Purkinje Cell Information
Purkinje cells, or Purkinje neurons ( / p ər ˈ k ɪ n dʒ iː / pər-kin-jee), are a class of GABAergic neurons located in the cerebellar cortex. They are named after their discoverer, Czech anatomist Jan Evangelista Purkyně (Czech: [ˈpurkɪɲɛ]).
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Anatomy
Transverse section of a cerebellar folium. (Purkinje Cell labeled at center top.) Purkinje cells. Bielschowsky stain.These cells are some of the largest neurons in the human brain (Betz cells being the largest),[1] with an intricately elaborate dendritic arbor, characterized by a large number of dendritic spines. Purkinje cells are found within the Purkinje layer in the cerebellum. Purkinje cells are aligned like dominos stacked one in front of the other. Their large dendritic arbors form nearly two-dimensional layers through which parallel fibers from the deeper-layers pass. These parallel fibers make relatively weaker excitatory (glutamatergic) synapses to spines in the Purkinje cell dendrite, whereas climbing fibers originating from the inferior olivary nucleus in the medulla provide very powerful excitatory input to the proximal dendrites and cell soma. Parallel fibers pass orthogonally through the Purkinje neuron's dendritic arbor, with up to 200,000 parallel fibers[2] forming a Granule-cell-Purkinje-cell synapse with a single Purkinje cell. Each Purkinje cell receives ca 500 climbing fiber synapses, all originating from a single climbing fiber.[3] Both basket and stellate cells (found in the cerebellar molecular layer) provide inhibitory (GABAergic) input to the Purkinje cell, with basket cells synapsing on the Purkinje cell axon initial segment and stellate cells onto the dendrites.
Purkinje cells send inhibitory projections to the deep cerebellar nuclei, and constitute the sole output of all motor coordination in the cerebellar cortex.
Electrophysiological activity
Microcircuitry of the cerebellum. Excitatory synapses are denoted by (+) and inhibitory synapses by (-). MF: Mossy fiber. DCN: Deep cerebellar nuclei. IO: Inferior olive. CF: Climbing fiber. GC: Granule cell. PF: Parallel fiber. PC: Purkinje cell. GgC: Golgi cell. SC: Stellate cell. BC: Basket cell.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.[4]
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[5]
Medical conditions related to Purkinje cells
In humans, Purkinje cells are affected in a variety of diseases ranging from toxic exposure (alcohol, lithium), to autoimmune diseases and to genetic mutations (spinocerebellar ataxias, Unverricht-Lundborg disease, autism) and neurodegenerative diseases that are not thought to have a known genetic basis (cerebellar type of multiple system atrophy, sporadic ataxias).
In some domestic animals, a condition where the Purkinje cells begin to atrophy shortly after birth, called Cerebellar abiotrophy, can lead to symptoms including ataxia, intention tremors, hyperreactivity, lack of menace reflex, stiff or high-stepping gait, apparent lack of awareness of wherein the feet are (sometimes standing or walking with a foot knuckled over), and a general inability to determine space and distance. A similar condition known as cerebellar hypoplasia occurs when Purkinje cells either fail to develop in utero or die off in utero prior to birth. The genetic conditions Ataxia Telangiectasia and Niemann Pick disease Type C, as well as cerebellar essential tremor, involve the progressive loss of Purkinje cells. Spinal pathology as well as loss of dendritic branches of the Purkinje cells have been also described in Alzheimer's disease.[6]
Links
- Cell Centered Database - Purkinje
- Disorders of cerebellum
- NIF Search - Purkinje Cell via the Neuroscience Information Framework
References
- ^ Purves, Dale, George J. Augustine, David Fitzpatrick, William C. Hall, Anthony-Samuel LaMantia, James O. McNamara, and Leonard E. White (2008). Neuroscience. 4th ed.. Sinauer Associates. pp. 432–4. ISBN 978-0-87893-697-7.
- ^ Tyrrell, T; Willshaw, D (1992-05-29). "Cerebellar cortex: its simulation and the relevance of Marr's theory.". Philosophical transactions of the Royal Society of London. Series B, Biological sciences 336 (1277): 239–57. doi:10.1098/rstb.1992.0059. PMID 1353267.
- ^ Wadiche, JI; Jahr, CE (2001-10-25). "Multivesicular release at climbing fiber-Purkinje cell synapses". Neuron 32 (2): 301–13. doi:10.1016/S0896-6273(01)00488-3. PMID 11683999.
- ^ Eric R. Kandel, James H. Schwartz, Thomas M. Jessell (2000). Principles of Neural Science. 4/e. McGraw-Hill. pp.837-40.
- ^ Kreitzer AC, Regehr WG (March 2001). "Retrograde inhibition of presynaptic calcium influx by endogenous cannabinoids at excitatory synapses onto Purkinje cells". Neuron 29 (3): 717–27. doi:10.1016/S0896-6273(01)00246-X. PMID 11301030.
- ^ Mavroudis, IA; Fotiou, DF, Adipepe, LF, Manani, MG, Njau, SD, Psaroulis, D, Costa, VG, Baloyannis, SJ (2010 Nov). "Morphological changes of the human purkinje cells and deposition of neuritic plaques and neurofibrillary tangles on the cerebellar cortex of Alzheimer's disease". American journal of Alzheimer's disease and other dementias 25 (7): 585–91. doi:10.1177/1533317510382892. PMID 20870670.
Further reading
- Llinás R, Hess R (July 1976). "Tetrodotoxin-resistant dendritic spikes in avian Purkinje cells". Proc. Natl. Acad. Sci. U.S.A. 73 (7): 2520–3. doi:10.1073/pnas.73.7.2520. PMC 430632. PMID 1065905.
- Llinás R, Sugimori M (August 1980). "Electrophysiological properties of in vitro Purkinje cell somata in mammalian cerebellar slices". J. Physiol. (Lond.) 305: 171–95. PMC 1282966. PMID 7441552. http://www.jphysiol.org/cgi/pmidlookup?view=long&pmid=7441552.
- Llinás RR, Sugimori M, Cherksey B (1989). "Voltage-dependent calcium conductances in mammalian neurons. The P channel". Ann. N. Y. Acad. Sci. 560 (1 Calcium Chann): 103–11. doi:10.1111/j.1749-6632.1989.tb24084.x. PMID 2545128.
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