Abstract
In the cerebellar network, a precise relationship between plasticity and neuronal discharge has been predicted. However, the potential generation of persistent changes in Purkinje cell (PC) spike discharge as a consequence of plasticity following natural stimulation patterns has not been clearly determined. Here, we show that facial tactile stimuli organized in theta-patterns can induce stereotyped N-methyl-D-aspartate (NMDA) and gamma-aminobutyric acid (GABA-A) receptor-dependent changes in PCs and molecular layer interneurons (MLIs) firing: invariably, all PCs showed a long-lasting increase (Spike-Related Potentiation or SR-P) and MLIs a long-lasting decrease (Spike-Related Suppression or SR-S) in baseline activity and spike response probability. These observations suggests that tactile sensory stimulation engages multiple long-term plastic changes that are distributed along the mossy fiber-parallel fiber (MF-PF) pathway and operate synergistically to potentiate spike generation in PCs. In contrast, theta-pattern electrical stimulation (ES) of PFs indistinctly induced SR-P and SR-S both in PCs and MLIs, suggesting that tactile sensory stimulation preordinates plasticity upstream of the PF-PC synapse. All these effects occurred in the absence of complex spike changes, supporting the theoretical prediction that PC activity is potentiated when the MF-PF system is activated in the absence of conjunctive climbing fiber (CF) activity.
Highlights
Long-term modifications in synaptic transmission and in neuronal intrinsic excitability, collectively called plasticity, are thought to provide a critical mechanism for learning and memory in brain circuits (Bliss and Collingridge, 1993)
The peri-stimulus time histogram (PSTH) slowly decayed toward basal frequency levels in about 30 ms (Figure 2A)
This latency and decay of the simple spikes (SSs) PSTH were well in line with the delays of the signals known to be transmitted through the trigemino-cerebellar pathway and from granule cells to Purkinje cell (PC) (Bower and Woolston, 1983; Jaeger and Bower, 1994; Roggeri et al, 2008)
Summary
Long-term modifications in synaptic transmission (either long-term potentiation or depression, LTP or LTD) and in neuronal intrinsic excitability, collectively called plasticity, are thought to provide a critical mechanism for learning and memory in brain circuits (Bliss and Collingridge, 1993). The main consequence of plasticity is to regulate neuronal spike discharge in response to specific inputs and to modify neural circuit operations. A precise relationship between plasticity and neuronal discharge has been predicted. According to the ‘‘motor learning theory’’, plasticity at the parallel fiber (PF)—Purkinje cell (PC) synapse is essential to regulate the PC output and motor learning (Marr, 1969; Albus, 1971). LTD should be driven by error-related signals carried by climbing fibers (CFs; Ito and Kano, 1982), LTP should occur when such error signals are absent (Sakurai, 1987).
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