0.5[6.3/13.4]�� -17.7[-5.1/-29.7] 12.5 [8.9/15.0] 9.1 [4.5/10.9]�� -26.6[-12.8/-49.8] 29.8[12.2/45.5] 129.0[45.5/215.5] 300[83/690] 7.2[4.2/12.3] 61.0[17.3/117.4]�� 476[115/1342] 363 [176/552] 1211[580/2112]�� -241[-81/475] 75 [39/154] 77[119/1159]�� -364[-98/-759] SNL4 26 44 12.7[7.9/15.9] 9.0[5.3/12.5]�� -24.5[-14.7/-28.7] 13.0 [9.6/14.7] 9.6[6.6/11.4]�� -24.1[-7.1/-39.7] 27.7 [17.1/38.4] 168.0[72.3/309.5]?358[197/856] 5.9 [4.0/12.4] 36.1[14.0/93.5]�� 299[120/1114] 294 [172/519] 993[369/1936] -194[-24/-485] 88 [52/151] 453[196/920]�� -351[-87/-680] SNL5 41 28 8.4[6.7/10.7] 6.1[4.0/8.3]�� -28.7[-12.6/-48.7] 8.8 [6.9/11.6] 7.4 [4.8/11.0] -8.7[-2.6/-24.3] 7.6 [4.8/13.3] 46.5[11.0/138.5] 309[44/1015] 8.4[5.5/19.6] 50.4[21.7/ONO-4059 biological activity 4-Hydroxytamoxifen web 99.0]�� 369[144/1158] 62 [33/131] 87 [-25/418] -50[-580/147] 51 [29/141] 624[145/1523]�� -609[-113/-1209] 0.002 0.002 0.55 0.038 0.34 0.014 <0.001 <0.01 0.02 0.75 0.38 0.44 <0.001 <0.001 <0.001 0.23 0.54 0.38 Injury effect PAoAHPdAiAoAHPareaAiAoValues are expressed as median [25th/75th percentile]. Amplitude and area hyperpolarized compared with the RMP are considered positive. Injury effect P indicates the ANOVA main effect of injury for the parameter in that row. For post hoc comparisons: different from Control P < 0.05, P < 0.01; different from SNL4 P < 0.05, P < 0.01; 20th different from single �P < 0.05, ��P < 0.01. AHPamp, afterhyperpolarization amplitude; AHParea, area of the afterhyperpolarization; AHPd, afterhyperpolarizarion duration; n, number of cells; SNL, spinal nerve ligation; SNL4, 4th lumbar ganglion after SNL; SNL5, 5th lumbar ganglion after SNL.Failure of the somatic depolarization reflects propagation failure at the T-junctionPrior observations in neurons from amphibians, embryonic rat DRGs and adult rabbit nodose ganglia (Stoney, 1990; Ducreux et al. 1993; Luscher et al. 1994b) have established the T-junction as the site with the lowest safety factor for propagation of APs between the opposing processes of the sensory neuron. We extended these findings to adult mammalian DRG neurons by employing collision experiments in which we monitored somatic membrane depolarizations induced by converging APs that were triggered in the peripheral and central processes (Fig. 3). We observed that whenever the second of a pair of peripheral pulses produced either an incomplete somatic depolarization (the electrotonic residue of a distant AP) or a full somatic AP, this is accompanied by blockade of the AP coming from the central process. Thus, both types of somatic depolarization are evidence for successful transit of the impulse between the peripheral and central processes (Fig. 3), which confirms findings in other preparations (Stoney, 1990). We further established that when the time between a pair of peripheral pulses was reduced to an interval at which the second AP fails to produce any type of somatic depolarization, this simultaneously allowed the arrival of an impulse generated in the central process.This indicates that whenever the AP approaching the T-junction from peripheral process fails to enter the stem axon, it also fails to enter the central process. Therefore, failure of longitudinal conduction from one process to the other can be inferred from complete loss of the somatic depolarization. On the basis of these observations, only complete failure of somatic depolarization was regarded as evidence of longitudinal propagation failure for the purpose of determining RP and following frequency.Pulse repetition ra.0.5[6.3/13.4]�� -17.7[-5.1/-29.7] 12.5 [8.9/15.0] 9.1 [4.5/10.9]�� -26.6[-12.8/-49.8] 29.8[12.2/45.5] 129.0[45.5/215.5] 300[83/690] 7.2[4.2/12.3] 61.0[17.3/117.4]�� 476[115/1342] 363 [176/552] 1211[580/2112]�� -241[-81/475] 75 [39/154] 77[119/1159]�� -364[-98/-759] SNL4 26 44 12.7[7.9/15.9] 9.0[5.3/12.5]�� -24.5[-14.7/-28.7] 13.0 [9.6/14.7] 9.6[6.6/11.4]�� -24.1[-7.1/-39.7] 27.7 [17.1/38.4] 168.0[72.3/309.5]?358[197/856] 5.9 [4.0/12.4] 36.1[14.0/93.5]�� 299[120/1114] 294 [172/519] 993[369/1936] -194[-24/-485] 88 [52/151] 453[196/920]�� -351[-87/-680] SNL5 41 28 8.4[6.7/10.7] 6.1[4.0/8.3]�� -28.7[-12.6/-48.7] 8.8 [6.9/11.6] 7.4 [4.8/11.0] -8.7[-2.6/-24.3] 7.6 [4.8/13.3] 46.5[11.0/138.5] 309[44/1015] 8.4[5.5/19.6] 50.4[21.7/99.0]�� 369[144/1158] 62 [33/131] 87 [-25/418] -50[-580/147] 51 [29/141] 624[145/1523]�� -609[-113/-1209] 0.002 0.002 0.55 0.038 0.34 0.014 <0.001 <0.01 0.02 0.75 0.38 0.44 <0.001 <0.001 <0.001 0.23 0.54 0.38 Injury effect PAoAHPdAiAoAHPareaAiAoValues are expressed as median [25th/75th percentile]. Amplitude and area hyperpolarized compared with the RMP are considered positive. Injury effect P indicates the ANOVA main effect of injury for the parameter in that row. For post hoc comparisons: different from Control P < 0.05, P < 0.01; different from SNL4 P < 0.05, P < 0.01; 20th different from single �P < 0.05, ��P < 0.01. AHPamp, afterhyperpolarization amplitude; AHParea, area of the afterhyperpolarization; AHPd, afterhyperpolarizarion duration; n, number of cells; SNL, spinal nerve ligation; SNL4, 4th lumbar ganglion after SNL; SNL5, 5th lumbar ganglion after SNL.Failure of the somatic depolarization reflects propagation failure at the T-junctionPrior observations in neurons from amphibians, embryonic rat DRGs and adult rabbit nodose ganglia (Stoney, 1990; Ducreux et al. 1993; Luscher et al. 1994b) have established the T-junction as the site with the lowest safety factor for propagation of APs between the opposing processes of the sensory neuron. We extended these findings to adult mammalian DRG neurons by employing collision experiments in which we monitored somatic membrane depolarizations induced by converging APs that were triggered in the peripheral and central processes (Fig. 3). We observed that whenever the second of a pair of peripheral pulses produced either an incomplete somatic depolarization (the electrotonic residue of a distant AP) or a full somatic AP, this is accompanied by blockade of the AP coming from the central process. Thus, both types of somatic depolarization are evidence for successful transit of the impulse between the peripheral and central processes (Fig. 3), which confirms findings in other preparations (Stoney, 1990). We further established that when the time between a pair of peripheral pulses was reduced to an interval at which the second AP fails to produce any type of somatic depolarization, this simultaneously allowed the arrival of an impulse generated in the central process.This indicates that whenever the AP approaching the T-junction from peripheral process fails to enter the stem axon, it also fails to enter the central process. Therefore, failure of longitudinal conduction from one process to the other can be inferred from complete loss of the somatic depolarization. On the basis of these observations, only complete failure of somatic depolarization was regarded as evidence of longitudinal propagation failure for the purpose of determining RP and following frequency.Pulse repetition ra.
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