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

Abstract

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.

Striatopallidal dysfunction underlies repetitive behavior in Shank3-deficient model of autism

“…We thus started out to test whether the induction protocol, pairing HFS (4 trains of 100 Hz/s given at 10-second interval) of presynaptic glutamatergic afferent fibers by placing a stimulating electrode at the inner edge of the corpus callosum (instead of intrastriatal stimulation) and postsynaptic depolarization (DP) of MSNs (HFS/DP), was able to induce LTD in both types of MSNs and whether LTD could be blocked by a CB1R antagonist in both types of neurons. Consistent with previous reports (55,56,58,(61)(62)(63), the HFS/DP stimulation paradigm led to the induction of robust LTD in WT D1 MSNs and D2 MSNs in the dorsal striatum, as evidenced by the reduction in the amplitude of evoked EPSCs (eEPSCs) (Figure 2). This reduction in eEPSC amplitude following LTD induction was also accompanied by an increase in PPR, which suggests a reduction in presynaptic glutamate release probability.…”

Dysfunctional play and dopamine physiology in the Fischer 344 rat

“…However, Fischer rats were, again, deficient in this DA-dependent form of cortical plasticity (Figure 6). This finding confirms earlier work from our laboratory showing young Fischer rats do not express corticostriatal LTD in vitro [97]. These findings in combination with the deficits in dopamine release we observed in Fischer rats indicates that insufficient dopamine release may underlie abnormalities in long-term plasticity seen with cortical synapses in Fischer rats and may contribute to the behavioral phenotype for this strain as well.…”

Temporal Sequence Learning, Prediction, and Control: A Review of Different Models and Their Relation to Biological Mechanisms

“…This is meant to facilitate the computational perspective and should allow us to design restricted but at least valid models without too many open degrees of freedom. References for the table rows 1: (Calabresi et al, 1992a;Choi and Lovinger, 1997;Calabresi et al, 1999), 2: (Calabresi et al, 1992b;Choi and Lovinger, 1997;Calabresi et al, 1999), 3: (Calabresi et al, 1987(Calabresi et al, , 1992bUmemiya and Raymond, 1997), 4:(LTD) (Calabresi et al, 1992b;Lovinger et al, 1993;Walsh, 1993;Wickens et al, 1996), 4: (LTP and mixed effects) (Charpier and Deniau, 1997;Charpier et al, 1999;Akopian et al, 2000;Partridge et al, 2000;Spencer and Murphy, 2000), 5: (nucleus accumbens) (Pennartz et al, 1993), 5:(striatum) , 6: , 7: (LTP with M g 2+ removed) (Calabresi et al, 1992c;Walsh and Dunia, 1993), 7: (LTD with normal conditions, i.e., with M g 2+ ) (Calabresi et al, 1992a,b;Tang et al, 2001), 7: (LTP with pulsed DA application) (Wickens et al, 1996). postsynaptic activation of the projection neuron, and 3) activation of the nigrostriatal, dopaminergic pathway.…”