Purkinje Cell - Electrophysiological Activity

Electrophysiological Activity

Purkinje cells show two distinct forms of electrophysiological activity:

• Simple spikes occur at rates of 17 – 150 Hz (Raman and Bean, 1999) either spontaneously, or when Purkinje cells are activated synaptically by the parallel fibers, the axons of the granule cells.

• Complex spikes are slow, 1–3 Hz spikes, characterized by an initial prolonged large-amplitude spike, followed by a high-frequency burst of smaller-amplitude action potentials. They are caused by climbing fiber activation, and can involve the generation of calcium-mediated action potentials in the dendrites. Following complex spike activity, simple spikes can be suppressed by the powerful complex spike input.

Purkinje cells show spontaneous electrophysiological activity in the form of trains of spikes both sodium- as well as calcium-dependent was initially shown by Rodolfo Llinas (Llinas and Hess (1977) and Llinas and Sugimori (1980). P-type calcium channels were named after Purkinje cells where they were initially encountered (Llinas et al. 1989), which are crucial in cerebellar function. It has recently been shown that climbing fiber activation of the Purkinje cell can shift its activity from a quiet state to a spontaneously-active state, and vice-versa, serving as a type of toggle switch (Loewenstein et al., 2005, Nature Neuroscience). However, these findings have recently been challenged by a study suggesting that such toggling by climbing fiber inputs occurs predominantly in anaesthetized animals, and that Purkinje cells in awake behaving animals, in general, operate almost continuously in the upstate (Schonewille et al., 2006, Nature Neuroscience).

Findings have suggested that Purkinje cell dendrites release endocannabinoids that can transiently downregulate both excitatory and inhibitory synapses

The sodium-potassium pump has been shown to control and set the intrinsic activity mode of Purkinje cells. This suggests that the pump might not simply be a homeostatic, "housekeeping" molecule for ionic gradients; but could be a computation element in the cerebellum and the brain. Indeed, a mutation in the Na+-K+ pump causes rapid onset dystonia parkinsonism, which has symptoms to indicate that it is a pathology of cerebellar computation. Furthermore, an ouabain block of Na+-K+ pumps in the cerebellum of a live mouse results in it displaying ataxia and dystonia.