Table 1.

BDNF does not alter intrinsic excitability

BDNFControlTrkB-IgG
Vm(mV)−50.7  ±  1.3,  n = 24−50.8  ±  1.3,  n = 20−49.3  ±  1.1,  n = 24
Rin(MΩ)175.8  ±  16.1,  n = 27213.4  ±  16.9,  n = 22220.7  ±  20.2,  n = 24
Cm (pF)69.1  ±  3.6,  n = 27*58.2  ±  3.3,  n = 2255.5  ±  2.8,  n = 24
VT (mV)−35.1  ±  1.0,  n = 24−33.0  ±  1.2,  n = 20−33.3  ±  0.9,  n = 24
AP ½-width (msec)2.1  ±  0.2,  n = 242.1  ±  0.2,  n = 201.8  ±  0.2,  n = 24
AP height (mV)93.2  ±  3.05,  n = 24101.4  ±  3.6,  n = 2096.7  ±  2.8,  n = 24
  • Neither long-term augmentation or depletion of BDNF affected the shape of action potentials or the voltage threshold for action potential initiation (Vm, resting potential; Rin, input resistance; Cm, membrane capacitance; VT, voltage threshold for action potential initiation; AP ½-width, width of action potential at half-height; AP height, height of action potential; procedures as described in Materials and Methods). A small increase in capacitance, however, suggested the possibility of minor morphological changes; asterisk denotes significant differences between BDNF and control groups (p < 0.03 by ANOVA) and between BDNF and TrkB-IgG groups (p < 0.005 by ANOVA) with respect to cell capacitance. No other differences were statistically significant at the 0.05 level by ANOVA for any parameter measured.