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Purkinje fibre cell

APD (microelectrode) Purkinje fibres papillary muscle mid-myocardial (M-cell) wedge preparation Abi-Gerges et al.,-88 Gintant et al.,-89 Lu et al. 90 Antzelevitch et al91... [Pg.257]

Q4 The cardiac impulse arises in the pacemaker tissue of the heart, the SA node. The nodal tissues of the heart-the SA and AV nodes in the right atrium - are spontaneously rhythmic. The impulse generated by the SA node spreads, rather like ripples on a pond, over the atria and reaches the AV node to excite it. From the AV node the impulse travels via the bundle of His along the Purkinje fibres, which are enlarged muscle cells with a high conduction velocity, to the ventricles. The cardiac impulse reaches the apex of the heart first and then spreads over the muscle of the two ventricles. [Pg.196]

In cardiac cells, there are two time-dependent outward currents which contribute to repolarization of the cell. Both of these outward currents may be decreased by calcium channel blocking drugs. Since an increase in the intracellular Ca2 + concentration activates one of the outward currents (7to), all the calcium channel blocking drugs should reduce Ito [ 159]. This has been shown with D600, nisoldipine and diltiazem [41-43, 159], The other time-dependent outward current (7X, delayed rectifier) is not calcium-activated [ 160]. Hume has found that D600, diltiazem and nisoldipine inhibit 7X in frog atrial cells [ 160]. However, a similar concentration of nisoldipine does not affect 7X in calf Purkinje fibres [43]. [Pg.279]

Importantly, depending on the areas measru ed, the distinct separation of phases are not quite feasible and the prevailing voltages invariably alter amongst the major cell types of the heart, viz., Purkinje fibres, AV-node, atrial cells, and the SA-node. [Pg.357]

Many antiarrhythmic drugs have local anaesihciic activity (i.c, block voliagc-dependetu Na channels) or are calcium aniagonisLs. These actions decrease the automaticity of pacemaker cells and increase the effective refrticlory jxrritxl of atrial, ventricular and Purkinje fibres. [Pg.40]

Activation Atrial preparation Biophysics Calcium channel Cardiac action potential Channel kinetics Comprehensive in vitro proarrhythmia assay Delayed rectifier Early afterdepolarisation ECG Hodgkin-Huxley ICHS7A ICHS7B In silico modelling Inactivation Inward rectifier Langendorff heart Purkinje fibre Safety assessment Sodium channel Stem cells... [Pg.150]

The properties of the current i in the cardiac SA node cells are investigated in the light of its resemblance to the current i 2 of cardiac Purkinje fibres in their quality of "pacemaker currents and in their role in mediating the adrenaline-induced acceleration of pacemaker activity. We find that ... [Pg.67]

The current if has been recently described as the one which controls the pacemaker activity of cardiac SA node cells and mediates the acceleratory effect of adrenaline (Brown, DiFrancesco Noble, 1979a). In this respect, i.e. in the voltage range of activation and in the response to adrenaline, i is similar to another current already described in the heart, the current i 2 Purkinje fibre... [Pg.67]

These specialised conduction cells are distributed throughout the heart forming specialised conduction pathways (Fig. 1.5). Depolarisation occurs in the Sinoatrial node (SAN). This is a collection of self-excitory (pacemaker) cells that normally fire at a rate of between 60 and 100 Beats Per Minute (BPM). The wave of Depolarisation moves from the SAN through an intra-atrial tract called Bachmanns bundle into the left atrium and to the Atrioventricular (AV) node. From here the impulse travels down the bundle of His into the right and Left bundle branches and finally into the Purkinje fibres activating the ventricles. [Pg.8]

Duguid IC, Smart TG (2004) Retrograde activation of presynaptic NMDA receptors enhances GABA release at cerebellar intemeuron-Purkinje cell synapses. Nat Neurosci 7 525 Eccles JC, Kostyuk PG, Schmidt RF (1962) Central pathways responsible for depolarization of primary afferent fibres. J Physiol 161 237-57... [Pg.517]

Batchelor AM, Madge DJ, Garthwaite J (1994) Synaptic activation of metabotropic glutamate receptors in the parallel fibre-Purkinje cell pathway in rat cerebellar slices. Neuroscience 63 9 1-915. [Pg.91]

Glutamate is a key neurotransmitter in the cerebellum mossy fibres onto granule cells parallel fibres onto Purkinje and stellate/basket cells, climbing fibres onto Purkinje cells, and also mossy fibre and climbing fibre inputs onto Golgi cells all use glutamate (Fig. 19) (Voogd... [Pg.129]

Purkinje cells express GluR-A flop, GluR-B flip and flop, and GluR-C flip mRNAs GluR-A expression is the weakest (Keinanen et al., 1990 Sommer et al., 1990 Monyer et al., 1991 Sato et al., 1993 see Fig. II-L for pan GluR-A to -D expression). There are thus probably multiple AMPA receptors on Purkinje cells for example, these could be differentially located at parallel fibre and climbing fibre synapses. [Pg.132]

In slices of rat cerebellum, LTD of parallel fibre inputs to Purkinje cells can be induced by pairing low-frequency stimulation (1 Hz for 5 min) with post-synaptic depolarisation. Both WIN55, 212-2 (1 pM) and CP55,940 (400 nM) reduced the EPSC by about 50%, and impaired the induction of LTD, an effect which was blocked by rimonabant (1 pM) (Levenes et al. 1998). In this pathway, therefore, it appears that cannabinoid effects on synaptic plasticity may be secondary to changes in baseline responses. [Pg.468]

Crepel F, Daniel H, Hemart N, Jaillard D (1991) Effects of ACPD and AP3 on parallel-fibre-mediated EPSPs of Purkinje cells in cerebellar slices in vitro. Exp, Brain Res., 86, 402-406. [Pg.322]

Fox CA, Barnard JW (1957) A quantitative study of the Purkinje cell dendritic branchlets and their relationship to afferent fibres. J. Anat., 91, 299-313. [Pg.328]

Ito M, Sakurai M, Tongroach P (1982) Climbing fibre induced depression of both mossy fibre responsiveness and glutamate sensitivity of cerebellar Purkinje cells. J. Physiol, 324, 113-134. [Pg.336]

The output of Purkinje cells is regulated by two distinct excitatory inputs, the parallel fibres and the climbing fibres. Conjunctive stimulation of parallel fibres and climbing fibres input at low frequencies results in a persistent attenuation of the parallel fibre- Purkinje neurone synapse, a process termed long-term depression (Ito et al. 1982). [Pg.538]

Golgi cells in the granule cell layer are interneurones involved in modulating input to the Purkinje cells from the mossy fibre pathway. They express phosphodiesterase II (Juilfs etal. 1999). In relation to the number of cells in the cerebellum these represent a minor cell population, however, signal intensity is high suggesting that there is a significant level of phosphodiesterase II protein expressed in these cells. [Pg.541]

The Bergmann fibres belong to the astroglia (Petersen 1969). They exhibit bundles of gUal filaments and are rich in glycogen particles. Most of the cell bodies of the Bergmann fibres lie in the granule cell layer, some in file Purkinje cell layer or the molecular layer. [Pg.541]

Miyazaki T, Fukaya M, Shimizu H et al (2003) Subtype switching of vesicular glutamate transporters at parallel fibre-Purkinje cell synapses in developing mouse cerebellum. Em J Neurosci 17 2563-2572... [Pg.310]


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See also in sourсe #XX -- [ Pg.357 ]




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