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.

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.

Amplitude/frequency of spontaneous mEPSC correlates to the degree of long-term depression in the CA1 region of the hippocampal slice

Prior synaptic or cellular activity influences degree or threshold for subsequent induction of synaptic plasticity, a process known as metaplasticity. Thus, the continual synaptic activity, spontaneous miniature excitatory synaptic current (mEPSC) may correlate to the induction of long-teen depression (LTD). Here, we recorded whole-cell EPSC and mEPSC alternately in the Schaffer-CA1 synapses in brain slice of young rats, and found that this recording configuration affected neither EPSC nor mEPSC. Low frequency stimulation (LFS) induced variable magnitudes of LTD. Remarkably, larger magnitudes of LTD were significantly correlated to smaller amplitude/lower frequency of the basal mEPSC. Furthermore, under the conditions reduced amplitude/frequency of the basal mEPSC by exposure to behavioral stress immediately before slice preparation or low concentration of calcium in bath solution, the magnitudes of LTD were still inversely correlated to mEPSC amplitude/frequency. These new findings suggest that spontaneous mEPSC may reflect functional and/or structural aspects of the synapses, the synaptic history ongoing metaplasticity. (C) 2005 Elsevier B.V. All rights reserved.

Long-term depression in rat CA1-subicular synapses depends on the G-protein coupled mACh receptors

The subiculum, which is the primary target of CA1 pyramidal neurons and sending efferent fibres to many brain regions, serves as a hippocampal interface in the neural information processes between hippocampal formation and neocortex. Long-term depression (LTD) is extensively studied in the hippocampus, but not at the CA1-subicular synaptic transmission. Using whole-cell EPSC recordings in the brain slices of young rats, we demonstrated that the pairing protocols of low frequency stimulation (LFS) at 3 Hz and postsynaptic depolarization of -50 mVelicited a reliable LTD in the subiculum. The LTD did not cause the changes of the paired-pulse ratio of EPSC. Furthermore, it did not depend on either NMDA receptors or voltage-gated calcium channels (VGCCs). Bath application of the G-protein coupled muscarinic acetylcholine receptors (mAChRs) antagonists, atropine or scopolamine, blocked the LTD, suggesting that mAChRs are involved in the LTD. It was also completely blocked by either the Ca2+ chelator BAPTA or the G-protein inhibitor GDP-beta-S in the intracellular solution. This type of LTD in the subiculum may play a particular role in the neural information processing between the hippocampus and neocortex. (c) 2005 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.

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

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

Exposure to chronic constant light impairs spatial memory and influences long-term depression in rats

Exposure to chronic constant light (CCL) influences circadian rhythms and evokes stress. Since hippocampus is sensitive to stress, which facilitates long-term depression (LTD) in the hippocampal CA1 area, we examined whether CCL exposure influenced hippoc

Opioid Withdrawal for 4 Days Prevents Synaptic Depression Induced by Low Dose of Morphine or Naloxone in Rat Hippocampal CA1 Area In Vivo

The formation of memory is believed to depend on experience- or activity-dependent synaptic plasticity, which is exquisitely sensitive to psychological stress since inescapable stress impairs long-term potentiation (LTP) but facilitates long-term depression (LTD). Our recent studies demonstrated that 4 days of opioid withdrawal enables maximal extents of both hippocampal LTP and drug-reinforced behavior; while elevated-platform stress enables these phenomena at 18 h of opioid withdrawal. Here, we examined the effects of low dose of morphine (0.5 mg kg(-1), i.p.) or the opioid receptor antagonist naloxone (1 mg kg(-1), i.p.) on synaptic efficacy in the hippocampal CA1 region of anesthetized rats. A form of synaptic depression was induced by low dose of morphine or naloxone in rats after 18 h but not 4 days of opioid withdrawal. This synaptic depression was dependent on both N-methyl-D-aspartate receptor and synaptic activity, similar to the hippocampal long-term depression induced by low frequency stimulation. Elevated-platform stress given 2 h before experiment prevented the synaptic depression at 18 h of opioid withdrawal; in contrast, the glucocorticoid receptor (GR) antagonist RU38486 treatment (20 mg kg(-1), s.c., twice per day for first 3 days of withdrawal), or a high dose of morphine reexposure (15 mg kg(-1), s.c., 12 h before experiment), enabled the synaptic depression on 4 days of opioid withdrawal. This temporal shift of synaptic depression by stress or GR blockade supplements our previous findings of potentially correlated temporal shifts of LTP induction and drug-reinforced behavior during opioid withdrawal. Our results therefore support the idea that stress experience during opioid withdrawal may modify hippocampal synaptic plasticity and play important roles in drug-associated memory. (C) 2009 Wiley-Liss, Inc.

Know thy neighbour: A normative theory of synaptic depression

Synapses exhibit an extraordinary degree of short-term malleability, with release probabilities and effective synaptic strengths changing markedly over multiple timescales. From the perspective of a fixed computational operation in a network, this seems like a most unacceptable degree of added variability. We suggest an alternative theory according to which short-term synaptic plasticity plays a normatively-justifiable role. This theory starts from the commonplace observation that the spiking of a neuron is an incomplete, digital, report of the analog quantity that contains all the critical information, namely its membrane potential. We suggest that a synapse solves the inverse problem of estimating the pre-synaptic membrane potential from the spikes it receives, acting as a recursive filter. We show that the dynamics of short-term synaptic depression closely resemble those required for optimal filtering, and that they indeed support high quality estimation. Under this account, the local postsynaptic potential and the level of synaptic resources track the (scaled) mean and variance of the estimated presynaptic membrane potential. We make experimentally testable predictions for how the statistics of subthreshold membrane potential fluctuations and the form of spiking non-linearity should be related to the properties of short-term plasticity in any particular cell type.

ESTIMATION OF THE RADIATION-INDUCED DAMAGE IN PTFE BY DEPRESSION OF THE MELTING AND CRYSTALLIZATION TEMPERATURES

The radiation induced depression of the melting and crystallization temperatures of PTFE irradiated at various temperatures followed by heat treatment at 380-degrees-C, and their relationship to structural changes, were investigated. The G(-units) values obtained in this work are different from those of samples which have not undergone heat treatment and seem to be more closely associated with radiation induced branched structures.

Hydrogeochemistry of formation water in relation to overpressures and fluid flow in the Qikou Depression of the Bohai bay basin, China

The Qikou Depression is the largest hydrocarbon bearing depression in the western part of the Bohai bay basin, dominated by fan delta and lacustrine strata with volcanic and volcaniclastic rocks. In this study, the formation pressures and hydrochemistry of the formation water in the Qikou depression are investigated. It is found that a significant overpressure occurs in the Dongying (Ed) Formation and the first member (Est), the second member (Es2), the third member (Es3) of the Shahejie Formation. The pressure coefficients commonly range from 1.2 to 1.6 with the highest pressure coefficient being 1.7. The analysis of hydrochemistry data shows that the whole depression is dominated by NaHCO3 water type. The concentration of total dissolved solid (TDS) ranges from 2.13 to 53.16 g/L and shows a distinct vertical variation of salinity and ion ratios. High salinity water (TDS> 10 g/L) occurs below a depth of 2500 m, which coincides with the presence of the overpressured system. However, the increasing trend of TDS is diminished below 3500 m because the generation of organic acids in Qikou Depression is inhibited in the presence of overpressure. The analysis of the relationship among different ions indicates that the present-day characteristics of the formation water result from the albitization of feldspar and the dissolution of sodium-rich silicate minerals and halite in the different hydrochemical and pressure systems. (C) 2009 Elsevier B.V. All rights reserved.