Stress-facilitated LTD induces output plasticity through a synchronized-spikes and spontaneous unitary discharges the CA1 region of the hippocampus

Long-term potentiation (LTP) and long-term depression (LTD) of the excitatory synaptic inputs plasticity in the hippocampus is believed to underlie certain types of learning and memory. Especially, stressful experiences, well known to produce long-lasting strong memories of the event themselves, enable LTD by low frequency stimulation (LFS, 3 Hz) but block LTP induction by high frequency stimulation (HFS, 200 Hz). However, it is unknown whether stress-affected synaptic plasticity has an impact on the output plasticity. Thus, we have simultaneously studied the effects of stress on synaptic plasticity and neuronal output in the hippocampal CA1 region of anesthetized Wistar rats. Our results revealed that stress increased basal power spectrum of the evoked synchronized-spikes and enabled LTD induction by LFS. The induction of stress-facilitated LTD but not LFS induced persistent decreases of the power spectrum of the synchronized-spikes and the frequency of the spontaneous unitary discharges; However, HFS induced UP in non-stressed animals and increased the power spectrum of the synchronized-spikes, without affecting the frequency of the spontaneous unitary discharges, but HFS failed to induce UP in stressed animals without affecting the power spectrum of the synchronized-spikes and the frequency of the spontaneous unitary discharges. These observations that stress-facilitated LTD induces the output plasticity through the synchronized-spikes and spontaneous unitary discharges suggest that these types of stress-related plasticity may play significant roles in distribution, amplification and integration of encoded information to other brain structures under stressful conditions. (C) 2004 Elsevier Ireland Ltd and The Japan Neuroscience Society. All rights reserved.

Gibbons under seasonal stress: the diet of the black crested gibbon (Nomascus concolor) on Mt. Wuliang, Central Yunnan, China

The diet of a habituated group of black crested gibbon (Nomascus concolor jingdongensis) was studied from March 2005 to April 2006 in the Wuliang Mountains, central Yunnan, China. Gibbons consumed 77 different plant species, one mammal-, two bird-, one li

Stress and long-term synaptic depression

Acute inescapable stress reverses the direction of synaptic plasticity in the intact hippocampus via a corticosterone-mediated activation of glucocorticoid receptors and protein/RNA synthesis.

Glucocorticoid receptor and protein/RNA synthesis-dependent mechanisms underlie the control of synaptic plasticity by stress

Learning and memory are exquisitely sensitive to behavioral stress, but the underlying mechanisms are still poorly understood. Because activity-dependent persistent changes in synaptic strength are believed to mediate memory processes in brain areas such as the hippocampus we have examined the means by which stress affects synaptic plasticity in the CA1 region of the hippocampus of anesthetized rats, Inescapable behavioral stress (placement on an elevated platform for 30 min) switched the direction of plasticity, favoring low frequency stimulation-induced decreases in synaptic transmission (long-term depression, LTD), and opposing the induction of long-term potentiation by high frequency stimulation, We have discovered that glucocorticoid receptor activation mediates these effects of stress on LTD and longterm potentiation in a protein synthesis-dependent manner because they were prevented by the glucocorticoid receptor antagonist RU 38486 and the protein synthesis inhibitor emetine. Consistent with this, the ability of exogenously applied corticosterone in non-stressed rats to mimic the effects of stress on synaptic plasticity was also blocked by these agents, The enablement of low frequency stimulation-induced LTD by both stress and exogenous corticosterone was also blocked by the transcription inhibitor actinomycin D, Thus, naturally occurring synaptic plasticity is liable to be reversed in stressful situations via glucocorticoid receptor activation and mechanisms dependent on the synthesis of new protein and RNA, This indicates that the modulation of hippocampus-mediated learning by acute inescapable stress requires glucocorticoid receptor-dependent initiation of transcription and translation.

The effect of acute stress on LTP and LTD induction in the hippocampal CA1 region of anesthetized rats at three different ages

Not all experiences are memorized equally well. Especially, some types of stress are unavoidable in daily life and the stress experience can be memorized for life. Previous evidence has showed that synaptic plasticity, such as long-term potentiation (LTP) that may be the major cellular model of the mechanism underlying learning and memory, is influenced by behavioral stress. However, the effect of behavioral stress on age-related synaptic plasticity in-vivo was primarily known. Here we found that the LTP induction in the hippocampal CA1 region of anesthetized rats obviously showed inverted-U shape related to ages (4, 10 and 74 weeks old rats), but low-frequency stimulation was unable to induce reliable long-term depression (LTD) in these animals. Furthermore, acute elevated platform (EP) stress enabled reliable LTD significantly and completely blocked LTP induction at these ages. Importantly, LTD after exposure to acute EP stress showed similar magnitude over these ages. The present results that stress enables LTD but impairs LTP induction at these three ages strengthen a view that stress experience-dependent LTD (SLTD) may underlie stress form of aberrant memories. (C) 2004 Elsevier B.V. All rights reserved.

Stress enables synaptic depression in CA1 synapses by acute and chronic morphine: Possible mechanisms for corticosterone on opiate addiction

The hippocampus, being sensitive to stress and glucocorticoids, plays significant roles in certain types of learning and memory. Therefore, the hippocampus is probably involved in the increasing drug use, drug seeking, and relapse caused by stress. We have studied the effect of stress with morphine on synaptic plasticity in the CA1 region of the hippocampus in vivo and on a delayed-escape paradigm of the Morris water maze. Our results reveal that acute stress enables long-term depression (LTD) induction by low-frequency stimulation (LFS) but acute morphine causes synaptic potentiation. Remarkably, exposure to an acute stressor reverses the effect of morphine from synaptic potentiation ( similar to 20%) to synaptic depression ( similar to 40%), precluding further LTD induction by LFS. The synaptic depression caused by stress with morphine is blocked either by the glucocorticoid receptor antagonist RU38486 or by the NMDA-receptor antagonist D-APV. Chronic morphine attenuates the ability of acute morphine to cause synaptic potentiation, and stress to enable LTD induction, but not the ability of stress in tandem with morphine to cause synaptic depression. Furthermore, corticosterone with morphine during the initial phase of drug use promotes later delayed-escape behavior, as indicated by the morphine-reinforced longer latencies to escape, leading to persistent morphine-seeking after withdrawal. These results suggest that hippocampal synaptic plasticity may play a significant role in the effects of stress or glucocorticoids on opiate addiction.

Stress evoked by opiate withdrawal facilitates hippocampal LTP in vivo

Stress impairs hippocampal long-term potentiation (LTP), but it is unknown whether the stress evoked by opiate withdrawal has the same effect. Here the authors report that opiate withdrawal for 4 days does not influence basal synaptic transmission, but re

NR2B-containing N-methyl-D-aspartate subtype glutamate receptors regulate the acute stress effect on hippocampal long-term potentiation/long-term depression in vivo

Behavioral stress facilitates long-term depression but impairs long-term potentiation in the hippocampus. Recent evidence in vitro demonstrates that the NIR2B-containing N-methyl-D-aspartate subtype glutamate receptor antagonist Ro25-6981 prevents the beh

Enriched environment experience overcomes the memory deficits and depressive-like behavior induced by early life stress

Stress in early life is believed to cause cognitive and affective disorders, and to disrupt hippocampal synaptic plasticity in adolescence into adult, but it is unclear whether exposure to enriched environment (EE) can overcome these effects. Here, we rep

Acute behavioural stress facilitates long-term depression in temporoammonic-CAI pathway

Behavioural stress facilitates long-term depression in Schaffer collaterals-CAI pathway, but it is unknown whether it influences long-term depression in temporoammonic fibres-CAI. Here, we report that low-frequency stimulation induced long-term depression

Prenatal stress modifies hippocampal synaptic plasticity and spatial learning in young rat offspring

Clinical studies demonstrate that prenatal stress causes cognitive deficits and increases vulnerability to affective disorders in children and adolescents. The underlying mechanisms are not yet fully understood. Here, we reported that prenatal stress (10

Enriched environment treatment restores impaired hippocampal synaptic plasticity and cognitive deficits induced by prenatal chronic stress

Prenatal stress can cause long-term effects on cognitive functions in offspring. Hippocampal synaptic plasticity, believed to be the mechanism underlying certain types of learning and memory, and known to be sensitive to behavioral stress, can be changed

Stress within the postseizure time window inhibits seizure recurrence

Recurrence is a key characteristic in the development of epilepsy. It remains unclear whether seizure recurrence is sensitive to postseizure stress. Here, tonic-clonic seizures were induced with a convulsive dose of pentylenetetrazole (PTZ), and acute seizure recurrence was evoked with a subconvulsive dose of the drug. We found that stress inhibited seizure recurrence when applied 30 minutes or 2 hours, but not 4 hours, after the tonic-clonic seizure. The time-dependent anti-recurrence effect of stress was mimicked by the stress hormone corticosterone and blocked by co-administration of mineralocorticoid and glucocorticoid receptor antagonists. Furthermore, in a PTZ-induced epileptic kindling model, corticosterone administered 30 minutes after each seizure decreased the extent of seizures both during the kindling establishment and in the following challenge test. These results provide novel insights into both the mechanisms of and therapeutic strategies for epilepsy. (C) 2010 Elsevier Inc. All rights reserved.

Physiological Responses of Microcystis aeruginosa PCC7806 to Nonanoic Acid Stress

A recent study has shown that nonanoic acid (NA) is one of the strongest allelochemicals to a cyanobacterium Microcystis aeruginosa, but the physiological responses of M. aeruginosa to NA stress remain unknown. In this study, physiological characters such as the growth rate, photosynthetic processes, phosphorus and nitrogen uptake kinetics, and the contents of intracellular microcystin of M. aeruginosa PCC7806 were studied under the NA stress. The results showed that the growth rates of M. aeruginosa PCC 7806 were significantly inhibited in all NA stress treatments during first 3 days after exposure, and the growth rate was recovered after 5-day exposure. After 2-day exposure, the contents of both phycocyanin and allophycocyanin per cell decreased at NA concentration of 4 mg L-1, and oxygen evolution was inhibited even at the concentration of 0.5 mg L-1, but carotenoid content per cell was slightly boosted in NA stress. Physiological recovery of M. aeruginosa PCC7806 was observed after 7-day exposure to NA. It was shown that NA stress had no effect on uptake of nitrogen, but could stimulate the uptake of phosphorus. The contents of intracellular microcystin have not been affected in all NA treatments in contrast with the control. (C) 2008 Wiley Periodicals, Inc. Environ Toxicol 24: 610-617, 2009.

Carbon and nitrogen metabolism of an eutrophication tolerative macrophyte, Potamogeton crispus, under NH4+ stress and low light availability

Submersed macrophytes in eutrophic lakes often experience high NH4+ concentration and low light availability in the water column. This study found that an NH4+-N concentration of 1 mgL(-1) in the water column apparently caused physiological stress on the macrophyte Potamogeton crispus; L The plants accumulated free amino acids (FAA) and lost soluble carbohydrates (SC) under NH4+ stress. These stressful effects of NH4+ were exacerbated under low light availability. Shading significantly increased NH4+ and FAA contents and dramatically decreased SC and starch contents in the plant shoots. At an NH4+-N concentration of 1 mg L-1 in the water column, neither growth inhibition nor NH4+ accumulation was observed in the plant tissues of P. crispus under normal light availability. The results showed that 1 mg L-1 NH4+-N in the water column was not toxic to P. crispus in a short term. To avoid NH4+ toxicity. active NH4+ transportation out of the cell may cost energy and thus result in a decline of carbohydrate. When NH4+ inescapably accumulates in the plant cell, i.e. under NH4+ Stress and shading, NH4+ is scavenged by FAA synthesis. (c) 2009 Published by Elsevier B.V.