2 'antidepressant' effects of galanin. Galanin has a role in behavioral adaptation to stressful events involving changes of molecules important for noradrenaline and/or serotonin transmission.

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“…CRF administration has been shown to increase probe burying, while this behavior was blocked by CRF antagonists (Basso et al 1999;Diamant et al 1992;Korte et al 1994). Furthermore, shock-probe burying is accompanied by increases in NE transmission (Bondi et al 2007;Korte et al 1992) and attenuated by pretreatment with noradrenergic antagonists (Morilak et al 2005). Taken together, these data suggest that burying by rodents may be a model response for stress associated with the activation of NE pathways from the LC.…”

Section: Burying Behavior Is Mediated By Forebrain Nementioning

confidence: 80%

“…Rodent burying behavior has long been described as a defensive coping strategy in natural habitats (Calhoun 1962;MacClintock 1970;Owings and Coss 1977). Furthermore, in the context of defensive avoidance, this proactive form of stress management provides an index of anxiety when directed at an electrified probe (Bondi et al 2007;De Boer et al 1990;Korte et al 1992;Treit et al 1981), and is enhanced and attenuated by anxiogenic and anxiolytic drugs, respectively (De Boer and Koolhaas 2003;Diamant et al 1992). To the best of our knowledge, the present studies are the first to specifically characterize and quantify the burying response to i.c.v.…”

Section: Characterization Of Crf-evoked Behaviorsmentioning

confidence: 99%

Differential blockade of CRF-evoked behaviors by depletion of norepinephrine and serotonin in rats

et al. 2008

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Rationale-Central administration of corticotropin-releasing factor (CRF) elicits a specific pattern of behavioral responses resembling a stress-like state, and is anxiogenic in rodent models of anxiety.Objectives-Specific behaviors evoked by the administration of CRF were measured. The roles of CRF receptor subtypes and that of serotonergic and noradrenergic systems in mediating these responses were studied.Methods-Burying, grooming and head shakes were quantified in rats following intracerebroventricular administration of CRF and urocortin II and after pretreatment with antagonists. The role of forebrain norepinephrine in the behavioral responses to CRF (0.3 μg) was examined following pretreatment with the neurotoxin DSP-4 and that of serotonin after depletion using systemic administration of para-chlorophenylalanine (p-CPA).Results-CRF at 0.3 and 3.0 μg caused robust increases in burying, grooming and head shakes, but urocortin II was ineffective. Pretreatment with either antalarmin or propranolol significantly attenuated the CRF-evoked behaviors. Destruction of forebrain NE pathways blocked spontaneous burying behavior elicited by CRF and conditioned burying directed towards an electrified shock probe. In contrast, depletion of 5-HT selectively attenuated CRF-evoked grooming.Conclusions-Overt behavioral responses produced by CRF, burying, grooming, and head shakes, appeared to be mediated through the CRF 1 receptor. Spontaneous burying behavior evoked by CRF or conditioned burying directed towards a shock probe were disrupted by lesion of the dorsal noradrenergic bundle and may represent anxiety-like behavior caused by CRF activation of the LC. In contrast, CRF-evoked increases in grooming were dependent on serotonin.

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Noradrenergic facilitation of shock-probe defensive burying in lateral septum of rats, and modulation by chronic treatment with desipramine

Cited by 46 publications

References 76 publications

Neurokinin 1 Receptor Antagonism Promotes Active Stress Coping Via Enhanced Septal 5-HT Transmission

Neurokinin 1 Receptor Antagonism Promotes Active Stress Coping Via Enhanced Septal 5-HT Transmission

Differential Role of Galanin Receptors in the Regulation of Depression-Like Behavior and Monoamine/Stress-Related Genes at the Cell Body Level

Differential blockade of CRF-evoked behaviors by depletion of norepinephrine and serotonin in rats

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