All recordings were in slices obtained from SAL-treated rats.
a. Recording traces illustrate that a
marked membrane hyperpolarization (more negative than −110 mV) was
immediately followed by a small, Vm rebound (i.e., a
subthreshold, low voltage-activated (LVA)-potential; upper trace). Tat (40 nM)
markedly enlarged this LVA potential (middle trace). The Tat-induced effect was
abolished by concurrent bath application of diltiazem (40 nM; lower trace).
b. Quantification of LVA-potential area.
Tat (40 nM) significantly enlarged the subthreshold LVA-potential area and this
effect was abolished by co-perfusion of diltiazem (40 nM) (n=9 neurons recorded
from 9 rats; one-way rmANOVA, p=0.008; post
hoc Dunnett’s test, **p<0.01).
c. Traces from a single neuron
illustrating that Tat-induced LVA-potential enhancement achieved the firing
threshold and elicited spontaneous action potentials.
d. Number of neurons that displayed the
LVA-potential and spontaneous firing triggered by the
LVA-Vm rebound; data are presented as%of
total neurons tested (n=22 from 17 rats). Only one neuron showed the
Vm rebound-triggered firing prior to Tat
perfusion. During Tat (40 nM) application, 10/22 neurons demonstrated
Vm rebound-triggered firing (Chi-squared test,
**p<0.01). e. In two
of the ten neurons showing the Vm rebound
(illustrated are traces from one of these two), Tat (40 nM) depolarized the RMP
to spiking threshold so that spontaneous firing occurred, and spiking was
further enhanced by the Vm rebound in response to a
hyperpolarizing stimulus