Purkinje cell specific

Feil R, Hartmann J, Luo C, Wolfsgruber W, Schilling K, Feil S, Barski JJ, et al. (2003) Impairment of LTD and cerebellar learning by Purkinje cell-specific ablation of cGMP-dependent protein kinase I. J Cell Biol 163 295-302... 

The IP3 receptor has been found to be identical to the Purkinje cell-specific P400... 

Cloning of the P400 protein cDNA revealed that it was identical to the IP3 receptor protein, as well as the Purkinje cell-specific PCPP-260 protein isolated by Walaas et al. 

Purkinje cell-specific markers include several glyco- and phosphoproteins, peptides, antigenic determinants that have not been identified or determinants that Purkinje cells share with other, non-cerebellar cell types. One of the first sera specific for rat Purkinje cells was obtained, using immunohistochemical screening, by Woodhams et al. (1979), but the antigen corresponding to this antibody has not been identified. Reeber et al. 

The large ealiber fibers within the compartments of the white matter could be identified as Purkinje cell axons with axonal tracing methods and immunohistochemistry with Purkinje cell-specific antibodies. They appear as discrete bundles, separated by narrow gaps with antibodies against cyelic GMP-dependent protein kinase (De Camilli et al.,... 

The possibility that zonally distributed differenees in size and connections of the Purkinje cells are correlated with specific chemical properties of these cells was first raised by Marani (Marani and Voogd, 1977 Marani, 1981, 1982a Marani, 1986) on the basis of the distribution of 5 -nucleotidase and acetyleholinesterase in the molecular layer and by Chan-Palay (1984) who reported a restricted distribution of certain peptides in subsets of Purkinje cells. More recently a complete pattern of alternating zones of immunoreactive and non-immunoreactive Purkinje cells was described by Hawkes and Leclerc (1986, 1987) with a Purkinje cell-specific antibody (anti Zebrin-I) in the rat and by Brochu et al. (1990) with anti-Zebrin II in the rat and other species (see Section... 

The particulars of several Purkinje cell-specific markers that define parasagittal zones in adult rat cerebellum have been discussed in the first part of this chapter (see Section... 

The distribution of 5 -nucleotidase (5 -N) (Section 3.5.) in alternate longitudinal bands of high and low enzyme activity in the molecular layer of the cerebellar cortex of the mouse (Scott, 1963,1964,1965,1967) was the first evidence for the biochemical compart-mentalization of the cerebellar cortex. The pattern of 5 -N-positive and -negative zones is complete in the sense that it is present in all the lobules of vermis and hemisphere and unequivocal, because, in the mouse at least, the bands are clearly delineated (Marani, 1986). The 5 -N band pattern is very similar, if not identical, to the more recently described distribution of Purkinje cells in the rat, reacting with Purkinje cell-specific monoclonal antibodies to Zebrin-I (mabQl 13) (Eisenman and Hawkes, 1989). 

The epitopes recognized by Hawkes family of monoclonal antibodies known as the anti-Zebrins are localized on Purkinje cells (see Section 3.1.8.). Zonal patterns that are identical or very similar to Zebrin I and II have been described for the distribution of 5 -nucleotidase (see above), the p75 low affinity nerve growth factor receptor protein in the rat (Section 3.1.10., Fig. 38), protein kinase C delta (Fig. 133) (see Section 3.1.5.) and the B30 antibody of Stainier and Gilbert (1989) (see Section 3.1.8.). Immunoreactiv-ity in mouse Purkinje cells for an antibody against HNK is partially congruent with the Zebrin negative Purkinje cells, but Zebrin+/HNK-l- Purkinje cells also exist (Hawkes, 1992 Eisenman and Hawkes, 1993). The similarity between the Zebrin pattern and the transient zonal patterns in the development of the Purkinje cell specific marker L7 is discussed in Section 6.2. 

Caffe AR, Von Schantz M, Szel A, Voogd J, Van Veen T (1994) Distribution of Purkinje cell-specific zebrin-ll/aldolase C immunoreactivity in the mouse, rat, rabbit, and human retina. J. Comp. Neurol, 348, 291-297. 

Langley OK, Reeber A, Vincendon G, Zanetta JP (1982) Fine structural localization of a new Purkinje cell-specific glycoprotein subunit Immunoelectron microscopical study. J. Comp. Neurol, 208, 335-344. 

Walaas SI, Naim AC, Greengard P (1986) PCPP-260, a purkinje cell-specific cyclic AMP-regulated membrane phosphoprotein of M, 260,000. J. Neurosci, 6, 954-961. 

Brown SP, Brenowitz SD, Regehr WG (2003) Brief presynaptic bursts evoke synapse-specific retrograde inhibition mediated by endogenous cannabinoids. Nat Neurosci 6 1048-57 Brown SP, Safo PK, Regehr WG (2004) Endocannabinoids inhibit transmission at granule cell to Purkinje cell synapses by modulating three types of presynaptic calcium channels. J Neurosci 24(24) 5623-31... 

Besides the variable functional outcome after ischemia in animal models, it is well established that specific neuronal populations within an individual vary substantially in ischemic tolerance. Neurons in the CA1 region of the hippocampus and other distinct cellular populations of the caudate, thalamus, neocortex and cerebellum are selectively vulnerable to relatively brief periods of ischemia (Kirino and Sano 1984 Siesjo 1988). The reasons for this phenomenon are not fully elucidated, but for example in cerebellar Purkinje cells it could be shown that a reduced level of aldolase may trigger energy failure after brief periods of anoxia (Welsh et al. 2002). Changes in microcirculation, as seen in focal stroke,... 

Purkinje cells A specific type of nerve cell that carries each and every piece of information output by the cerebellum. These cells possess a great deal of control over the refinement of motor activities PVC Polyvinylchloride... 

Purkinje cells is demonstrated in Figure 12.1 and, like all cardiac myocytes, can be divided into four phases. Phase 4 (pacemaker potential) involves the slow influx of sodium ions, depolarizing the cell until the threshold potential is reached. Once the threshold potential is reached, the fast sodium current is activated, resulting in a rapid influx of sodium ions causing cell depolarization (phase 0 rapid depolarization). Phase 1 (partial repolarization) involves the inactivation of sodium channels and a transient outward current. Phase 2 (plateau phase) results from the slow influx of calcium ions. Repolarization (phase 3) occurs as a result of outflow of potassium ions from the cell and restores the resting potential. There are variations between the different areas of the heart, specifically the nodal tissues do not possess fast sodium channels and slow L-t5rpe calcium channels generate phase 0 current (Fig. 12.1). Phase 4 activity varies between nodal areas the sinoatrial node depolarizes more rapidly than the atrioventricular (AV) node. Automaticity is under autonomic nervous system control. Parasympathetic neurons... 

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