Changes in reliability of synaptic function as a mechanism for plasticity

Stevens, Charles F.; Wang, Yanyan

doi:10.1038/371704a0

Cited by 340 publications

(254 citation statements)

References 16 publications

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“…2f). These properties of the induction of LTD agree with those previously described for glutamatergic synapses in hippocampal cultures 26 and slices [28][29][30][31][32] . The properties of GABAergic LTD remain to be further characterized.…”

Section: Induction Of Ltdsupporting

confidence: 89%

Propagation of activity-dependent synaptic depression in simple neural networks

Fitzsimonds

Song

Poo

1997

Nature

164

123

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Triple whole-cell recordings from simple networks of cultured hippocampal neurons show that induction of long-term depression at glutamatergic synapses is accompanied by a back propagation of depression to input synapses on the dendrite of the presynaptic neuron. The depression also propagates laterally to divergent outputs of the presynaptic neuron and to convergent inputs on the postsynaptic neuron. There is no forward propagation of depression to the output of the postsynaptic neuron and no presynaptic propagation accompanying long-term depression at GABAergic synapses. Activity-induced synaptic modification is therefore not restricted to the activated synapse, but selectively propagates throughout the neural network.The development and plasticity of the nervous system involve activity-dependent modification of synaptic connections 1-3 . Longterm potentiation (LTP) and long-term depression (LTD) of central synapses induced by repetitive activity in various regions of the brain have been implicated as the cellular mechanisms that underlie learning and memory [4][5][6][7] . These modifications are known to be input-specific, so only activated pathways are affected. But within the vicinity of activated pathways, other non-activated synapses also become modified, leading to more distributed synaptic modifications within a neural network. For example, LTP generated at one synaptic input to a CA1 hippocampal neuron was found to spread to adjacent synapses on the same or on a different postsynaptic neuron [8][9][10][11] and to result in LTD in more distant neurons 12,13 . Such spread of synaptic modification appears to depend on membranepermeable or secreted factors released by the activated synapse, and the extent of influence on other synapses depends on their physical proximity. On the other hand, the spread of synaptic modification can also be mediated by signalling within the neuron. On the postsynaptic side, LTP at one synaptic input can result in heterosynaptic modification of other convergent inputs [14][15][16][17][18][19] . On the presynaptic side, changes may spread through the cytoplasm to other divergent outputs. In Xenopus nerve-muscle cultures, LTD induced at one neuromuscular synapse can propagate to other synapses made by the same neuron onto other myocytes, apparently by signalling within the neuronal cytoplasm 20 . A similar presynaptic cytoplasmic mechanism may also account for the spread of shortterm depression of inhibitory synapses observed in cerebellar slices 21 .Here we find that induction of LTD at glutamatergic synapses within small networks of cultured hippocampal neurons is accompanied by a retrograde spread of depression to synapses on the dendrites of the presynaptic neurons (back propagation). The depression also spreads laterally to synapses made by divergent outputs of the presynaptic neuron (presynaptic lateral propagation) or to convergent inputs on the postsynaptic neurons (postsynaptic lateral propagation). In contrast, there was no forward propagation of depression to output s...

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Section: Induction Of Ltdsupporting

confidence: 89%

Propagation of activity-dependent synaptic depression in simple neural networks

Fitzsimonds

Song

Poo

1997

Nature

164

123

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“…Consistent with these findings, changes in quantal amplitude as well as frequency associated with LTP and LTD have been detected using analysis of Sr 2ϩ -induced asynchronous quantal release in the CA1 region of hippocampus (Oliet et al, 1996(Oliet et al, , 1997. It should be noted, however, that a presynaptic expression mechanism has also been suggested for CA1 LTP and LTD (Malinow and Tsien, 1990;Bolshakov and Siegelbaum, 1994;Stevens and Wang, 1994;Kullmann and Siegelbaum, 1995). In contrast to hippocampal LTP, analysis of asynchronous quanta at corticostriatal synapses indicates that striatal LTD involves a decrease in quantal frequency without any significant change in quantal amplitude.…”

Section: Discussionsupporting

confidence: 66%

“…It should be noted, however, that more than one form of LTD appears to exist in the hippocampal CA1 region (Oliet et al, 1997). A form of LTD that depends on NMDA receptor activation for its initiation can be induced at these same hippocampal synapses and appears to have a postsynaptic locus of expression (Stevens and Wang, 1994;Selig et al, 1995;Oliet et al, 1996Oliet et al, , 1997.…”

Section: Discussionmentioning

confidence: 99%

Decreased Frequency But Not Amplitude of Quantal Synaptic Responses Associated with Expression of Corticostriatal Long-Term Depression

Choi¹,

Lovinger

1997

J. Neurosci.

102

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We have investigated the site of expression of striatal long-term synaptic depression (LTD) using analysis of Sr 2ϩ -induced asynchronous release of quanta from stimulated synapses. The cumulative amplitude distribution of Sr 2ϩ -induced asynchronous synaptic responses overlaps with that of miniature EPSCs (mEPSCs), suggesting that Sr 2ϩ -induced asynchronous responses are quantal. Quantal amplitude at stimulated synapses is not significantly altered after LTD induction, whereas quantal frequency decreases after LTD induction. The decrease in quantal frequency is prevented when LTD expression is blocked by dialyzing 10 mM EGTA into the postsynaptic neuron. Our findings are most consistent with the idea that expression of striatal LTD involves decreased neurotransmitter release with no change in quantal amplitude, despite the fact that induction of striatal LTD involves postsynaptic mechanisms.

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“…To assess presence of multiquantal release during the minimal-like stimulation, AMPAR currents elicited by paired stimuli were recorded from a subset of neurons (eight from control and nine from OF mice). When release is multiquantal, changes in failure rate of response from the first to the second pulse Emotional trauma generates silent synapses W Ito et al are expected to negatively correlate with changes in response potency (Stevens and Wang, 1994). Despite the failure rate of the second response being higher on average and in majority of cells (13 out of 17) (first: 0.61 ± 0.05, second: 0.69 ± 0.05, n = 17, P = 0.009, paired t-test) (Figure 3c), there were no significant differences between potencies of the first and second responses (P = 0.58, paired t-test) (Figure 3b and c) and no correlations between the ratio of potencies at the first and second stimulation and the ratio of failure rates (R 2 = 0.037).…”

Section: Of Alters Glutamatergic Transmission In the Input From Dmpfcmentioning

confidence: 99%

Observation of Distressed Conspecific as a Model of Emotional Trauma Generates Silent Synapses in the Prefrontal-Amygdala Pathway and Enhances Fear Learning, but Ketamine Abolishes those Effects

Ito

Erişir

Morozov

2015

Neuropsychopharmacol

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Witnessing pain and distress in others can cause psychological trauma and increase odds of developing PTSD in the future, on exposure to another stressful event. However, the underlying synaptic process remains unknown. Here we report that mice exposed to a conspecific receiving electrical footshocks exhibited enhanced passive avoidance (PA) learning when trained 24 h after the exposure. The exposure activated neurons in the dorsomedial prefrontal cortex (dmPFC) and basolateral amygdala (BLA) and altered synaptic transmission from dmPFC to BLA. It increased amplitude, slowed decay of NMDA receptor-mediated currents, and generated silent synapses. Administration of sub-anesthetic ketamine immediately after the exposure prevented the enhancement of PA learning and silent synapse formation. These findings suggest that ketamine can prevent pathophysiological consequences of psychological trauma.

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Changes in reliability of synaptic function as a mechanism for plasticity

Cited by 340 publications

References 16 publications

Propagation of activity-dependent synaptic depression in simple neural networks

Propagation of activity-dependent synaptic depression in simple neural networks

Decreased Frequency But Not Amplitude of Quantal Synaptic Responses Associated with Expression of Corticostriatal Long-Term Depression

Observation of Distressed Conspecific as a Model of Emotional Trauma Generates Silent Synapses in the Prefrontal-Amygdala Pathway and Enhances Fear Learning, but Ketamine Abolishes those Effects

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