SPONTANEOUS AND AMPHETAMINE-EVOKED RELEASE OF CEREBELLAR NORADRENALINE AFTER SENSORIMOTOR CORTEX CONTUSION - AN IN-VIVO MICRODIALYSIS STUDYIN THE AWAKE RAT
Ka. Krobert et al., SPONTANEOUS AND AMPHETAMINE-EVOKED RELEASE OF CEREBELLAR NORADRENALINE AFTER SENSORIMOTOR CORTEX CONTUSION - AN IN-VIVO MICRODIALYSIS STUDYIN THE AWAKE RAT, Journal of neurochemistry, 62(6), 1994, pp. 2233-2240
Microdialysis sampling combined with HPLC was used to assess spontaneo
us and d-amphetamine (AMPH)-evoked release of noradrenaline (NA) in th
e cerebellum 1 day after probe implantation and 1 day after contusion
of the right sensorimotor cortex (SMCX) in rats. In normal controls th
e mean +/- SEM basal NA release was 10.08 +/- 0.97 pg in the left cere
bellar hemisphere and 8.21 +/- 1.17 pg in the right hemisphere 22-24 h
after probe implantation. The average +/- SEM NA release in a 3-h per
iod after administration of AMPH (2 mg/kg, i.p.) increased to 453 +/-
47.35 pg in the left and to 402 +/- 49.95 pg in the right cerebellar h
emisphere. NA release (range of 413-951% increase over baseline) was m
aximal 20-40 min postdrug, returned to basal levels within 5 h, and re
mained unchanged for the 22-24-h postdrug measurement period. Animals
with a focal SMCX contusion had a marked depression of both spontaneou
s and AMPH-evoked NA release. Mean +/- SEM basal NA release was 4.84 /- 1.09 pg in the left and 4.95 +/- 0.43 pg in the right cerebellar he
misphere from 22 to 24 h postinjury, with NA levels increasing to 259
+/- 75.44 and 219 +/- 23.45 pg in the respective hemispheres over a 3-
h period after AMPH. The maximal AMPH-induced increase in NA release r
anged from 522 to 1,088% of basal levels in contused rats, with NA rel
ease returning to predrug levels within 5 h and remaining depressed fo
r at least 48 h postinjury. These data indicate that although neocorti
cal injury results in a bilateral reduction of extracellular levels of
NA in cerebellum, AMPH-releasable NA stores are present in the cerebe
llum. These effects may be related to locomotor impairments and AMPH-f
acilitated behavioral recovery after cortical injury.