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50°C to give a latency of about 10 s for control rats. Withdrawal
latency was defined as the time between placing the rat on the hot
plate and the time of withdrawal, or licking the hind paw. Each ani-
mal was tested twice, separated by a 30-min rest interval.
The mechanical nociceptive threshold was quantified by using
the Randal-Selitto paw withdrawal test with an analgesy meter
(Ugo Basile, Comerio, Italy), which generates a linearly increasing
mechanical force. The paw withdrawal reflex is automatically
recorded using the latency until withdrawal, in seconds, and the
force at which paw was withdrawn, in grams.
In agreement with others, in these experiments, diabetes was
associated with an increase in the threshold of thermal with-
drawal and a decrease in threshold for mechanical stimulation
(Fig.
2
). As expected, after STZ treatment hind paw thermal
withdrawal latency significantly changed from week 2 until week
6, being 1.8 times higher in STZ untreated group as compared
with the control group (Fig.
2a
). EPO treatment progressively
and significantly did prevent the increases in latency. The
mechanical paw force withdrawal threshold in diabetic rats was
lower at all times than for controls (by about 30%) and EPO
significantly increase: the mechanical threshold in diabetic rats
(Fig.
2b
). EPO did not affect the response latencies in nondia-
betic rats at any time (Fig.
2
).
Figure
3a
shows the hind paw thermal withdrawal threshold
measured over the 5 weeks after beginning EPO treatment accord-
ing to the Therapeutic schedule. Five weeks after STZ injection the
thermal response latency was significantly changed, with hypoalge-
sia in the diabetic untreated group. EPO did not affect the laten-
cies in control treated rats at any time. Noteworthy, EPO was able
to significantly ameliorate thermal nociceptive threshold from week
9 until week 11.
Figure
3b
presents the hind paw force withdrawal thresholds
according to the Therapeutic protocol. Diabetic rats showed a
decrease in the mechanical thresholds at all times (by 30-45%).
Starting from a comparable situation, EPO only partially restore
the diabetic mechanical hyperalgesia.
Antidromic tail NCV was measured for each animal by a method
already used in neuroprotection experiments (
36
). Briefly, the anti-
dromic NCV in the tail nerve was assessed by placing recording
ring electrodes distally in the tail, and stimulating electrodes (stim-
ulus duration 100 ms, filter 1 Hz to 5 MHz) were placed 5 and
10 cm proximally from the recording point. The latencies of the
potentials recorded at the two sites after nerve stimulation were
determined (peak-to-peak) and NCV was calculated. All the neu-
rophysiological determinations were done under standard condi-
tions in room and animal controlled temperature.
3.2 Nerve
Conduction Velocity
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