Author Correction: Kv1 potassium channels control action potential firing of putative GABAergic deep cerebellar nuclear neurons.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

A Slow Short-Term Depression at Purkinje to Deep Cerebellar Nuclear Neuron Synapses Supports Gain-Control and Linear Encoding over Second-Long Time Windows.

Modifications in the sensitivity of neural elements allow the brain to adapt its functions to varying demands. Frequency-dependent short-term synaptic depression (STD) provides a dynamic gain-control mechanism enabling adaptation to different background conditions alongside enhanced sensitivity to input-driven changes in activity. In contrast, synapses displaying frequency-invariant transmission can faithfully transfer ongoing presynaptic rates enabling linear processing, deemed critical for many functions.

Kv1 potassium channels control action potential firing of putative GABAergic deep cerebellar nuclear neurons.

Low threshold voltage activated Kv1 potassium channels play key roles in regulating action potential (AP) threshold, neural excitability, and synaptic transmission. Kv1 channels are highly expressed in the cerebellum and mutations of human Kv1 genes are associated to episodic forms of ataxia (EAT-1). Besides the well-established role of Kv1 channels in controlling the cerebellar basket-Purkinje cells synapses, Kv1 channels are expressed by the deep cerebellar nuclear neurons (DCNs) where they regulate the activity of principal DCNs carrying the cerebellar output.

Nuclear factor of activated T cells (NFATc4) is required for BDNF-dependent survival of adult-born neurons and spatial memory formation in the hippocampus.

New neurons generated in the adult dentate gyrus are constantly integrated into the hippocampal circuitry and activated during encoding and recall of new memories. Despite identification of extracellular signals that regulate survival and integration of adult-born neurons such as neurotrophins and neurotransmitters, the nature of the intracellular modulators required to transduce those signals remains elusive. Here, we provide evidence of the expression and transcriptional activity of nuclear factor of activated T cell c4 (NFATc4) in hippocampal progenitor cells.

Rebound excitation triggered by synaptic inhibition in cerebellar nuclear neurons is suppressed by selective T-type calcium channel block.

Following hyperpolarizing inputs, many neurons respond with an increase in firing rate, a phenomenon known as rebound excitation. Rebound excitation has been proposed as a mechanism to encode and process inhibitory signals and transfer them to target structures. Activation of low-voltage-activated T-type calcium channels and the ensuing low-threshold calcium spikes is one of the mechanisms proposed to support rebound excitation.

BK and Kv3.1 potassium channels control different aspects of deep cerebellar nuclear neurons action potentials and spiking activity.

Deep cerebellar nuclear neurons (DCNs) display characteristic electrical properties, including spontaneous spiking and the ability to discharge narrow spikes at high frequency. These properties are thought to be relevant to processing inhibitory Purkinje cell input and transferring well-timed signals to cerebellar targets. Yet, the underlying ionic mechanisms are not completely understood.

Intrinsic plasticity complements long-term potentiation in parallel fiber input gain control in cerebellar Purkinje cells.

Synaptic gain control and information storage in neural networks are mediated by alterations in synaptic transmission, such as in long-term potentiation (LTP). Here, we show using both in vitro and in vivo recordings from the rat cerebellum that tetanization protocols for the induction of LTP at parallel fiber (PF)-to-Purkinje cell synapses can also evoke increases in intrinsic excitability. This form of intrinsic plasticity shares with LTP a requirement for the activation of protein phosphatases 1, 2A, and 2B for induction.

Mechanisms supporting transfer of inhibitory signals into the spike output of spontaneously firing cerebellar nuclear neurons in vitro.

Cerebellar cortical signals are carried to their principal target, the deep cerebellar nuclear neurons (DCNs), via the inhibitory pathway formed by Purkinje cell (PC) axons. Two different intrinsic properties of DCNs, rebound excitation and automatic firing, have been proposed to support ensuing mechanisms for information transfer via inhibitory synapses. The efficacy of these mechanisms was investigated using whole-cell recordings of spontaneously firing DCNs in cerebellar slices.

Glycinergic synaptic currents in the deep cerebellar nuclei.

Despite evidence of local glycinergic circuits in the mature cerebellar nuclei the result of their activation remains unknown. Here, using whole cell recordings in rat cerebellar slices we demonstrated that after postnatal day 17 (>P17) glycinergic IPSCs can be readily evoked in large deep cerebellar nuclear neurons (DCNs), in the same way as in neonatal DCNs (P7-P10). Spontaneous glycinergic IPSCs were very rare but direct presynaptic depolarization by superfusion with elevated potassium concentration or application of 4-aminopyridine consistently evoked strychnine sensitive IPSCs.

Efficacy and short-term plasticity at GABAergic synapses between Purkinje and cerebellar nuclei neurons.

Although the entire output of the cerebellar cortex is conveyed to the deep cerebellar nuclei neurons (DCNs) via the GABAergic synapses established by Purkinje cells (PCs), very little is known about the strength and dynamic properties of PC-DCN connections. Here we show that activation of PC-DCN unitary connections induced large conductance changes (11.7 nS) in DCNs recorded in whole cell patch configuration in acute slices, suggesting that activity of single PCs might significantly affect the output of its target neurons.