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Results for “Long-Term Synaptic Depression”

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At least 19 recordsLinked to original sources
PubMed1992

Priming of associative long-term depression in the dentate gyrus by theta frequency synaptic activity.

Associative long-term synaptic depression (LTD) was investigated utilizing negatively correlated activity patterns in the medial and lateral perforant path inputs to the dentate gyrus in anesthetized rats. Normally only nonassociative, or heterosynaptic, LTD is elicited in naive pathways. We report here, however, that associative LTD in the lateral path is readily induced after being "primed" by a brief period of lateral path synaptic activity at a theta rhythm frequency (5 Hz). Priming of associative LTD lasts at least 2 hr and is not seen following priming activity at non-theta frequencies (1 and 15 Hz). N-methyl-D-aspartate receptor activation is critical for establishing the priming effect, but not for the subsequent induction of the associative LTD. These data suggest that theta rhythm activity in the dentate gyrus may predispose the system to a specific form of synaptic plasticity, associative LTD.

Animals↗
PubMed1978

Long-term potentiation and depression of synaptic responses in the rat hippocampus: localization and frequency dependency.

1. The consequences of repetitive activation of excitatory synaptic inputs to the CA1 pyramidal cells of rat hippocampus have been studied using in vitro techniques. 2. Single stimulation trains of 100 pulses at rates of 5-100/sec resulted in potentiation of population spike amplitudes lasting the duration of a 5 min test period in thirty-four out of thirty-five cases. Trains of 100 pulses delivered at 1/sec resulted in depression of the stimulated pathway in ten out of twelve experiments. 3. Responses to test stimulation of other excitatory inputs to the same cell population were depressed following conditioning trains at frequencies in the range 1-100/sec. Depression was seen both in the population spike amplitude (reflecting synchronous cell discharge) as well as the extracellularly recorded population e.p.s.p., and appeared to be maximal at lower frequencies. 4. Trains of antidromic stimulation of the CA1 cell population produced subsequent decreases in synaptically evoked responses, indicating that repetitive firing of pyramidal neurones or interneurones do not cause potentiation, but may be involved in heterosynaptic depression. 5. The results suggest that potentiation and heterosynaptic depression arise from different mechanisms, and that potentiation is confined to the set of terminals activated by a conditioning train, whereas the depression is generalized to the whole neurone.

Animals↗
PubMed1992

Synaptic excitation produces a long-lasting rebound potentiation of inhibitory synaptic signals in cerebellar Purkinje cells.

Persistent changes in synaptic efficacy are thought to underlie the formation of learning and memory in the brain. High-frequency activation of an afferent excitatory fibre system can induce long-term potentiation, and conjunctive activation of two distinct excitatory synaptic inputs to the cerebellar Purkinje cells can lead to long-term depression of the synaptic activity of one of the inputs. Here we report a new form of neural plasticity in which activation of an excitatory synaptic input can induce a potentiation of inhibitory synaptic signals to the same cell. In cerebellar Purkinje cells stimulation of the excitatory climbing fibre synapses is followed by a long-lasting (up to 75 min) potentiation of gamma-aminobutyric acid A (GABAA) receptor-mediated inhibitory postsynaptic currents (i.p.s.cs), a phenomenon that we term rebound potentiation. Using whole-cell patch-clamp recordings in combination with fluorometric video imaging of intracellular calcium ion concentration, we find that a climbing fibre-induced transient increase in postsynaptic calcium concentration triggers the induction of rebound potentiation. Because the response of Purkinje cells to bath-applied exogenous GABA is also potentiated after climbing fibre-stimulation with a time course similar to that of the rebound potentiation of i.p.s.cs, we conclude that the potentiation is caused by a calcium-dependent upregulation of postsynaptic GABAA receptor function. We propose that rebound potentiation is a mechanism by which in vivo block of climbing fibre activity induces an increase in excitability in Purkinje cells. Moreover, rebound potentiation of i.p.s.cs is a cellular mechanism which, in addition to the long-term depression of parallel fibre synaptic activity, may have an important role for motor learning in the cerebellum.

Animals↗
PubMed1992

Intracellular injection of Ca2+ chelators blocks induction of long-term depression in rat visual cortex.

In a variety of brain structures repetitive activation of synaptic connections can lead to long-term potentiation (LTP) or long-term depression (LTD) of synaptic transmission, and these modifications are held responsible for memory formation. Here we examine the role of postsynaptic Ca2+ concentration in the induction of LTD in the neocortex. In layer III cells of the rat visual cortex, LTD can be induced by tetanic stimulation of afferent fibers ascending from the white matter. We show that LTD induction is reliably blocked by intracellular injection of either EGTA or BAPTA [bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetate], two different Ca2+ chelators. This confirms that the processes underlying the induction of LTD in neocortex are located postsynaptically and indicates that they depend on intracellular Ca2+ concentration. Thus, both LTP and LTD induction appear to involve calcium-mediated processes in the postsynaptic neuron. We propose that LTD is caused by a surge of calcium either through voltage-gated Ca2+ conductances and/or by transmitter-induced release of calcium from intracellular stores.

Animals↗
PubMed1978

Cellular analysis of long-term habituation of the gill-withdrawal reflex of Aplysia californica.

Long-term habituation training in Aplysia californica produces a profound depression in the efficacy of synaptic transmission between mechanoreceptor neurons and gill motor neurons. This depression persists for more than 3 weeks. Thus a critical synaptic site for plasticity underlying long-term habituation is the same as that for short-term habituation. For this simple form of learning, short- and long-term memory share a common locus and aspects of a common mechanism: synaptic depression.

Animals↗
PubMed1992

[Tachykinins in the central mechanisms of biological motivation].

The studies have indicated that tachykinin peptides are selectively involved in the central mechanisms of biological motivations. The injections of tachykinins suppress food motivation, salt appetite, to a lesser extent modifying defensive behaviour. Neuropeptides, including tachykinins, affect the prompt induction of early genes, which in turn enables a neuron to transform a short-term synaptic stimulation to long-term changes of synaptic sensitivity.

Animals↗
PubMed2026

AAV-mediated CBLN1 replacement rescues hereditary ataxia caused by bi-allelic CBLN1 variants.

Cbln1 is a secreted synaptic organizer required for parallel fiber-Purkinje cell (PF-PC) synapse integrity, climbing fiber (CF) refinement, and cerebellar motor learning but has not previously been implicated in human disease. We identified bi-allelic CBLN1 missense variants (A63P and Y112C) in two unrelated families with early-onset cerebellar ataxia accompanied by oculomotor abnormalities, cerebellar atrophy, and variable cognitive delay. In heterologous cells, both variants showed reduced steady-state protein abundance, impaired maturation through the early secretory pathway, and little or no detectable secretion, resulting in markedly reduced extracellular CBLN1 availability. Consistently, cerebellar granule cells expressing CBLN1-Y112C failed to induce excitatory synapses onto glutamate receptor δ2 (GluD2)-expressing cells in vitro. A knockin mouse harboring Y112C lacked synaptic Cbln1 and recapitulated key features of Cbln1 deficiency, including disrupted PF-PC synapse organization, persistent CF multi-innervation, impaired PF-PC transmission, and long-term depression, and deficits in motor coordination and oculomotor learning. Notably, systemic delivery of an astrocyte-targeted adeno-associated virus expressing wild-type CBLN1 in adult mutant mice restored synaptic CBLN1 localization, cerebellar synaptic function, plasticity, and behavior. These findings establish CBLN1 deficiency as a cause of hereditary ataxia and identify extracellular CBLN1 replacement as a therapeutic strategy for a reversible cerebellar synaptopathy.

CBLN1↗
PubMed1979

Sensitization in Aplysia: restoration of transmission in synapses inactivated by long-term habituation.

Long-term habituation of a simple withdrawal reflex in Aplysia leads to an inactivation of synaptic transmission between identified sensory and gill motor neurons that persists for more than 3 weeks. A single sensitizing stimulus rapidly reactivates both the depressed behavioral response and the inactivated synaptic transmission. Thus sensitization, a simple competitive form of learning, provides a mechanism whereby changing environmental demands can rapidly override the long-term memory of habituation.

Animals↗
PubMed1992

Longevity of synaptic depression in the hippocampal dentate gyrus.

This study used urethane-anesthetized rats to investigate the longevity of heterosynaptically evoked depression of the monosynaptic response generated by synapses between entorhinal cortical (EC) afferents and the cells of the dentate gyrus (DG). Brief, high-frequency activation of the converging ipsilateral EC-DG input depressed the synaptic response of the contralateral EC-DG synapses without prior experimentally induced potentiation. This depression lasted for hours. Such observations are consistent with a role for heterosynaptically induced long-term depression in the encoding functions of synapses.

Animals↗
PubMed1992

Maintenance of long-term adaptation of synaptic transmission requires axonal transport following induction in an identified crayfish motoneuron.

Motoneurons can adapt to altered levels of electrical activity by effecting semi-permanent changes in their neuromuscular synaptic physiology. In the present study, we tested the hypothesis that maintenance of activity-dependent long-term adaptation of synaptic transmission in a crayfish abdominal extensor motoneuron (phasic axon 3) required axonal transport following induction. Intact crayfish were chronically wired for periodic in vivo stimulation of axon 3. Periodic unilateral stimulation for 3-5 consecutive days (2 h/day) induced long-term adaptation (LTA) of neuromuscular synaptic transmission in axon 3. Initial EPSP amplitudes (measured at 0.1 Hz) were significantly reduced to approximately 40% of contralateral control amplitudes over a 7-day poststimulation period. Additionally, synaptic depression during 5 Hz test stimulation of axon 3 was significantly less in chronically stimulated neurons: excitatory postsynaptic potential (EPSP) amplitudes measured after 20 min of 5 Hz test stimulation (final EPSPs) were significantly larger in conditioned neurons than in unstimulated controls. The depression of initial EPSP amplitudes persisted for 7 days postinduction, while the increased synaptic stamina persisted for 4 days but was absent at 7 days postinduction. Axotomy of axon 3 following induction of LTA had no effect on long-term maintenance of the activity-induced reduction in initial EPSP amplitudes. Initial EPSP amplitudes in conditioned, axotomized neurons were still reduced to 42% of control amplitudes over the 7-day postinduction period. In contrast, postinduction axotomy of axon 3 elicited an accelerated decay of the enhanced synaptic stamina. Following axotomy, final EPSP amplitudes were significantly larger in conditioned neurons for only 1 day poststimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1976

Long term changes in augmentation, potentiation, and depression of transmitter release as a function of repeated synaptic activity at the frog neuromuscular junction.

1. End-plate potentials (e.p.p.s) were recorded from frog neuromuscular junctions under conditions of low quantal content to study the long-term effects of repeated synaptic activity on transmitter release. 2. The nerve terminal was presented with 30-100 successive conditioning-testing trials applied once every 7-10 min over a 4-16 hr perod. Each conditioning-testing trial consisted of a 200-600 impulse conditioning train followed by a series of testing impulses. The magnitudes and time constants of decay of augmentation and potentiation following each successive conditioning train were determined by measuring the e.p.p. amplitudes resulting from the testing impulses. 3. The magnitude of augmentation immediately following the conditioning trains increased an average of 3-4 times (range 1-20) with sucessive trials. 4. As the magnitude of augmentation increased with successive trials the decay of augmentation deviated from a simple exponential, decaying faster immediately after the conditioning train. This faster decay led to a 20% decrease with successive trials in estimates of the time constant obtained from the first 10 or 20 sec of the decay of augmentation. The deviation of the decay of augmentation from a simple exponential could be accounted for if augmentation is related to the 4th power of some substance which decays with a simple exponential time course. Some alternative explantations for the non-exponential decay of augmentation are also discussed. 5. The magnitude of potentiation increased or decreased about 25% with successive trials. 6. The time constant characterizing the decay of potentiation inceased an average of 1-5 times (range 0-8-5 times) with successive trials. 7. The increase in the magnitude of augmentation with successive trials was accompanied by a similar increase in the magnitude of the e.p.p. amplitudes during the conditioning trains, suggesting that augmentation develops during the conditioning train. In some preparatons augmentation appeared to be the major factor acting to increase e.p.p. amplitudes during the conditioning train, having a greater effect than facilitation or potentiation. 8. If a sufficiently large number of successive trials were applied, a depression of e.p.p. amplitudes developed during the conditioning trains and estimates of the magnitude of potentiation following the depressed conditioning trains were reduced...

Animals↗
PubMed2026

Altered Excitation-Inhibition Balance and mGluR1/5-Driven Plasticity in the Motor Cortical Surface in a Rat Model of Parkinson's Disease.

Parkinson's disease (PD) is characterized by progressive dopaminergic degeneration and maladaptive motor cortical plasticity. However, the cellular pathways underlying cortical surface activity in the primary motor cortex (M1) remain unclear, despite serving as a potential target for electrotherapy. We investigated the excitatory-inhibitory (E-I) balance and synaptic plasticity of superficial M1 circuits in a unilateral 6-hydroxydopamine (6-OHDA)-induced rat model of PD. Using extracellular local field potential and whole-cell patch recordings from the contralateral and ipsilateral M1 hemispheres of hemi-parkinsonian rats, we observed a significantly elevated field excitatory postsynaptic potential (fEPSP) input-output function but unchanged intrinsic neuronal excitability in the M1 superficial layer. An altered relative contribution between alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)- and N-methyl-D-aspartate receptor (NMDAR)-mediated transmission was reflected by a significantly increased AMPA/NMDA ratio. Markedly reduced inhibitory synaptic tone was also evidenced by the decreased amplitude and frequency of spontaneous inhibitory postsynaptic currents (sIPSCs), supporting an E-I imbalance favoring excitation in PD. Furthermore, group I metabotropic glutamate receptor (mGluR1/5)-dependent long-term depression (LTD) was abolished in the ipsilateral PD hemisphere, whereas NMDAR-dependent LTD remained intact. In summary, dopamine depletion appears to enhance network excitation and disrupt mGluR1/5-mediated control of M1 surface circuitry. Our findings identify altered cortical surface mGluR-dependent plasticity in the hemi-parkinsonian model; however, the relationship between these electrophysiological alterations and individual motor outcomes remains to be determined.

Animals↗
PubMed1976

Tardive dyskinesia and depressive illness.

Tardive dyskinesia has been regarded as a long-term complication of neuroleptic administration to patients with the diagnosis of schizophrenia. However, nine of the first fourteen patients evaluated for an investigation of tardive dyskinesia met diagnostic criteria for depression. Neuroleptics produce blockade of post-synaptic dopaminergic receptors. Tardive dyskinesia occurs when neuroleptics are discontinued, and is regarded as a manifestation of super-sensitive post-synaptic dopaminergic receptors. Tardive dyskinesia occurs when neuroleptics are discontinued, and is regarded as a manifestation of super-sensitive post-synaptic dopaminergic receptors. Chronically decreased neurotransmission in the synapse of a patient with depression may contribute to the development of a super-sensitive receptor and could explain the high proportion of patients with depression seen in this sample of patients with tardive dyskinesia.

Antidepressive Agents, Tricyclic↗
PubMed1975

[Short and long term depression of neuromuscular transmission in crayfish].

Following single excitation of the abdominal giant motoneuron of crayfish, an important depression of neuro-muscular transmission is observed for about 15 mn. The time course of recovery is not modified even after low frequency (1/30 Hz) repetitive stimulation. Recovery curves obtained for different Mg++ concentration in physiological solutions show two phases of depression: short-term depression which is largely reduced in high Mg++ concentrations - thus probably depending on transmitter depletion in motoneuron terminals - long-term depression which is not modified by changing Mg++ concentration and seems to be independent of depletion.

Abdomen↗
PubMed1978

Further evidence for a change in central alpha-adrenergic receptor sensitivity after withdrawal from long-term haloperidol treatment.

Phenoxybenzamine, FLA-63 and alpha-MT produced less locomotor depression in mice withdrawn for 4 days from a 21 day treatment with haloperidol than that produced in vehicle-treated animals. There were no differences between the two groups when challenged with yohimbine or phentolamine. The data support the hypothesis that central alpha-adrenergic receptors had become supersensitive and suggest that the sensitivity changes are restricted to post-synaptic receptors.

Animals↗
PubMed1979

[Dopa and dopamine agonists in depression (author's transl)].

Following a summary of the functional organisation of the ascending dopamine systems, the pharmacology of the dopamine synaptic receptors is considered. The stress is placed upon the differences induced by dopamine agonists during short-term and long-term treatment. In this connection, recent ideas on the heterogeneous nature of the dopamine receptors, on their specificity and on their functional role will be discussed. The dopaminergic action of certain antidepressants will be studied by analysing the different types of activity: presynaptic release, direct pre- or post-synaptic agonism. The role of dopaminergic transmission in depression of mood is considered finally on the basis of clinico-biochemical correlations. Finally, dopaminergic activity is linked with the other possible changes in cerebral monoamines by drafting a table of the interactions between the neurotransmitters.

Animals↗
PubMed1979

Heterosynaptic postactivation potentiation in hippocampal CA 3 neurons: long-term changes of the postsynaptic potentials.

CA 3 neurons were excited synaptically by stimulation in the dentate hilus and the stratum radiatum of CA 1 in guinea pig hippocampal slices. Following repetitive stimulation (10--20 c/s, 10 s) of either stimulation site, the amplitudes of orthodromic population spikes or the probability of unitary discharges increased. Changes of the intracellularly recorded potentials were either (a) increased EPSP amplitudes associated with decreased IPSP amplitudes, or (b) increased IPSP amplitudes. A cell showing enhanced IPSPs after repetitive activation could respond with increased EPSP amplitudes and decreased IPSP amplitudes upon further repetitive activation. The potentiation, which was always preceded by a 5--10 min depression, lasted up to 3 h. This potentiation was heterosynaptic, since the responses to the non-stimulated input also changed and since the inputs were found to excite the pyramidal cells through separate synapses in double shock experiments. The heterosynaptic mode of the potentiation as well as the changes of the IPSPs indicate that not only the excitatory pathway but also the inhibitory pathway must be considered in explaining postactivation potentiation in this hippocampal field.

Animals↗