Facilitatory effect of olfactory bulbectomy on 2-deoxyglucose uptake in rat amygdala slices

Shibata, Shigenobu; Watanabe, Soichi

doi:10.1016/0006-8993(94)91165-7

Cited by 15 publications

(6 citation statements)

References 17 publications

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“…Infusion of the mixed V1a/b peptide antagonist d(CH2)5Tyr(Me)AVP into the amygdala using a retrodialysis technique in rats produced antidepressant-like behaviors (Ebner et al 2002). The amygdala has been implicated in the regulation of depressive-related behavior or in the actions of antidepressant drugs in the forced-swimming test and the olfactory bulbectomized paradigm (Gorka et al 1979;Duncan et al 1986;Shibata and Watanabe 1994;Wrynn et al 2000;Ho et al 2001;Rutkoski et al 2002). For example, unilateral lesion of the amygdala reduced the antidepressant-like effects of imipramine on immobility time and microinjection of imipramine into the CeA, BlA, or MeA produced antidepressant-like effects (Gorka et al 1979;Araki et al 1984;Duncan et al 1986).…”

Section: Discussionmentioning

confidence: 98%

Differential roles of amygdaloid nuclei in the anxiolytic- and antidepressant-like effects of the V1b receptor antagonist, SSR149415, in rats

et al. 2006

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Microinjection of SSR149415 into the BlA (1-10 ng), but not into the CeA or the MeA, increased the percentage of time spent in the open arms of the elevated plus-maze, indicating anxiolytic-like effects. Furthermore, in the forced-swimming test, microinjection of the drug into the CeA (1, 10, and 100 ng), BlA (1-10 ng), or MeA (100 ng) decreased immobility, an effect which is indicative of an antidepressant-like action. Together, these findings indicate that while the antidepressant-like effects of SSR149415 are mediated by different amygdaloid nuclei, its anxiolytic-like effects appear to involve only the basolateral nucleus of the amygdala. Moreover, these results add further evidence to the role of extrahypothalamic vasopressinergic systems in the control of emotional responses.

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Section: Discussionmentioning

confidence: 98%

Differential roles of amygdaloid nuclei in the anxiolytic- and antidepressant-like effects of the V1b receptor antagonist, SSR149415, in rats

et al. 2006

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“…Also the olfactory bulb has been implicated in anxiety behavior [58]. Olfactory bulbectomy has been suggested as an animal model of comorbid anxiety and leads to hyperexcitability of amygdala neurons [58,59]. Indeed, olfactory information converges in the amygdala, where the involvement of PI3K signaling has recently been observed in fear learning [2].…”

Section: Discussionmentioning

confidence: 99%

Phosphatidylinositide Dependent Kinase Deficiency Increases Anxiety and Decreases GABA and Serotonin Abundance in the Amygdala

Ackermann¹,

Hörtnagl²,

Wolfer³

et al. 2008

Cell Physiol Biochem

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Pathological anxiety is paralleled by deficits in serotonergic and GABAergic neurotransmission in the amygdala. Conversely, anxiety disorders and depression may be reversed by brain-derived neurotrophic factor (BDNF). BDNF signaling involves Phosphatidylinositol 3-Kinase / 3-phosphoinositide-dependent protein kinase 1 (PI3K/PDK1). We thus hypothesized that impaired function of PDK1 might be associated with increased anxiety and concomitant neurotransmitter changes. Here we used the hypomorphic PDK1^hm mouse to investigate anxiety behavior in different settings: PDK1^hm mice differed from Wt littermates PDK1^WT in several behavioral measures related to anxiety and exploration, namely in the open field, dark-light box, O-maze and startle response. Further we analyzed the brain substrate underlying this phenotype and found significantly decreased GABA, taurine and serotonin concentrations in the amygdala and olfactory bulb of PDK1^hm mice, while BDNF and nerve growth factor (NGF) concentrations were not significantly different between PDK1^hm and PDK1^WT mice. These results suggest that impaired PI3K signaling in the PDK1^hm mouse reduces concentrations of GABA and serotonin in anxiety related brain regions and can serve as a molecular substrate for behavior indicative for anxious and depressive-like mood states.

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“…In addition, the medial amygdala plays an important role in mediating defensive behaviours due to its monosynaptic substance P projections to the medial hypothalamus [60,61]. Disinhibition of the amygdala has been proposed to underlie the behavioural changes observed following olfactory bulbectomy including emotional blunting and deficit in defensive behaviours [62][63][64][65][66]. The present study demonstrated enhanced NK1 receptor expression in the medial amygdaloid nuclei following bulbectomy, and thus it is tempting to speculate that the increased receptor density observed in the amygdala may underlie the altered behavioural response to stress observed in the model.…”

Section: Discussionmentioning

confidence: 99%

Neurokinin-1 receptor deletion modulates behavioural and neurochemical alterations in an animal model of depression

Roche

Kerr

Hunt

et al. 2012

Behavioural Brain Research

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Facilitatory effect of olfactory bulbectomy on 2-deoxyglucose uptake in rat amygdala slices

Cited by 15 publications

References 17 publications

Differential roles of amygdaloid nuclei in the anxiolytic- and antidepressant-like effects of the V1b receptor antagonist, SSR149415, in rats

Differential roles of amygdaloid nuclei in the anxiolytic- and antidepressant-like effects of the V1b receptor antagonist, SSR149415, in rats

Phosphatidylinositide Dependent Kinase Deficiency Increases Anxiety and Decreases GABA and Serotonin Abundance in the Amygdala

Neurokinin-1 receptor deletion modulates behavioural and neurochemical alterations in an animal model of depression

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