Progressive alterations of hippocampal CA3-CA1 synapses in an animal model of depression

Qiao, Hui; An, Shu-Cheng; Ren, Wei; Ma, Xin−Ming

doi:10.1016/j.bbr.2014.08.040

Cited by 81 publications

(105 citation statements)

References 89 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…(Willner, 1997). In the present study, CUMS successfully induced depressive-like behaviors in rats, including decreased body weight and locomotor activity, loss of interest and behavioral despair as expected (Qiao et al, 2014). In rodents, the sucrose preference and tail suspension test were used to assess the prominent symptom of depression, anhedonia (Der-Avakian and Markou, 2012) and despair behavior (Cryan et al, 2005, Ge et al, 2014 respectively.…”

Section: -Ht 2a Receptors In Cums-induced Depressive-like Behaviors mentioning

confidence: 96%

“…Therefore, CUMS is widely used as an experimental model of depression. In our previous studies (Luo et al, 2008, Qiao et al, 2014, we successfully established a CUMS rat model for studying the mechanisms of depression.…”

Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 99%

“…All group rats (n=6，except n=4 for Ket/CON group) were used for labeling dendritic spines in the OFC pyramidal neurons, using a modified Golgi-Cox method (Qiao et al, 2014). Briefly, rats were fixed by perfusion and the whole brain was removed.…”

Section: Labeled Dendritic Spinesmentioning

confidence: 99%

See 2 more Smart Citations

Orbitofrontal cortex 5-HT2A receptor mediates chronic stress-induced depressive-like behaviors and alterations of spine density and Kalirin7

Chen

et al. 2016

Neuropharmacology

Self Cite

View full text Add to dashboard Cite

Section: -Ht 2a Receptors In Cums-induced Depressive-like Behaviors mentioning

confidence: 96%

Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 99%

See 1 more Smart Citation

Orbitofrontal cortex 5-HT2A receptor mediates chronic stress-induced depressive-like behaviors and alterations of spine density and Kalirin7

Chen

et al. 2016

Neuropharmacology

Self Cite

View full text Add to dashboard Cite

“…Changes in hippocampal synaptic plasticity were dependent on the duration of CUS, the functional changes at CA3-CA1 hippocampal synapses occurring earlier than the structural alterations. Qiao et al [32] reported that CUS during three weeks induced depressive-like behaviors, impaired LTP induction, and decreased basal synaptic transmission at hippocampal CA3-CA1 synapses recorded in vivo; a decrease in density of dendritic spines in CA1 and CA3 pyramidal neurons and brain-derived neurotrophic factor (BDNF) level in the hippocampus accompanied changes in synaptic plasticity. After a two week CUS, some depressive-like behaviors were observed, accompanied by depressed basal synaptic transmission, enhanced LTP induction at the CA3-CA1 synapses and decreased BDNF.…”

Section: Literaturementioning

confidence: 99%

Studies on stress-induced modulation of long term potentiation in rodent hippocampus: what can we learn about pathogenesis of depression?

Gulyaeva¹

2016

Transl Brain Rhythmicity

View full text Add to dashboard Cite

Long-term potentiation (LTP) reflecting continuous changes in synaptic efficacy is regarded as a cellular model of learning and memory. In this mini-review the data relating to hippocampal LTP alterations in rodent models of depression are analyzed to learn whether disturbances in LTP may be reliable markers of synaptic plasticity impairments underlying depressive and anxiety states. LTP disturbances result from synaptic reorganizations induced by multiple inter-related and mutually dependent events: hypothalamic-pituitary-adrenal axis disfunction; malfunction of neurotransmitter systems; failure to maintain the balance of neurotrophic systems; neuroinflammatory processes; disturbance in neurogenesis. Stable deficits in hippocampal LTP reflect the synapse-related basic mechanisms for cognitive and emotional behavioral deficits characterisic for depression/anxiety, and altered LTP is indicative of the development of stress-induced psychopathology.Correspondence to: Natalia V.Gulyaeva, Institute of Higher Nervous Activity and Neurophysiology RAS, 5a Butlerov Street, Moscow, 117485, Russia, E-mail: nata_gul@pisem.net Key words: depression, anxiety, synaptic plasticity, long term potentiation (LTP), stress LiteratureChronic stress is considered to be a major risk factor in the development of mood diseases. In order to study mechanisms involved in the etiology of human affective disorders, there is an abundant use of various animal models based on different stress paradigms. Depressive disorders are the most common psychiatric pathology, and a great number of people who experience depression also experience anxiety. Sometimes, anxiety is more expressed than depression, while in many cases neither is clearly predominant. In rodent stress-based models anxiety and depression symptoms often are demonstrated in parallel.Activity-dependent changes in synaptic strength are widely accepted as key mechanisms for information storage in the brain [1]. Long-term potentiation (LTP) is an electrophysiological phenomenon, an hours-lasting increase of postsynaptic potentials after tetanization. It is believed to reflect long-term changes in synaptic efficacy in distributed networks, associated with constant changes in the behavioral phenomena, which are often interpreted as the retention of information [2]. Thus, hippocampal LTP is regarded as a cellular model of learning and memory. Cognitive impairments and LTP impairments are increasingly recognized as events accompanying and reflecting experimental depression, anxiety and other experimental stress-related chronic psychological disorders, therefore, disturbances in LTP may be reliable markers of synaptic plasticity impairments underlying depressive and anxiety states. The dentate gyrus (DG) of the hippocampus is supposed to play a critical role in defining the impact of stress on hippocampal functioning. The DG is a dynamic structure susceptible to stress, its variable and complex stress response being reflected in changes of LTP and local circuit activity associated wit...

show abstract

“…It has been strikingly implicated in the genesis of depressive disorders [41][42][43][44][45][46][47][48]. The neurothrophin BDNF is a molecule extremely sensible to stress, and its expression or production is reduced in key brain regions of animal model of depression [49][50][51] and also in the blood of depressed patients [52][53][54]. In order to better understand the possible mechanisms underlying these changes, researchers have investigated the role of DNA methylation within BDNF promoter regions.…”

mentioning

confidence: 99%

A Brief Review on Epigenetic Aspects involved in Depression

Conti¹,

Silva-Conforti²

2016

Biol Med (Aligarh)

View full text Add to dashboard Cite

It is known that external environmental or internal physiologic factors interact with an individual's genetic constitution to determine risk for depression throughout life. This can be possible through epigenetic mechanisms that lead to changes in gene expression -with transgenerational abilities -that do not involve a change in the DNA sequence. Here we briefly summarize the link between depressive disorders and epigenetics, considering stressful events as important triggers for these modifications. The increasing knowledge in this issue is relevant for updating and expanding comprehension in the molecular basis of this mood disorder. Keywords Epigenetic aspects involved in depressionGrowing evidences support the hypothesis that epigenetics is a key mechanism through which environmental exposures interact with our genetic constitution and this interaction is able to cause depression throughout life. The term epigenetics ("epi" means above in Greek) is used to denote transgenerational transmission of traits without a change in the nucleotide sequence of DNA [1][2][3][4]. It had emerged as a mechanism initiated by environmental cues and cellular events mediated by various cellular mechanisms that originate phenotypes during the development. However, recently, it has been postulated that these cellular modifications can be converted into alterations in chromatin structure -non related with DNA sequence alteration -that finally lead to expression or suppression of altered gene programs [5].While the genome defines the potential genetic information, the epigenome defines which genes are actually expressed. This regulation over the gene expression without altering the sequence of the DNA is possible by epigenetic modifications including microRNAs (small RNA molecules that can negatively control their target gene expression posttranscriptionally), covalent modifications of histone proteins, mechanisms controlling higher order chromatin organization and DNA methylation. Among numerous epigenetic processes, DNA methylation is one of the major mechanisms studied in the context of early life adversities as a potential via to explain the long-term effects on gene transcription [3]. It is a stable mark that is important for diverse cellular processes [6]. Methyl group is added to the C5 position catalyzed by DNA methyltransferases (DNMTs) [7]. Considering all cytosines in the human genome, about 3% is methylated and proper cytosine methylation is required for cell differentiation, genetic imprinting and suppression of repetitive elements. In the central nervous system, DNA methylation is a physiological process, relevant for normal brain development, differentiation and maintenance of function [8,9]. Indeed, during development, pluripotent stem cells undergo division and differentiate into different cell types that ultimately become different organs and tissues with specific patterns of gene expression [10].Epigenetics refers to how both the external environment and internal physiologic environment can interact wit...

show abstract

Progressive alterations of hippocampal CA3-CA1 synapses in an animal model of depression

Cited by 81 publications

References 89 publications

Orbitofrontal cortex 5-HT2A receptor mediates chronic stress-induced depressive-like behaviors and alterations of spine density and Kalirin7

Orbitofrontal cortex 5-HT2A receptor mediates chronic stress-induced depressive-like behaviors and alterations of spine density and Kalirin7

Studies on stress-induced modulation of long term potentiation in rodent hippocampus: what can we learn about pathogenesis of depression?

A Brief Review on Epigenetic Aspects involved in Depression

Contact Info

Product

Resources

About