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'''Purkinje cells''', or '''Purkinje neurons''' ({{IPAc-en|p|ər|ˈ|k|ɪ|n|dʒ|iː}} {{respell|pər|KIN|jee}}), are a class of [[GABA]]ergic neurons located in the [[cerebellum]]. They are named after their discoverer, [[Czech people|Czech]] [[anatomist]] [[Jan Evangelista Purkyně]] ({{IPA-cs|ˈpurkɪɲɛ|lang}}).
[[Fil:Neuron, LangNeutral.svg|thumb|370x370px|Simpel oversigt over nervecellens opbygning. a: [[Dendrit]], b: [[Soma|Cellelegeme]], c: [[Cellekerne]], d: Aksonets rod, e, [[Myelinskede]], f: [[Schwann-celle|Schwann Celle]], g: '''Ranviersk indsnøring''', h: [[Synapse]]]]
 
<nowiki>'''</nowiki>Ranvierske indsnøringer<nowiki>'''</nowiki> er mellemrum mellem de fedtholdige [[myelinskede]]<nowiki/>r, der omgiver [[Nervecelle|nervecellernes]] [[akson]]. Myelinskeden er isolerende, hvorimod indsnøringen er uisoleret, og udgøres af aksonmembranen, der indeholder et højt antal spændingsstyrede Na+-kanaler. Dette gør indsnøringerne elektrisk ledende for [[Aktionspotentiale|aktionspotential]][[Aktionspotentiale|er]] opstået ved aksonets rod (mod cellelegemet). Herved forstås at aktionspotentialet "hopper" fra ranviersk indsnøring til ravniersk indsnøring pga. den isolerende myelinskede. Nettoresultatet er en øget ledningshastighed - et fænomen kaldet saltatorisk ledning.
==Electrophysiological activity==
[[Image:CerebCircuit.png|thumb|right|200px|Microcircuitry of the cerebellum. [[Excitatory synapses]] are denoted by (+) and [[inhibitory synapses]] by (-).<BR>MF: [[Mossy fiber (cerebellum)|Mossy fiber]].<BR>DCN: [[Deep cerebellar nuclei]].<BR>IO: [[Inferior olivary nucleus|Inferior olive]].<BR>CF: [[Climbing fiber]].<BR>GC: [[Granule cell]].<BR>PF: [[Parallel fiber]].<BR>PC: Purkinje cell.<BR>GgC: [[Golgi cell]].<BR>SC: [[Stellate cell]].<BR>BC: [[Basket cell]].]]
 
Purkinje cells show two distinct forms of electrophysiological activity:
 
* '''Simple spikes''' occur at rates of 17 – 150&nbsp;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&nbsp;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.<ref>Eric R. Kandel, James H. Schwartz, Thomas M. Jessell (2000). ''Principles of Neural Science. 4/e.'' McGraw-Hill. pp.837-40.</ref>
Purkinje cells show spontaneous electrophysiological activity in the form of trains of spikes both sodium-dependent and calcium-dependent. This 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. We now know that activation of the Purkinje cell by climbing fibers can shift its activity from a quiet state to a spontaneously active state and vice-versa, serving as a kind 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 [[endocannabinoid]]s that can transiently downregulate both excitatory and inhibitory synapses.<ref>{{cite journal |author=Kreitzer AC, Regehr WG |title=Retrograde inhibition of presynaptic calcium influx by endogenous cannabinoids at excitatory synapses onto Purkinje cells |journal=Neuron |volume=29 |issue=3 |pages=717–27 |date=March 2001 |pmid=11301030 |doi=10.1016/S0896-6273(01)00246-X}}</ref>
 
The intrinsic activity mode of Purkinje cells is set and controlled by the [[sodium-potassium pump]].<ref>{{cite journal |author=Forrest MD, Wall MJ, Press DA, Feng J |title=The Sodium-Potassium Pump Controls the Intrinsic Firing of the Cerebellar Purkinje Neuron |journal=PLoS ONE |volume=7 |issue=12 |pages=e51169 |date=December 2012 |pmid=23284664 |pmc=3527461 |url=http://dx.plos.org/10.1371/journal.pone.0051169 |doi=10.1371/journal.pone.0051169 |editor1-last=Cymbalyuk |editor1-first=Gennady}}</ref> This suggests that the pump might not be simply a [[homeostatic]], "housekeeping" molecule for ionic gradients. Instead, it could be a [[computation]] element in the cerebellum and the brain. Indeed, a [[mutation]] in the {{chem|Na|+}}-{{chem|K|+}} pump causes rapid onset dystonia parkinsonism; its symptoms indicate that it is a pathology of cerebellar computation.<ref>{{cite journal |author=Cannon C |title=Paying the Price at the Pump: Dystonia from Mutations in a Na+/K+-ATPase |journal=Neuron |volume=43 |issue=2 |pages=153–154 |date=July 2004 |pmid=15260948 |url=http://www.cell.com/neuron/retrieve/pii/S089662730400426X |doi=10.1016/j.neuron.2004.07.002}}</ref> Furthermore, using the poison [[ouabain]] to block {{chem|Na|+}}-{{chem|K|+}} pumps in the cerebellum of a live mouse induces [[ataxia]] and [[dystonia]].<ref>{{cite journal |author=Calderon DP, Fremont R, Kraenzlin F, Khodakhah K |title=The neural substrates of rapid-onset Dystonia-Parkinsonism |journal=Nature Neuroscience |volume=14 |issue=3 |pages=357–65 |date=March 2011 |pmid=21297628 |pmc=3430603 |url=http://www.nature.com/neuro/journal/v14/n3/full/nn.2753.html |doi=10.1038/nn.2753}}</ref>
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