Enhancement of Anxiety and Modulation of TH and pERK Expressions in Amygdala by Repeated Injections of Corticosterone

Lim, Heejin; Jang, Soyong; Lee, Yeon-Ju; Moon, Sohyeon; Kim, Jieun; Oh, Seikwan

doi:10.4062/biomolther.2012.20.4.418

Cited by 16 publications

(10 citation statements)

References 43 publications

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“…In order to focus on cell-autonomous mechanisms of vulnerability, we deleted the D2R gene selectively in DA neurons by crossing Drd2 loxP mice with DAT IREScre mice. Using these DAT IREScre /Drd2 loxP mice, we surprisingly did not find any changes in TH signal in the striatum, an observation that could reflect the highly plastic and homeostatic nature of TH expression in response to perturbations such as neurotoxins, which might make it somewhat unreliable to assess the extent of loss of axonal processes [30–36]. On the other hand, we did observe a significant increase in DAT immunoreactive processes in the dorsal striatum, as shown previously in the constitutive KO model [17], with no increase in the number of DA neurons.…”

Section: Discussionmentioning

confidence: 99%

Increased vulnerability of nigral dopamine neurons after expansion of their axonal arborization size through D2 dopamine receptor conditional knockout

et al. 2019

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Parkinson’s disease (PD) is a neurodegenerative disorder characterized by the loss of dopamine (DA) neurons in the substantia nigra pars compacta (SNc). Rare genetic mutations in genes such as Parkin, Pink1, DJ-1, α-synuclein, LRRK2 and GBA are found to be responsible for the disease in about 15% of the cases. A key unanswered question in PD pathophysiology is why would these mutations, impacting basic cellular processes such as mitochondrial function and neurotransmission, lead to selective degeneration of SNc DA neurons? We previously showed in vitro that SNc DA neurons have an extremely high rate of mitochondrial oxidative phosphorylation and ATP production, characteristics that appear to be the result of their highly complex axonal arborization. To test the hypothesis in vivo that axon arborization size is a key determinant of vulnerability, we selectively labeled SNc or VTA DA neurons using floxed YFP viral injections in DAT-cre mice and showed that SNc DA neurons have a much more arborized axon than those of the VTA. To further enhance this difference, which may represent a limiting factor in the basal vulnerability of these neurons, we selectively deleted in mice the DA D2 receptor (D2-cKO), a key negative regulator of the axonal arbour of DA neurons. In these mice, SNc DA neurons have a 2-fold larger axonal arborization, release less DA and are more vulnerable to a 6-OHDA lesion, but not to α-synuclein overexpression when compared to control SNc DA neurons. This work adds to the accumulating evidence that the axonal arborization size of SNc DA neurons plays a key role in their vulnerability in the context of PD.

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Section: Discussionmentioning

confidence: 99%

Increased vulnerability of nigral dopamine neurons after expansion of their axonal arborization size through D2 dopamine receptor conditional knockout

et al. 2019

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“…MAPK/ERK signaling in the amygdala has been repeatedly shown to contribute to anxiety regulation in rodents. For example, exposure to novel environments or repeated intraperitoneal injection of corticosterone, which enhances anxiety-like behavior in the EPM test, increases ERK activation in the rat amygdala 41 42 , whereas ERK inhibition in the mouse BLA abolishes restraint stress-induced increase in anxiety-like behavior in the EPM test 43 . Given the crosstalk reported for MAPK/ERK and AKT/GSK3β signaling pathways, it is therefore of interest to examine how SCOP regulates these anxiety-related signaling pathways in the BLA in vivo .…”

Section: Discussionmentioning

confidence: 99%

SCOP/PHLPP1β in the basolateral amygdala regulates circadian expression of mouse anxiety-like behavior

Nakano

Shimizu

Shimba

et al. 2016

Sci Rep

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While disruption of the circadian clock triggers a spectrum of affective abnormalities, how the clock regulates mammalian emotionality remains unclear. Here, we characterized the time-of-day-dependent regulation of mouse anxiety-like behaviors. We show that anxiety-like behaviors are expressed in a circadian manner in mice and demonstrate that the clock machineries in the dorsal telencephalon (dTel) are required for the time-of-day-dependent regulation of anxiety-like behaviors. We identify suprachiasmatic nucleus circadian oscillatory protein (SCOP/PHLPP1β) as an essential intracellular signaling molecule mediating this temporal regulation downstream of the clock. Using viral-mediated, basolateral amygdala (BLA)-specific knockout of Scop, we demonstrate that deletion of SCOP in the BLA exerts anxiolytic effects on the elevated plus maze at early subjective night, thereby blunting the circadian variation in the anxiety-like behavior. We conclude that the circadian expression of SCOP in the BLA plays a key role in generating circadian rhythmicity in the anxiety-like behavior. Our results demonstrate SCOP as a regulator of anxiety-like behaviors and reveal its key roles in the anxiogenic functions of the BLA.

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“…The ERK pathway is one of several signal transduction pathways that propagate and amplify cellular signaling ( Lim et al ., 2012 ). Several studies have reported modulation of sleeping behavior by ERK activation.…”

Section: Discussionmentioning

confidence: 99%

Quinpirole Increases Melatonin-Augmented Pentobarbital Sleep via Cortical ERK, p38 MAPK, and PKC in Mice

Hong

Kwon

Hwang

et al. 2016

Biomolecules & Therapeutics

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Sleep, which is an essential part of human life, is modulated by neurotransmitter systems, including gamma-aminobutyric acid (GABA) and dopamine signaling. However, the mechanisms that initiate and maintain sleep remain obscure. In this study, we investigated the relationship between melatonin (MT) and dopamine D2-like receptor signaling in pentobarbital-induced sleep and the intracellular mechanisms of sleep maintenance in the cerebral cortex. In mice, pentobarbital-induced sleep was augmented by intraperitoneal administration of 30 mg/kg MT. To investigate the relationship between MT and D2-like receptors, we administered quinpirole, a D2-like receptor agonist, to MT- and pentobarbital-treated mice. Quinpirole (1 mg/kg, i.p.) increased the duration of MT-augmented sleep in mice. In addition, locomotor activity analysis showed that neither MT nor quinpirole produced sedative effects when administered alone. In order to understand the mechanisms underlying quinpirole-augmented sleep, we measured protein levels of mitogen-activated protein kinases (MAPKs) and cortical protein kinases related to MT signaling. Treatment with quinpirole or MT activated extracellular-signal-regulated kinase 1 and 2 (ERK1/2), p38 MAPK, and protein kinase C (PKC) in the cerebral cortex, while protein kinase A (PKA) activation was not altered significantly. Taken together, our results show that quinpirole increases the duration of MT-augmented sleep through ERK1/2, p38 MAPK, and PKC signaling. These findings suggest that modulation of D2-like receptors might enhance the effect of MT on sleep.

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Enhancement of Anxiety and Modulation of TH and pERK Expressions in Amygdala by Repeated Injections of Corticosterone

Cited by 16 publications

References 43 publications

Increased vulnerability of nigral dopamine neurons after expansion of their axonal arborization size through D2 dopamine receptor conditional knockout

Increased vulnerability of nigral dopamine neurons after expansion of their axonal arborization size through D2 dopamine receptor conditional knockout

SCOP/PHLPP1β in the basolateral amygdala regulates circadian expression of mouse anxiety-like behavior

Quinpirole Increases Melatonin-Augmented Pentobarbital Sleep via Cortical ERK, p38 MAPK, and PKC in Mice

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