The role of basolateral amygdala in the regulation of stress-induced phosphorylated extracellular signal-regulated kinase expression in the hippocampus

Jeon, B.; Hwang, Yoo Kyeong; Lee, S.-Y.; Kim, D.; Chung, ChiHye; Han, Jung‐Soo

doi:10.1016/j.neuroscience.2012.08.035

Cited by 19 publications

(9 citation statements)

References 51 publications

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“…In addition, lesion of the basolateral nucleus of the amygdala results in the reduction of nuclear translocation of the GR in the DG and in CA1 (Jeon et al, 2012). Since the functioning of this nucleus is an important component of the neural circuit of fear conditioning, where the sensory information converges and conditioned and unconditioned stimuli are also associated (Phillips and LeDoux, 1992;Goosens and Maren, 2001;Cardinal et al, 2002), the increase in pSer246 that we observed in the DG and CA1 might be modulated by the basolateral amygdala.…”

Section: Discussionmentioning

confidence: 54%

Differential Phosphorylation of the Glucocorticoid Receptor in Hippocampal Subregions Induced by Contextual Fear Conditioning Training

Ponce-Lina

Serafín

Carranza

et al. 2020

Front. Behav. Neurosci.

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Aversive events induce the release of glucocorticoid stress hormones that facilitate long-term memory consolidation, an effect that depends on the activation of glucocorticoid receptors (GRs). GRs are distributed widely in the hippocampus. The dorsal region of the hippocampus has been related to cognitive functions and the ventral region to stress and emotion. GR acts as a transcription factor which after hormone binding becomes phosphorylated, affecting its cellular distribution and transcriptional activity. Two functionally well-described GR phosphorylation sites are serine 232 (pSer232), which enhances gene expression, and serine 246 (pSer246), having the opposite effect. Since gene expression is one of the plastic mechanisms needed for memory consolidation, we investigated if an aversive learning task would induce GR phosphorylation in the dorsal (DH) and the ventral (VH) hippocampus. We trained rats in contextual fear conditioning (CFC) using different foot-shock intensities (0.0, 0.5, or 1.5 mA). One subgroup of animals trained with each intensity was sacrificed 15 min after training and blood was collected to quantify corticosterone (CORT) levels in serum. Another subgroup was sacrificed 1 h after training and brains were collected to evaluate the immunoreactivity (IR) to GR, pSer232 and pSer246 by SDS-PAGE/Western blot in DH and VH, and by immunohistochemistry in dorsal and ventral CA1, CA2, CA3, and dentate gyrus (DG) hippocampal regions. The conditioned freezing response increased in animals trained with 0.5 and 1.5 mA during training and extinction sessions. The degree of retention and CORT levels were directly related to the intensity of the foot-shock. Although total GR-IR remained unaffected after conditioning, we observed a significant increase of pSer246-IR in the dorsal region of CA1 and in both dorsal and ventral DG. The only region in which pSer232-IR was significantly elevated was ventral CA3. Our results indicate that fear conditioning training is related to GR phosphorylation in specific

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Section: Discussionmentioning

confidence: 54%

Differential Phosphorylation of the Glucocorticoid Receptor in Hippocampal Subregions Induced by Contextual Fear Conditioning Training

Ponce-Lina

Serafín

Carranza

et al. 2020

Front. Behav. Neurosci.

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“…To test this, hippocampal pERK and pMEK levels were measured immediately after oxytocin and stress treatments. A previous study showed that pERK levels, measured immediately after termination of uncontrollable stress, were reduced in both cytosol and nucleus 18 . Cytoplasmic levels of pERK revealed no main effects of stress ( F 1,28 = 2.54, P = 0.12) and drug ( F 1,28 = 3.59, P = 0.07), but a significant stress x drug interaction ( F 1,28 = 8.70, P = 0.006).…”

Section: Resultsmentioning

confidence: 91%

“…Because stress alters the ERK pathway 18 , we examined whether oxytocin might dampen the stress effects on the hippocampus through the ERK signaling. To test this, hippocampal pERK and pMEK levels were measured immediately after oxytocin and stress treatments.…”

Section: Resultsmentioning

confidence: 99%

“…Thus, we investigated whether oxytocin, administered intranasally 16 17 , modifies the uncontrollable stress effects on the hippocampal plasticity and memory. Because MEK-extracellular signal-regulated kinase (ERK) signaling in hippocampus is involved in regulation of both stress and the action of oxytocin 18 19 , we further examined whether oxytocin counters stress effects on the MEK-ERK signaling pathway in the hippocampus.…”

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confidence: 99%

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Oxytocin Protects Hippocampal Memory and Plasticity from Uncontrollable Stress

Lee

Park

Chung

et al. 2015

Sci Rep

101

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The hippocampus is vulnerable to uncontrollable stress and is enriched with oxytocin receptors, but their interactive influences on hippocampal functioning are unknown. This study aimed to determine the effects of intranasal oxytocin administration on stress-induced alterations in synaptic plasticity and spatial memory in male rats. While vehicle-administered stressed rats showed impairment in long-term potentiation, enhancement in long-term depression, and weakened spatial memory, these changes were not observed in oxytocin-administered stressed rats. To reveal the potential signaling mechanism mediating these effects, levels of phosphorylated extracellular signal-regulated kinases (pERK) in the hippocampus was examined. Western blotting showed that oxytocin treatment blocked stress-induced alterations of pERK. Additionally, the oxytocin receptor antagonist L-368,899 inhibited the oxytocin’s protective effects on hippocampal memory to stress. Thus, intranasal administration of oxytocin reduced stress effects on hippocampal synaptic plasticity and memory in rats via acting on oxytocin receptors and regulating ERK activity. This study suggests that exogenous oxytocin may be a therapeutically effective means to counter the detrimental neurocognitive effects of stress.

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“…Then 8-μm sections of frozen brain were cut and mounted directly on APC-coated slides (Matsunami, Kishiwada, Japan). After drying, the brain sections were stained with 0.25% thionin solution (0.25% thionin, 0.55 μM lithium carbonate) [26].…”

Section: Methodsmentioning

confidence: 99%

Abnormal Behaviors and Developmental Disorder of Hippocampus in Zinc Finger Protein 521 (ZFP521) Mutant Mice

et al. 2014

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Zinc finger protein 521 (ZFP521) regulates a number of cellular processes in a wide range of tissues, such as osteoblast formation and adipose commitment and differentiation. In the field of neurobiology, it is reported to be an essential factor for transition of epiblast stem cells into neural progenitors in vitro. However, the role of ZFP521 in the brain in vivo still remains elusive. To elucidate the role of ZFP521 in the mouse brain, we generated mice lacking exon 4 of the ZFP521 gene. The birth ratio of our ZFP521 Δ/Δ mice was consistent with Mendel's laws. Although ZFP521 Δ/Δ pups had no apparent defect in the body and were indistinguishable from ZFP521+/+ and ZFP521 +/Δ littermates at the time of birth, ZFP521 Δ/Δ mice displayed significant weight reduction as they grew, and most of them died before 10 weeks of age. They displayed abnormal behavior, such as hyper-locomotion, lower anxiety and impaired learning, which correspond to the symptoms of schizophrenia. The border of the granular cell layer of the dentate gyrus in the hippocampus of the mice was indistinct and granular neurons were reduced in number. Furthermore, Sox1-positive neural progenitor cells in the dentate gyrus and cerebellum were significantly reduced in number. Taken together, these findings indicate that ZFP521 directly or indirectly affects the formation of the neuronal cell layers of the dentate gyrus in the hippocampus, and thus ZFP521 Δ/Δ mice displayed schizophrenia-relevant symptoms. ZFP521 Δ/Δ mice may be a useful research tool as an animal model of schizophrenia.

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The role of basolateral amygdala in the regulation of stress-induced phosphorylated extracellular signal-regulated kinase expression in the hippocampus

Cited by 19 publications

References 51 publications

Differential Phosphorylation of the Glucocorticoid Receptor in Hippocampal Subregions Induced by Contextual Fear Conditioning Training

Differential Phosphorylation of the Glucocorticoid Receptor in Hippocampal Subregions Induced by Contextual Fear Conditioning Training

Oxytocin Protects Hippocampal Memory and Plasticity from Uncontrollable Stress

Abnormal Behaviors and Developmental Disorder of Hippocampus in Zinc Finger Protein 521 (ZFP521) Mutant Mice

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