Long-Term Synaptic Potentiation

Brown, Thomas H.; Chapman, Paul F.; Kairiss, Edward W.; Keenan, Claude L.

doi:10.1126/science.2903551

Cited by 396 publications

(149 citation statements)

References 76 publications

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“…In many types of neurons, Ca 2ϩ entry through NMDA receptors is a critical step for LTP induction (39). Consistent with this observation, we found that addition of the NMDA receptor antagonist 2-amino-5-phosphonopentanoic acid (AP5; 100 M) to the artificial cerebrospinal fluid (aCSF) shortly before and during BLA-cortex pairings prevented LTP induction (114.6 Ϯ 11.2%, P ϭ 0.27; n ϭ 5; Fig.…”

Section: Resultssupporting

confidence: 67%

NMDA-dependent facilitation of corticostriatal plasticity by the amygdala

Popescu

Saghyan

Paré

2007

Proc. Natl. Acad. Sci. U.S.A.

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Emotions generally improve memory, and the basolateral amygdala (BLA) is believed to mediate this effect. After emotional arousal, BLA neurons increase their firing rate, facilitating memory consolidation in BLA targets. The enhancing effects of BLA activity extend to various types of memories, including motor learning, which is thought to involve activity-dependent plasticity at corticostriatal synapses. However, the underlying mechanisms are unknown. Here we show that the NMDA-to-AMPA (␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) ratio is nearly twice as high at BLA as compared with cortical synapses onto principal striatal neurons and that activation of BLA inputs greatly facilitates long-term potentiation induction at corticostriatal synapses. This facilitation was NMDA-dependent, but it occurred even when BLA and cortical stimuli were 0.5 s apart during long-term potentiation induction. Overall, these results suggest that BLA activity opens long time windows during which the induction of corticostriatal plasticity is facilitated.basolateral ͉ emotion ͉ memory ͉ synaptic plasticity

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Section: Resultssupporting

confidence: 67%

NMDA-dependent facilitation of corticostriatal plasticity by the amygdala

Popescu

Saghyan

Paré

2007

Proc. Natl. Acad. Sci. U.S.A.

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“…Perturbation of Ca 2+ signalling can promote alterations in neurosecretion, affect cell differentiation and plasticity and, eventually, cause cell death, necrosis or apoptosis (Suarez, 1984;Meldolesi and Ceccarelli, 1988;Brown et al, 1988;Choi, 1989. In a previous study, we showed that exposure of PC12 cells to low Hg 2+ concentra- tions (0.3 ± 0.5 mM) increased L-type Ca 2+ channel conductance and potentiated NGF-induced differentiation (Rossi et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

Inorganic mercury modifies Ca2+ signals, triggers apoptosis and potentiates NMDA toxicity in cerebellar granule neurons

et al. 1997

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, CGCs underwent apoptosis, which was identified by the cleavage of DNA into large (700 ± 50 kbp) and oligonucleosomal DNA fragments, and by the appearance of typical apoptotic nuclei. Combined treatment with 0.1 ± 0.3 mM Hg 2+ and a sublethal NMDA concentration (50 mM) potentiated DNA fragmentation and apoptotic cell death. When the exposure to Hg 2+ was carried out in Ca 2+ -free media or in the presence of Ca 2+ channel blockers (L-type or NMDA-R antagonists), the effects on signalling and apoptosis were prevented. Our results suggest that very low Hg 2+ concentrations can trigger apoptosis in CGCs by facilitating Ca 2+ entry through membrane channels.

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“…[9][10][11]. The induction of one form of LTP requires an increase in the [Ca"] at a postsynaptic site (12,13).…”

mentioning

confidence: 99%

Biophysical model of a Hebbian synapse.

Zador

Koch

Brown

1990

Proc. Natl. Acad. Sci. U.S.A.

212

126

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We present a biophysical model of electrical and Ca2' dynamics following activation of N-methyl-Daspartate (NMDA) receptors located on a dendritic spine. The model accounts for much of the phenomenology of the induction of long-term potentiation at a Hebbian synapse in hippocampal region CAI. (12,13). This increase is thought to be mediated by Ca>2 influx through the N-methyl-D-aspartate (NMDA) receptor-gated channel (13,14). Because the channel requires both ligand binding and postsynaptic depolarization for activation, it is ideally suited to contribute to the interactive requirement (4) for a Hebbian synapse.We have been interested in the role of the dendritic spine in LTP induction (9,11,15) and have constructed a biophysical model of electrical and Ca>2 dynamics in a spine after activation of NMDA receptors. Computer simulations indicate that the model can account for much of the known phenomenology of LTP induction at a Hebbian synapse in the CA1 region of the hippocampus. The results suggest that the microphysiology of the spine plays a critical role in the induction of this form of LTP. MODELThe biophysical mechanism of LTP induction has been best studied at the Schaffer collateral/commissural inputs to pyramidal cells of the CA1 region of the rodent hippocampus in the in vitro brain slice preparation. At least two pharmacologically distinguishable receptors mediate the excitatory postsynaptic response in this system. NMDA receptors mediate a slow current (16) with a substantial Ca2" component. The associated channel is voltage-dependent due to block byMg2`that is relieved by membrane depolarization (17-19).Non-NMDA receptors mediate a more rapid current with a negligible Ca`component.We simulated Ca`influx, transport, and buffering following activation of NMDA receptor-gated channels located on a spine head. The model (Fig. 1) consisted of separate electrical and Ca2+ components (15). The equations describing electrical and chemical dynamics were advanced independently and at the end of each time step electrical current was converted to ionic flux through Faraday's constant. These equations were discretized and then solved using alternating implicit-explicit steps (20, 21). Spine and Synapse. Total synaptic current (Fig. 1) was the sum of separate NMDA and non-NMDA components. An alpha function (22), I(t) = (Esyn -Vm) Kgpt exp(-t/tp), [1] was used for the non-NMDA current, with K = e/tp, e the base of the natural logarithm, tp = 1.5 msec, Esyn = 0 mV, and the peak conductance gp = 0.5 nS (9,23 tTo whom reprint requests should be addressed. 6718The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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Long-Term Synaptic Potentiation

Cited by 396 publications

References 76 publications

NMDA-dependent facilitation of corticostriatal plasticity by the amygdala

NMDA-dependent facilitation of corticostriatal plasticity by the amygdala

Inorganic mercury modifies Ca2+ signals, triggers apoptosis and potentiates NMDA toxicity in cerebellar granule neurons

Biophysical model of a Hebbian synapse.

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