Stellate cell inhibition of Purkinje cells in the turtle cerebellum in vitro.

Midtgaard, Jens

doi:10.1113/jphysiol.1992.sp019382

Cited by 68 publications

(65 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To completely avoid long-duration responses on parallel fibers, a model must rely on the intrinsic dynamics of Purkinje cells. Purkinje cells are known to exhibit complex Ca ++ dynamics in the dendrites which can interalia lead to long-duration plateau potentials in vitro (Llimis & Sugimori, 1980, 1992. We have developed models of Purkinje cell Ca ++ dynamics which demonstrate the feasibility of this approach for timing responses.…”

Section: Discussionmentioning

confidence: 99%

“…In other words, parallel fibers stimulate the inhibitory interneurons as well as the Purkinje cells. These interneurons produce a graded inhibitory postsynaptic potential in Purkinje cells (Midtgaard, 1992). While the synaptic weight between parallel fibers and Purkinje cells is modifiable, the efficacy of the parallel fiber to basket and stellate cells is not modified by climbing fiber input (Ito, 1984, p. 129).…”

Section: Spectral Timing In the Cerebellummentioning

confidence: 99%

See 1 more Smart Citation

A neural model of timed response learning in the cerebellum

1994

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Section: Spectral Timing In the Cerebellummentioning

confidence: 99%

A neural model of timed response learning in the cerebellum

1994

View full text Add to dashboard Cite

“…Cerebellar stellate cells are inhibitory interneurons that receive excitatory and inhibitory inputs from parallel fibers and other stellate cells, respectively (Palay and Chan-Palay, 1974;Midtgaard, 1992a,b). By projecting onto Purkinje cell dendrites, stellate cells can modify the output of the cerebellar cortex (Midtgaard, 1992b;Hausser and Clark, 1997;Jorntell and Ekerot, 2002;Mittmann et al, 2005). Indeed, even single spikes in stellate cells have been shown to significantly delay Purkinje cell firing (Hausser and Clark, 1997), revealing the potential impact of stellate cell spike timing.…”

Section: Introductionmentioning

confidence: 99%

A-Type and T-Type Currents Interact to Produce a Novel Spike Latency-Voltage Relationship in Cerebellar Stellate Cells

Molineux¹,

Fernandez²,

Mehaffey³

et al. 2005

J. Neurosci.

View full text Add to dashboard Cite

The modification of first-spike latencies by low-threshold and inactivating K ϩ currents (I A ) have important implications in neuronal coding and synaptic integration. To date, cells in which first-spike latency characteristics have been analyzed have shown that increased hyperpolarization results in longer first-spike latencies, producing a monotonic relationship between first-spike latency and membrane voltage. Previous work has established that cerebellar stellate cells express members of the K v 4 potassium channel subfamily, which underlie I A in many central neurons. Spike timing in stellate cells could be particularly important to cerebellar output, because the discharge of even single spikes can significantly delay spike discharge in postsynaptic Purkinje cells. In the present work, we studied the first-spike latency characteristics of stellate cells. We show that first-spike latency is nonmonotonic, such that intermediate levels of prehyperpolarization produce the longest spike latencies, whereas greater hyperpolarization or depolarization reduces spike latency. Moreover, the range of first-spike latency values can be substantial in spanning 20 -128 ms with preceding membrane shifts of Ͻ10 mV. Using patch clamp and modeling, we illustrate that spike latency characteristics are the product of an interplay between I A and lowthreshold calcium current (I T ) that requires a steady-state difference in the inactivation parameters of the currents. Furthermore, we show that the unique first-spike latency characteristics of stellate cells have important implications for the integration of coincident IPSPs and EPSPs, such that inhibition can shift first-spike latency to differentially modulate the probability of firing.

show abstract

“…CF activity has also been shown to trigger plasticity at inhibitory synapses onto Purkinje cells, expressed as long-term potentiation of spontaneous IPSCs (Kano et al, 1992(Kano et al, , 1996. Purkinje cells are ideally suited to read out the strength of inhibitory synapses even in the absence of excitation, because they are spontaneously active (Häusser and Clark, 1997;Bean, 1997, 1999) and because inhibitory inputs have a powerful influence on Purkinje cell spiking (Midtgaard, 1992;Häusser and Clark, 1997). Moreover, PFs activate a feedforward inhibitory microcircuit, generating a precise, stereotyped excitatory-inhibitory temporal sequence (Eccles et al, 1966;Brunel et al, 2004;Mittmann et al, 2005), such that the strength of synaptic inhibition can control the timing and number of spikes activated by PFs (Mittmann et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Linking Synaptic Plasticity and Spike Output at Excitatory and Inhibitory Synapses onto Cerebellar Purkinje Cells

Mittmann¹,

Häusser²

2007

J. Neurosci.

View full text Add to dashboard Cite

Understanding the relationship between synaptic plasticity and neuronal output is essential if we are to understand how plasticity is encoded in neural circuits. In the cerebellar cortex, motor learning is thought to be implemented by long-term depression (LTD) of excitatory parallel fiber (PF) to Purkinje cell synapses triggered by climbing fiber (CF) input. However, theories of motor learning generally neglect the contribution of plasticity of inhibitory inputs to Purkinje cells. Here we describe how CF-induced plasticity of both excitatory and inhibitory inputs is reflected in Purkinje cell spike output. We show that coactivation of the CF with PF input and interneuron input leads not only to LTD of PF synapses but also to comparable, "balanced" LTD of evoked inhibitory inputs. These two forms of plasticity have opposite effects on the spike output of Purkinje cells, with the number and timing of spikes sensitively reflecting the degree of plasticity. We used dynamic clamp to evaluate plasticity-induced changes in spike responses to sequences of excitation and feedforward inhibition of varied relative and absolute amplitude. Balanced LTD of both excitatory and inhibitory components decreased the net spike output of Purkinje cells only for inputs with small inhibitory components, whereas for inputs with a larger proportion of feedforward inhibition CF-triggered LTD resulted in an increase in the net spike output. Thus, the net effect of CF-triggered plasticity on Purkinje cell output depends on the balance of excitation and feedforward inhibition and can paradoxically increase cerebellar output, contrary to current theories of cerebellar motor learning.

show abstract

Stellate cell inhibition of Purkinje cells in the turtle cerebellum in vitro.

Cited by 68 publications

References 21 publications

A neural model of timed response learning in the cerebellum

A neural model of timed response learning in the cerebellum

A-Type and T-Type Currents Interact to Produce a Novel Spike Latency-Voltage Relationship in Cerebellar Stellate Cells

Linking Synaptic Plasticity and Spike Output at Excitatory and Inhibitory Synapses onto Cerebellar Purkinje Cells

Contact Info

Product

Resources

About