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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possible influence of the sleep-waking cycle on evoked neurotransmission and on the induction of long-term potentiation (LTP) and depression (LTD) was studied in the perforant path-granule cell system. Freely moving rats received a high-frequency stimulus train (8 bursts at 400 Hz) during slow-wave sleep (SWS), rapid eye movement (REM) sleep, and a still-alert (SAL) behavioral state. Trains applied during SAL and REM reliably elicited LTP of the excitatory postsynaptic potential (EPSP) slope, population spike height, and spike onset latency. Granule cell excitability was also enhanced, as indicated by a leftward shift of the EPSP-population spike (E-S) relation. In contrast, tetanization in SWS rarely produced 'classical' LTP and often failed to elicit any lasting change in field potentials. Furthermore, the following types of E-S change occurred almost exclusively after tetanization in SWS: (1) LTP of the EPSP accompanied by depression of the population spike, and (2) E-S potentiation without a change in EPSP. When LTP occurred, however, its magnitude was independent of the animal's behavioral state at the time of the train. In agreement with previous reports, the efficacy of low-frequency neurotransmission varied with behavioral state. A modulation index (MI) was introduced to quantify the difference between field potentials evoked in SAL and SWS. Interestingly, both the occurrence and magnitude of LTP were related to the strength of the MI, as determined in each rat before the train. After trains, the state-dependent modulation of transmission was maintained and was superimposed on LTP and LTD. The results suggest that synaptic plasticity is dynamically modulated during the sleep-wakefulness cycle.
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PMID:Synaptic plasticity in the hippocampus is modulated by behavioral state. 277 12

The present study evaluates whether the associative interactions between synapses that lead to long-term potentiation and depression (LTP and LTD) can occur between spatially segregated synapses of the medial and lateral temporodentate pathway of the rat. Coconditioning of crossed and ipsilateral pathways resulted in LTP of the crossed system only when the current sinks of the two conditioned pathways overlapped sufficiently. Likewise, conditioning of an ipsilateral pathway alone resulted in LTD of the crossed pathway only when those current sinks overlapped sufficiently. These observations support the idea that associative events that lead to LTP or LTD can be restricted to a local dendritic domain. The postsynaptic cell can therefore serve as more than one unit of integration for synaptic modification.
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PMID:Evidence that associative interactions between synapses during the induction of long-term potentiation occur within local dendritic domains. 335 84

Leukotriene D4 (LTD4) is the major constituent of slow-reacting substance of anaphylaxis (SRS-A). Cardiovascular depression and hypotensive shock represent the major manifestations that attend systemic anaphylaxis. To further evaluate the hemodynamic effects of LTD4, we measured blood pressure (BP), heart rate (HR) and blood flow (BF) (directional pulsed Doppler flowmeter) to different vascular beds (hindquarter, mesenteric and renal) of the urethane-anesthetized rat. LTD4 (3, 10 and 30 micrograms/kg, i.v.) caused a dose-dependent increase in BP: 15 +/- 3, 20 +/- 4 and 24 +/- 2 mm Hg, respectively, which was maximum after 2 min and returned to control level at 10 min; HR was not significantly altered. BF to different vascular beds was differentially altered: mesenteric (-59%) greater than hindquarter (-38%) greater than renal (-10%). Vascular resistance (VR) increased by 195, 85 and 40% in mesenteric, hindquarter and renal beds, respectively. Thyrotropin-releasing hormone (TRH) (2-5 mg/kg, i.v.) injected after LTD4 increased BP, reversed the decrease in BF and the increase in VR in the mesenteric and hindquarter vascular beds. These data suggest that LTD4 receptors are unevenly distributed in various vascular beds and that the splanchnic area is particularly vulnerable to anaphylaxis-induced ischemia. Furthermore, Thyrotropin Releasing Hormone (TRH) might be useful to antagonize the hemodynamic consequences mediated by SRS-A or leukotriene.
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PMID:Differential hemodynamic effects of leukotriene D4 in anesthetized rats: evaluation by directional pulsed Doppler technique. 385 95

The effect of activation of cholinergic receptors on long-term potentiation (LTP) in rat piriform cortex pyramidal cells was studied using extracellular and intracellular recordings in brain slice preparations. The functional role of this modulation was studied in a realistic network biophysical stimulation. Repetitive stimuli were applied in two paradigms: one in which the recorded cell was held at its resting potential and one in which synaptic activity was superimposed on a depolarizing pulse strong enough to evoke four action potentials. In the absence of cholinergic modulation, stimulation at 5 Hz induced LTP primarily in the second condition (13.7%, n = 6 out of 9, measured at 10 min after tetanus). When stimuli were applied in the presence of the muscarinic agonist carbachol (20 microM), LTP of greater amplitude was induced in both paradigms (resting: 41.5%, n = 11 out of 16, depolarized: 36%, n = 5 out of 7, measured at 10 min after tetanus). Increases in excitatory postsynaptic potential (EPSP) amplitudes in the presence of carbachol were gradual, starting at the time 5 Hz stimuli were applied and continuing until an action potential was evoked synaptically. In the presence of the NMDA receptor antagonist 2-amino-5-phosphonovaleric acid (APV), LTP could not be induced. The muscarinic antagonist atropine also prevented LTP induction in the presence of carbachol. Cholinergic modulation of synaptic plasticity was examined in a previously developed realistic biophysical network simulation. In simulations, use of a gradual rate of synaptic modification prevented excessive strengthening of synapses, which could cause interference between stored patterns. The effect of excess synaptic strengthening can be avoided by introducing activity dependent depression of synaptic strength. Coactivation of learning and depression rules results in a stable system where no interference occurs, at any rate of learning. Implementing the depression rule only during recall does not improve the network's performance. This implies that reduction in the strength of synaptic connections should occur in the presence of ACh, more than in normal conditions. We propose that two effects of ACh--enhancement of LTP and enhancement of LTD--should act together to increase the stability of the cortical network in the process of acquiring information.
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PMID:Cholinergic modulation of activity-dependent synaptic plasticity in the piriform cortex and associative memory function in a network biophysical simulation. 747 21

In standard protocols, the frequency of synaptic stimulation determines whether CA1 hippocampal synapses undergo long-term potentiation or depression. Here we show that during cholinergically induced theta oscillation (theta) synaptic plasticity is greatly sensitized and can be induced by a single burst (4 pulses, 100 Hz). A burst given at the peak of theta induces homosynaptic LTP; the same burst at a trough induces homosynaptic LTD of previously potentiated synapses. Heterosynaptic LTD is produced at inactive synapses when others undergo LTP. The synaptic modifications during theta require NMDA receptors and muscarinic receptors. The enhancement is cooperative and occludes with standard LTP. These results suggest that the similar bursts observed during theta rhythm in vivo may be a natural stimulus for inducing LTP/LTD.
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PMID:Bidirectional synaptic plasticity induced by a single burst during cholinergic theta oscillation in CA1 in vitro. 757 49

The long-term posttetanic modifications of the efficacy of excitatory synaptic connections were studied in auditory thalamo-cortical assemblies. We demonstrate that intracortical microstimulation--ICMS (high frequency pulses of 5 uA), which activated a small group of cortical neurons, produced long-term (at least 30 min) modifications (potentiation-LTP and depression-LTD) of the efficacy of excitatory monosynaptic transmission between numerous elements of thalamo-cortical network. Effectivity of "common input" also was potentiated or depressed. The amount of effective connections between neurons located in stimulated and nonstimulated loci of the cortex increased after ICMS. Some neurons in the network were favourable for inducing LTP. The efficacy of the synapses formed by terminals of one axon on different cells can be modified variously. The efficacy of the synapses formed by neurons from different loci of auditory cortex and MGB on the same target cell also can be modified variously.
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PMID:[Long-term changes in the efficiency of excitatory synaptic transmission in the thalamocortical networks evoked by microstimulation of the neocortex]. 759 29

The hippocampus and related structures are thought to be capable of 1) representing cortical activity in a way that minimizes overlap of the representations assigned to different cortical patterns (pattern separation); and 2) modifying synaptic connections so that these representations can later be reinstated from partial or noisy versions of the cortical activity pattern that was present at the time of storage (pattern completion). We point out that there is a trade-off between pattern separation and completion and propose that the unique anatomical and physiological properties of the hippocampus might serve to minimize this trade-off. We use analytical methods to determine quantitative estimates of both separation and completion for specified parameterized models of the hippocampus. These estimates are then used to evaluate the role of various properties and of the hippocampus, such as the activity levels seen in different hippocampal regions, synaptic potentiation and depression, the multi-layer connectivity of the system, and the relatively focused and strong mossy fiber projections. This analysis is focused on the feedforward pathways from the entorhinal cortex (EC) to the dentate gyrus (DG) and region CA3. Among our results are the following: 1) Hebbian synaptic modification (LTP) facilitates completion but reduces separation, unless the strengths of synapses from inactive presynaptic units to active postsynaptic units are reduced (LTD). 2) Multiple layers, as in EC to DG to CA3, allow the compounding of pattern separation, but not pattern completion. 3) The variance of the input signal carried by the mossy fibers is important for separation, not the raw strength, which may explain why the mossy fiber inputs are few and relatively strong, rather than many and relatively weak like the other hippocampal pathways. 4) The EC projects to CA3 both directly and indirectly via the DG, which suggests that the two-stage pathway may dominate during pattern separation and the one-stage pathway may dominate during completion; methods the hippocampus may use to enhance this effect are discussed.
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PMID:Hippocampal conjunctive encoding, storage, and recall: avoiding a trade-off. 770 10

It has been demonstrated that long-term posttetanic heterosynaptic depression (LTHD), manifested in the form of a prolonged decrease in the probability of monosynaptic responses of the cell to stimulation of that afferent pathway which was not activated during conditioning tetanization of another input, takes place in the neocortex, as it does in the hippocampus. LTHD is characterized by such properties as its long-term character, cooperativity, and nonspecificity of input. LTHD in the nonconditioned input and long-term posttetanic potentiation or long-term posttetanic homosynaptic depression in the conditioned input may develop both in parallel or independantly of one another. It is hypothesized on the basis of the results obtained that LTHD (as is the case with LTP and LTD) is a calcium-dependant phenomenon, and that the achievement of a specific level of depolarization of the membrane in the region of the disposition of the inactive synapses is required for its occurrence. "Contrasting," i.e., a relative increase in the efficiency of transmission in the activating synapse, may be effected through LTHD; LTHD may be one of the mechanisms underlying forgetting.
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PMID:Neurobiology of the integrative activity of the brain: some properties of long-term posttetanic heterosynaptic depression in the motor cortex of the cat. 771 72

To investigate the function of the autophosphorylated form of CaMKII in synaptic plasticity, we generated transgenic mice that express a kinase that is Ca2+ independent as a result of a point mutation of Thr-286 to aspartate, which mimics autophosphorylation. Mice expressing the mutant form of the kinase show an increased level of Ca(2+)-independent CaMKII activity similar to that seen following LTP. The mice nevertheless exhibit normal LTP in response to stimulation at 100 Hz. However, at lower frequencies, in the range of 1-10 Hz, there is a systematic shift in the size and direction of the resulting synaptic change in the transgenic animals that favors LTD. The regulation of this frequency-response function by Ca(2+)-independent CaMKII activity seems to account for two previously unexplained synaptic phenomena, the relative loss of LTD in adult animals compared with juveniles and the enhanced capability for depression of facilitated synapses.
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PMID:CaMKII regulates the frequency-response function of hippocampal synapses for the production of both LTD and LTP. 778 Oct 66

Extra- and intracellular recordings in slices were used to examine what types of synaptic plasticity can be found in the core of the nucleus accumbens, and how these forms of plasticity may be modulated by dopamine. Stimulus electrodes were placed at the rostral border of the nucleus accumbens in order to excite primarily infralimbic and prelimbic afferents, as was confirmed by injections of the retrograde tracer fluoro-gold. In extracellular recordings, tetanization induced long-term potentiation (LTP) of the population spike in 20 out of 53 slices. The presynaptic compound action potential did not change following LTP induction. For the intracellularly recorded excitatory postsynaptic potentiation, three types of synaptic plasticity were noted: long-term potentiation (16 out of 54 cells), decremental potentiation (eight cells) and long-term depression (LTD; six cells). No correlation was found between the occurrence of potentiation or depression and various parameters of the tetanic depolarization (e.g. peak voltage, integral under the curve). The N-methyl-D-aspartate receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid (50 microM; D-AP5) reduced, but did not completely prevent, the induction of LTP. The incidence of LTD was not markedly affected by D-AP5. No difference in LTP was found when comparing slices bathed in dopamine (10 microM) and controls. Likewise, slices treated with a mixture of the D1 receptor antagonist Sch 23390 (1 microM) and the D2 antagonist S(-)-sulpiride (1 microM) generated a similar amount of LTP as controls. In conclusion, both LTP and LTD can be induced in a key structure of the limbic-innervated basal ganglia. LTP in the nucleus accumbens strongly depends on N-methyl-D-aspartate receptor activity, but is not significantly affected by dopamine.
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PMID:Synaptic plasticity in an in vitro slice preparation of the rat nucleus accumbens. 790 83


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