Effects of Repeated Citalopram Treatments on Chronic Mild Stress-Induced Growth Associated Protein-43 mRNA Expression in Rat Hippocampus

Park, Sang Ha; Choi, Songa; Lee, Jimin; Kang, Seungwoo; Shin, You Chan; Kim, Hyun Ju; Kim, Hyun Jung; Shin, Seung Keon; Lee, Min Soo; Shin, Kyung Ho

doi:10.4196/kjpp.2008.12.3.117

Cited by 6 publications

(4 citation statements)

References 54 publications

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“…An alternative interpretation is that tinnitus suppresses auditory plasticity and GAP-43 expression. Chronic stress (Chao et al 1993; Kuroda and McEwen, 1998; Park et al, 2008; Kavushansky et al 2009) or stress hormones (Federoff et al, 1988; Chao et al, 1998) are capable of reducing GAP-43 expression in the limbic system and in cell culture. Since stress or stress hormones are also capable of affecting the auditory system (Tahera et al, 2006; Bose et al, 2010), we cannot rule out a possibility that tinnitus may affect synaptic plasticity in VCN.…”

Section: Discussionmentioning

confidence: 99%

Relationship between noise-induced hearing-loss, persistent tinnitus and growth-associated protein-43 expression in the rat cochlear nucleus: does synaptic plasticity in ventral cochlear nucleus suppress tinnitus?

et al. 2011

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Aberrant, lesion-induced neuroplastic changes in the auditory pathway are believed to give rise to the phantom sound of tinnitus. Noise-induced cochlear damage can induce extensive fiber growth and synaptogenesis in the cochlear nucleus, but it is currently unclear if these changes are linked to tinnitus. To address this issue, we unilaterally exposed nine rats to narrowband noise centered at 12 kHz at 126 dB SPL for two hours and sacrificed them 10 weeks later for evaluation of synaptic plasticity (GAP-43 expression) in the cochlear nucleus. Noise-exposed rats along with three age-matched controls were screened for tinnitus-like behavior with gap prepulse inhibition of the acoustic startle (GPIAS) before, 1–10 days after and 8–10 weeks after the noise exposure. All nine noise-exposed rats showed similar patterns of severe hair cell loss at high- and mid-frequency regions in the exposed ear. Eight of the 9 showed strong up-regulation of GAP-43 in auditory nerve fibers and pronounced shrinkage of the ventral cochlear nucleus (VCN) on the noise-exposed side, and strong up-regulation of GAP-43 in the medial ventral VCN, but not in the lateral VCN or the dorsal cochlear nucleus. GAP-43 up-regulation in VCN was significantly greater in Noise-No-Tinnitus rats than in Noise-Tinnitus rats. One Noise-No-Tinnitus rat showed no up-regulation of GAP-43 in auditory nerve fibers and only little VCN shrinkage, suggesting that auditory nerve degeneration plays a role in tinnitus generation. Our results suggest that noise-induced tinnitus is suppressed by strong up-regulation of GAP-43 in the medial VCN. GAP-43 up-regulation most likely originates from medial olivocochlear neurons. Their increased excitatory input on inhibitory neurons in VCN may possibly reduce central hyperactivity and tinnitus.

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Section: Discussionmentioning

confidence: 99%

Relationship between noise-induced hearing-loss, persistent tinnitus and growth-associated protein-43 expression in the rat cochlear nucleus: does synaptic plasticity in ventral cochlear nucleus suppress tinnitus?

et al. 2011

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“…Thus, it was recently shown that C57Bl/6 mice, exposed to chronic mild stress, displayed decreased hippocampal PKC activity [66]. Besides, Park et al [67] showed that a chronic mild stress protocol reduced the expression of the PKC substrate GAP-43 mRNA in the rat dentate gyrus. In the olfactory bulbectomy paradigm, a significant decrease of both the PKCα autophosphorylation and the phosphorylation of the NMDA receptor subunit NR1 on its PKC-dependent site (Ser 896) was observed in the CA1 region of the hippocampus [68,69].…”

Section: Depression-like Behaviorsmentioning

confidence: 97%

A Role for the PKC Signaling System in the Pathophysiology and Treatment of Mood Disorders: Involvement of a Functional Imbalance?

et al. 2011

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Mood disorders, such as bipolar and major depressive disorders, are frequent, severe, and often disabling neuropsychiatric diseases affecting millions of individuals worldwide. Available mood stabilizers and antidepressants remain unsatisfactory because of their delayed and partial therapeutic efficacy. Therefore, the development of targeted therapies, working more rapidly and being fully effective, is urgently needed. In this context, the protein kinase C (PKC) signaling system, which regulates multiple neuronal processes implicated in mood regulation, can constitute a novel therapeutic target. This paper reviews the currently available knowledge regarding the role of the PKC signaling pathway in the pathophysiology of mood disorders and the therapeutic potential of PKC modulators. Current antidepressants and mood stabilizers have been shown to modulate the PKC pathway, and the inhibition of this intracellular signaling cascade results in antimanic-like properties in animal models. Disrupted PKC activity has been found both in postmortem brains and platelet from patients with mood disorders. Finally, the PKC inhibitor tamoxifen has recently demonstrated potent antimanic properties in several clinical trials. Overall, emerging data from preclinical and clinical research suggest an imbalance of the PKC signaling system in mood disorders. Thus, PKC may be a critical molecular target for the development of innovative therapeutics.

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“…They are endogenous neuromodulators, which can be synthesized in the brain, adrenal gland, ovary, and testis, and mainly comprise progesterone, deoxycortone, dehydroepiandrosterone, testosterone, and the latter's metabolites[ 23 ]. By binding to intracellular receptors, neuroactive steroids regulate synaptic inhibitory transmission, inflammation, myelination, central nervous system development and post-injury repair, and the HPA axis and its stress effect[ 32 33 ]. Recently, increasing attention has been paid to the role of the stress hypothesis in the onset of depression.…”

Section: Discussionmentioning

confidence: 99%

Hippocampal gene expression in a rat model of depression after electroacupuncture at the Baihui and Yintang acupoints

Duan¹,

Yang

Tu³

et al. 2014

Neural Regen Res

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Preliminary basic research and clinical findings have demonstrated that electroacupuncture therapy exhibits positive effects in ameliorating depression. However, most studies of the underlying mechanism are at the single gene level; there are few reports regarding the mechanism at the whole-genome level. Using a rat genomic gene-chip, we profiled hippocampal gene expression changes in rats after electroacupuncture therapy. Electroacupuncture therapy alleviated depression-related manifestations in the model rats. Using gene-chip analysis, we demonstrated that electroacupuncture at Baihui (DU20) and Yintang (EX-HN3) regulates the expression of 21 genes. Real-time PCR showed that the genes Vgf, Igf2, Tmp32, Loc500373, Hif1a, Folr1, Nmb, and Rtn were upregulated or downregulated in depression and that their expression tended to normalize after electroacupuncture therapy. These results indicate that electroacupuncture at Baihui and Yintang modulates depression by regulating the expression of particular genes.

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Effects of Repeated Citalopram Treatments on Chronic Mild Stress-Induced Growth Associated Protein-43 mRNA Expression in Rat Hippocampus

Cited by 6 publications

References 54 publications

Relationship between noise-induced hearing-loss, persistent tinnitus and growth-associated protein-43 expression in the rat cochlear nucleus: does synaptic plasticity in ventral cochlear nucleus suppress tinnitus?

Relationship between noise-induced hearing-loss, persistent tinnitus and growth-associated protein-43 expression in the rat cochlear nucleus: does synaptic plasticity in ventral cochlear nucleus suppress tinnitus?

A Role for the PKC Signaling System in the Pathophysiology and Treatment of Mood Disorders: Involvement of a Functional Imbalance?

Hippocampal gene expression in a rat model of depression after electroacupuncture at the Baihui and Yintang acupoints

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