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

Choi, Sukwoo; Lovinger, David M.

doi:10.1523/jneurosci.17-21-08613.1997

Cited by 105 publications

(76 citation statements)

References 24 publications

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“…8 A2). Consistent with previous studies (Oliet et al, 1996;Choi and Lovinger, 1997), our result suggests that Sr 2ϩ -induced asynchronous synaptic events are quantal. Another important consideration is whether Sr 2ϩ -induced asynchronous mIPSCs are sensitive to presynaptic and postsynaptic manipulations.…”

Section: Both Presynaptic and Postsynaptic Mechanisms Contribute To Isupporting

confidence: 93%

“…This may explain why we did not detect any significant changes in the amplitude or frequency of mIPSCs during I-LTD. To record quantal synaptic responses selectively from the stimulated synapses, we induced asynchronous quantal responses by substituting Ca 2ϩ with strontium (Sr 2ϩ ) in the ACSF (Goda and Stevens, 1996;Oliet et al, 1996;Choi and Lovinger, 1997). When Sr 2ϩ is substituted for Ca 2ϩ , the fast synchronous component of evoked IPSCs is markedly reduced, but the slow asynchronous release of quanta is greatly enhanced.…”

Section: Both Presynaptic and Postsynaptic Mechanisms Contribute To Imentioning

confidence: 99%

“…When Sr 2ϩ is substituted for Ca 2ϩ , the fast synchronous component of evoked IPSCs is markedly reduced, but the slow asynchronous release of quanta is greatly enhanced. Analysis of Sr 2ϩ -induced asynchronous quantal events has revealed that LTP/LTD in the hippocampus is expressed postsynaptically (Oliet et al, 1996), whereas LTD in the dorsal striatum is expressed presynaptically (Choi and Lovinger, 1997). A distinct advantage of this approach is that it permits us to analyze quantal events from the stimulated synapses.…”

Section: Both Presynaptic and Postsynaptic Mechanisms Contribute To Imentioning

confidence: 99%

“…Twenty minutes after the 10 Hz stimulation, Sr 2ϩ -containing ACSF was washed in while the synaptic stimulation was continued. Sr 2ϩ has been shown to substitute for Ca 2ϩ in inducing and maintaining LTD in cultured hippocampal neurons and striatal slices (Goda and Stevens, 1996;Choi and Lovinger, 1997). Asynchronous mIPSCs recorded 10 min after Sr 2ϩ wash-in from these three groups were analyzed and compared (Fig.…”

Section: Both Presynaptic and Postsynaptic Mechanisms Contribute To Imentioning

confidence: 99%

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Endocannabinoid Signaling Mediates Cocaine-Induced Inhibitory Synaptic Plasticity in Midbrain Dopamine Neurons

Pan¹,

Hillard²,

Liu³

2008

J. Neurosci.

128

152

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Drugs that increase GABA levels in the brain reduce cocaine seeking in rodents and humans, suggesting that GABAergic inhibition regulates cocaine-seeking behavior. We previously reported that repeated cocaine exposure in vivo facilitates long-term potentiation by reducing the strength of GABAergic inhibition in dopamine neurons of the ventral tegmental area (VTA). Selective blockade of cocaineinduced reduction of GABAergic inhibition in the VTA might diminish cocaine-induced aberrant synaptic plasticity and addictive behavior. Here, we investigated the mechanism for cocaine-induced reduction of GABAergic inhibition. We show that a pathophysiologically relevant concentration of cocaine enables a normally ineffective stimulus to induce long-term depression (LTD) of IPSCs (I-LTD) in VTA dopamine neurons of midbrain slices. Activation of D 2 dopamine receptors and group I metabotropic glutamate receptors and subsequent recruitment of endocannabinoid signaling are required for I-LTD induction. We further demonstrate that in vivo pretreatment with antagonists to these receptors blocks cocaine-induced reduction of GABAergic inhibition and that repeated cocaine exposure in vivo occludes the subsequent induction of I-LTD ex vivo. Together, these results suggest that repeated cocaine exposure reduces the strength of GABAergic inhibition in dopamine neurons by inducing I-LTD-like modification in vivo.

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Section: Both Presynaptic and Postsynaptic Mechanisms Contribute To Isupporting

confidence: 93%

Section: Both Presynaptic and Postsynaptic Mechanisms Contribute To Imentioning

confidence: 99%

Section: Both Presynaptic and Postsynaptic Mechanisms Contribute To Imentioning

confidence: 99%

Section: Both Presynaptic and Postsynaptic Mechanisms Contribute To Imentioning

confidence: 99%

See 2 more Smart Citations

Endocannabinoid Signaling Mediates Cocaine-Induced Inhibitory Synaptic Plasticity in Midbrain Dopamine Neurons

Pan¹,

Hillard²,

Liu³

2008

J. Neurosci.

128

152

View full text Add to dashboard Cite

show abstract

“…Alternatively, we measured evoked asynchronous release by substitution of extracellular Ca 2ϩ with strontium (Sr 2ϩ ), a manipulation that increases delayed asynchronous release after a major peak current while decreasing synchronous release. Analysis of Sr 2ϩ -induced asynchronous events, which mimics the miniature postsynaptic responses, has been widely used as an approach to examine presynaptic quantal events (Choi and Lovinger, 1997;Oliet et al, 1997;Caillard et al, 1999;Xu-Friedman and Regehr, 2000;Hagler and Goda, 2001). Dual whole-cell recordings were performed on neurons (DIV12) 6 d after transfection with siRNAs, allowing us to selectively measure the frequency of asynchronous release from a single transfected presynaptic neuron.…”

Section: Syntabulin Is Essential For the Axonal Transport Of The Az Cmentioning

confidence: 99%

Syntabulin–Kinesin-1 Family Member 5B-Mediated Axonal Transport Contributes to Activity-Dependent Presynaptic Assembly

Cai

Pan²,

Sheng³

2007

J. Neurosci.

138

143

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The mechanism by which microtubule-based axonal transport regulates activity-dependent presynaptic plasticity in developing neurons remains mostly unknown. Our previous studies established that syntabulin is an adaptor capable of conjoining the kinesin family member 5B (KIF5B) motor and syntaxin-1. We now report that the complex of syntaxin-1-syntabulin-KIF5B mediates axonal transport of the active zone (

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Functional state of corticostriatal synapses determines their expression of short- and long-term plasticity

Akopian

Musleh

Smith

et al. 2000

Synapse

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Relationships between presynaptic function and short‐ and long‐term plasticity were investigated at adult corticostriatal synapses. Wide variability was observed in the expression of short‐ and long‐term synaptic plasticity. Intracellular records from 47 cells produced 17 examples of LTD (<90% of control), 10 examples of no long‐term change (between 90–110% of control), and 20 examples of LTP (>110% of control). Similar variation existed in paired‐pulse and posttetanic plasticities. The variability expressed in all three forms of plasticity appears to be related, based on correlations found between the paired‐pulse ratio (PPR) and tetanus‐induced short‐ (3 min posttetanus) and long‐term plasticities (16–20 min posttetanus). These data suggest that tetanus‐induced changes in synaptic strength are related to the intrinsic, preconditioned behavior of synapses. Every cell showing paired‐pulse depression also expressed LTD in response to high‐frequency activation of its afferents. Those synapses showing paired‐pulse potentiation tended to express LTP, although exceptions did exist. Similar relationships were found in a parallel analysis of population spikes. PPR also changed in association with the expression of posttetanic and long‐term depression. Greater paired‐pulse potentiation was observed in medial intracellular recordings, but no medial to lateral differences were seen in posttetanic plasticities. Field recordings also showed a medial bias toward paired‐pulse and posttetanic potentiation, but not in long‐term plasticity. Block of postsynaptic L‐type Ca2+ channels with nifedipine eliminated LTD expression, but overall no differences were found between nifedipine and control cells. Synapse 38:271–280, 2000. © 2000 Wiley‐Liss, Inc.

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

Cited by 105 publications

References 24 publications

Endocannabinoid Signaling Mediates Cocaine-Induced Inhibitory Synaptic Plasticity in Midbrain Dopamine Neurons

Endocannabinoid Signaling Mediates Cocaine-Induced Inhibitory Synaptic Plasticity in Midbrain Dopamine Neurons

Syntabulin–Kinesin-1 Family Member 5B-Mediated Axonal Transport Contributes to Activity-Dependent Presynaptic Assembly

Functional state of corticostriatal synapses determines their expression of short- and long-term plasticity

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