159:, the case represents the non-synaptic nature of PDS. Finally, the Na/K pump and calcium activated potassium channel might play a role in terminating PDS. Paradoxically, there might arise the argument whether intracellular calcium could be able to repolarize the single neuron while blocking this calcium entry from the extracellular milieu. However, the other opportunity such as Na-Ca exchange as well as small contribution from intracellular stores need to be explored.
144:.. The amount of calcium entry through ion channels is critical in determining the physiological or pathological state of individual neurons,). For example, high concentration of calcium perturbs Ca-signalling cascades, leading to the death of neurons and circuits, while adequate amount of calcium will help in maintaining normal physiological function.
64:) and ionic conductances (persistent sodium current and high-threshold calcium current) and the post-PDS hyperpolarization is governed by multiple potassium currents, activated by calcium or sodium entry, as well as by leak current. The next cycle of depolarization is initiated by both synaptic drive and the hyperpolarization-activated IH current.
357:
Ayala, G.F.; Dichter, M.; Gumnit, R.J.; Matsumoto, H.; Spencer, W.A. (1973). "Genesis of epileptic interictal spikes. New knowledge of cortical feedback systems suggests a neurophysiological explanation of brief paroxysms".
155:
such as Ni. Further evidence for Na dependent PDS is highlighted in leeches with the possibility of studying PDS in detail. It is likely that such type of PDS is sustained in the absence of
140:, which sustain calcium-dependent PDS. As usual, these Ca-ions will activate calcium dependent potassium channels and PDS will terminate. This is the case that provides a clue for
94:, and some hypothalamic neurons. The possibility of spontaneous bursting in these neurons is implicated in regulating hormonal secretion. The significance of PDS may increase the
32:. Little is known about the initiation, propagation and termination of PDS. Previously, electrophysiological studies have provided the evidence that there is a
117:, PDS can be theoretically categorized into two types. Ca dependent PDS requires the entry of Ca while Na dependent PDS is presumed to be non-synaptic.
232:Üre, Atik; Altrup, Ulrich (2006). "Block of spontaneous termination of paroxysmal depolarizations by forskolin (buccal ganglia, Helix pomatia)".
202:
Pathak, Dhruba; Lopicic, Srdjan; Stanojevic, Marija; Nedeljkov, Aleksandra; Pavlovic, Dragan; Cemerikic, Dusan; Nedeljkov, Vladimir (2009).
99:
76:
57:
203:
180:
if there is an underlying predisposition, and recording the spike can be an important aid in distinguishing seizure types.
72:
49:
351:
274:
Pathak et al. (2010), Modulation of Nickel-Induced
Bursting with 4-Aminopyridine in Leech Retzius Nerve Cells.
152:
68:
166:
107:
67:
In contrast, there lies non-synaptic mechanism of PDS. Unmasking persistent sodium current in presence of
141:
95:
275:
288:
60:, and the plateau potential of the PDS is maintained by a combination of synaptic potentials (EPSPs,
103:
257:
409:
375:
308:
249:
214:
204:"Ethanol and magnesium suppress nickel-induced bursting activity in leech Retzius nerve cells"
177:
91:
367:
300:
241:
83:
model systems. The initiation of PDS without blocking any channel is much more prevalent in
41:
341:
330:
148:
45:
289:"Sodium-dependent plateau potentials in cultured Retzius cells of the medicinal leech"
56:
channels or GABA-activated Cl influx.. In general, synaptic PDS could be initiated by
403:
371:
133:
129:
53:
261:
173:
137:
80:
245:
147:
Alternatively the PDS can still occur and is less frequently studied by blocking
33:
388:
304:
170:
125:
37:
71:
has been well studied. It is likely that calcium channel blockers will block
352:
http://www.aesnet.org/index.cfm?objectid=AB567D39-E7FF-0F41-282DBE7D52DE97DF
346:
335:
253:
218:
379:
312:
29:
136:. The evidence shows that there is a probable increase in intracellular
156:
387:
Bromfield, Edward B; Cavazos, José E; Sirven, Joseph I, eds. (2006).
87:
84:
276:
http://serbiosoc.org.rs/arch_old/VOL62/SVESKA_4/21%20-%20Pathak.pdf
163:
61:
162:
If several million neurons discharge at once, it shows up on a
128:
are assumed to be predominantly generated by activation of the
114:
176:
spike. Paroxysmal depolarizing shifts can lead to an
75:
and ligand gated calcium channels, thereby affecting
36:
mediated depolarization, which causes voltage gated
389:"Basic Mechanisms Underlying Seizures and Epilepsy"
106:. In contrast, the PDSs could be generated by
8:
132:, subsequently leading to activation of the
90:, for example, thalamocortical neurons, CA3
395:. West Hartford: American Epilepsy Society.
110:or chemical stimulation of single neurons.
28:is a hallmark of cellular manifestation of
197:
195:
193:
189:
120:The PDS found in invertebrates such as
7:
77:calcium-activated potassium channel
14:
211:General Physiology and Biophysics
287:Angstadt, JD; Choo, JJ (1996).
40:channels to open, resulting in
1:
18:paroxysmal depolarizing shift
372:10.1016/0006-8993(73)90647-1
246:10.1016/j.neulet.2005.08.045
393:An Introduction to Epilepsy
98:, and play a vital role in
48:is followed by a period of
426:
293:Journal of Neurophysiology
305:10.1152/jn.1996.76.3.1491
52:mediated by Ca-dependent
69:calcium channel blockers
342:Epileptiform Discharges
113:Depending on influx of
100:information processing
331:Epilepsy and Seizures
142:synaptic transmission
96:signal-to-noise ratio
234:Neuroscience Letters
213:. 28 Spec No: 9–17.
104:synaptic plasticity
26:depolarizing shift
178:epileptic seizure
92:pyramidal neurons
50:hyperpolarization
42:action potentials
417:
396:
383:
317:
316:
284:
278:
272:
266:
265:
229:
223:
222:
208:
199:
149:calcium channels
425:
424:
420:
419:
418:
416:
415:
414:
400:
399:
386:
356:
326:
324:Further reading
321:
320:
299:(3): 1491–502.
286:
285:
281:
273:
269:
231:
230:
226:
206:
201:
200:
191:
186:
12:
11:
5:
423:
421:
413:
412:
402:
401:
398:
397:
384:
360:Brain Research
354:
349:
338:
325:
322:
319:
318:
279:
267:
224:
188:
187:
185:
182:
46:depolarization
13:
10:
9:
6:
4:
3:
2:
422:
411:
408:
407:
405:
394:
390:
385:
381:
377:
373:
369:
365:
361:
355:
353:
350:
348:
344:
343:
339:
337:
333:
332:
328:
327:
323:
314:
310:
306:
302:
298:
294:
290:
283:
280:
277:
271:
268:
263:
259:
255:
251:
247:
243:
240:(1–2): 10–5.
239:
235:
228:
225:
220:
216:
212:
205:
198:
196:
194:
190:
183:
181:
179:
175:
172:
168:
165:
160:
158:
154:
150:
145:
143:
139:
135:
134:NMDA receptor
131:
130:AMPA receptor
127:
124:, and higher
123:
118:
116:
111:
109:
105:
101:
97:
93:
89:
86:
82:
78:
74:
70:
65:
63:
59:
55:
51:
47:
43:
39:
35:
31:
27:
23:
19:
392:
363:
359:
340:
329:
296:
292:
282:
270:
237:
233:
227:
210:
174:epileptiform
161:
153:heavy metals
146:
138:calcium ions
121:
119:
112:
81:invertebrate
66:
25:
21:
17:
15:
169:as a focal
126:vertebrates
184:References
171:interictal
108:electrical
347:eMedicine
336:eMedicine
85:mammalian
410:Epilepsy
404:Category
366:: 1–17.
262:27619277
254:16171948
219:19893074
44:. This
30:epilepsy
380:4573428
313:8890269
157:Calcium
88:neurons
73:voltage
378:
311:
260:
252:
217:
258:S2CID
207:(PDF)
164:scalp
151:with
122:Helix
62:IPSPs
58:EPSPs
24:) or
376:PMID
309:PMID
250:PMID
215:PMID
115:ions
368:doi
345:at
334:at
301:doi
242:doi
238:392
167:EEG
79:in
22:PDS
406::
391:.
374:.
364:52
362:.
307:.
297:76
295:.
291:.
256:.
248:.
236:.
209:.
192:^
102:,
38:Na
34:Ca
16:A
382:.
370::
315:.
303::
264:.
244::
221:.
54:K
20:(
Text is available under the Creative Commons Attribution-ShareAlike License. Additional terms may apply.