Pacemaker types

Figure 2.9 Hyperpolarisation-activated cation current 4 and its role in pacemaking in a guinea-pig thalamic relay neuron. (Adapted from Figs 2 and 14 in McCormick, DA and Pape, H-C (1990) J. Physiol. 431 291-318. Reproduced by permission of the Physiological Society.) (a) Records showing the time-dependent activation of the h-current by hyperpolarisation and its deactivation on repolarising, (b) Interpretation of rhythmic activity in a thalamic relay neuron. (1) The inter-spike hyperpolarisation activates 7h to produce a slowly rising pacemaker depolarisation. (2) This opens T-type Ca " channels to give a more rapid depolarisation, leading to (3) a burst of Na" spikes (see Fig. 2.8). At (4) the depolarisation has closed (deactivated) the h-channels and has inactivated the T-channels. The membrane now hyperpolarises, assisted by outward K+ current (5). This hyperpolarisation now removes T-channel in-activation and activates 7h (6), to produce another pacemaker potential...

Class I recalls are those that have been judged to present a serious threat to the health of the consumer. Examples of this type of recall include brewers yeast tablets (product contaminated with Salmonella), defective pacemakers (electronically unsafe), and numerous cases of mislabeling of drug substances, such as the belladonna alkaloids [20]. 

A pacemaker potential involves gradual depolarization of the cell membrane to threshold. The subsequent generation of an action potential causes smooth muscle contraction. This type of spontaneous depolarization is referred to as a "pacemaker potential" because it creates a regular rhythm of contraction. 

The sinoatrial (SA) node is located in the wall of the right atrium near the entrance of the superior vena cava. The specialized cells of the SA node spontaneously depolarize to threshold and generate 70 to 75 heart beats/ min. The "resting" membrane potential, or pacemaker potential, is different from that of neurons, which were discussed in Chapter 3 (Membrane Potential). First of all, this potential is approximately -55 mV, which is less negative than that found in neurons (-70 mV see Figure 13.2, panel A). Second, pacemaker potential is unstable and slowly depolarizes toward threshold (phase 4). Two important ion currents contribute to this slow depolarization. These cells are inherently leaky to sodium. The resulting influx of Na+ ions occurs through channels that differ from the fast Na+ channels that cause rapid depolarization in other types of excitable cells. Toward the end of phase... 

Enteric Neuropathies. Different kinds of familial visceral neuropathies have been described the dominant type 1 [134], the recessive type 2 [135] and a recessive form with calcified basal ganglia [134], Furthermore, aganglionosis of the small bowel (Hirschsprung s disease) [136], hypergan-glionosis (neurofibromatosis) [137], neuronal intestinal dysplasia [138] and Parkinson s disease [139] are neuropathies to consider. The recognition of the pacemaker cells of the small bowel, the interstitial cells of Cajal, has prompted studies to detect abnormalities of these cells, another possible cause of pseudoobstruction [140],... 

FIGURE 37-4 Antiseizure mediated reduction of IT. Certain antiseizure drugs reduce the flow of calcium through T-type Ca2+ channels (ethosuximide, valproate), thereby reducing the pacemaker current that underlies spike-wave discharges of generalized absence epilepsy. 

What type of battery is used in pacemakers to regulate a patient s heartbeat What are some of the benefits of this battery ... 

Phase 4 Hyperpolarization occurs before K+ efflux has completely stopped and is followed by a gradual drift towards threshold (pacemaker) potential. This is reflects a Na+ leak, T-type Ca2+ channels and a Na+/Ca2+ pump, which all encourage cations to enter the cell. The slope of your line during phase 4 is altered by sympathetic (increased gradient) and parasympathetic (decreased gradient) nervous system activity. 

Numerical simulations indicate that relay of cAMP pulses represents a different mode of dynamic behavior, closely related to oscillations. Just before autonomous oscillations break out, cells in a stable steady state can amplify suprathreshold variations in extracellular cAMP in a pulsatory manner. Thus, relay and oscillations of cAMP are produced by a unique mechanism in adjacent domains in parameter space. The two types of dynamic behavior are analogous to the excitable or pacemaker behavior of nerve cells. 

The molecular assays in Clk"mAic2As bom fide rhythms with a predominant effect on circadian rhythm amplitude and no more than a modest effect on phase or period. With circadian per and tim enhancers, we observed reduced enhancer activity and a reduced cycling amplitude in a Clk" background, consistent with the role of Clk in regulating these enhancers. Nonetheless, the phase of oscillating bioluminescence is similar to that of wild-type flies. The presence of molecular rhythms contrasts with the absence of detectable behavioural rhythms. We favour the notion that this reflects a level or amplitude reduction below a critical threshold for behavioural rhythmicity. The absence of anticipation of light—dark transitions makes it very unlikely that an effect restricted to the lateral neurons — the absence of the neuropeptide PDF, for example — is primarily responsible for the behavioural phenotypes. This is also because LD behavioural rhythms are largely normal in flies devoid of PDF or the pacemaker lateral neurons (Renn et al 1999). However, we cannot exclude the possibility of selective effects of Clk" on other behaviourally relevant neurons. 

Contraindications include hypersensitivity to local anesthetics of the amide type (a very rare occurrence), severe hepatic dysfunction, a history of grand mal seizures due to lidocaine, and age 70 or older. Lidocaine is contraindicated in the presence of second- or third-degree heart block, since it may increase the degree of block and can abolish the idioventricular pacemaker responsible for maintaining the cardiac rhythm. 

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