REGIONAL VARIATION IN GAMMA-AMINOBUTYRIC-ACID TURNOVER - EFFECT OF CASTRATION ON GAMMA-AMINOBUTYRIC-ACID TURNOVER IN MICRODISSECTED BRAIN-REGIONS OF THE MALE-RAT
Dr. Grattan et M. Selmanoff, REGIONAL VARIATION IN GAMMA-AMINOBUTYRIC-ACID TURNOVER - EFFECT OF CASTRATION ON GAMMA-AMINOBUTYRIC-ACID TURNOVER IN MICRODISSECTED BRAIN-REGIONS OF THE MALE-RAT, Journal of neurochemistry, 60(6), 1993, pp. 2254-2264
This study compared the turnover of GABA neurons in different brain ar
eas of the male rat and examined the effect of castration on GABA turn
over in regions of the brain associated with the control of gonadotrop
in secretion. To estimate GABA turnover, GABA was quantified by HPLC i
n microdissected brain regions 0, 30, 60, 90, and 120 min after inhibi
tion of GABA degradation by aminooxyacetic acid (100 mg/kg, i.p.). GAB
A accumulation was linear in all areas for 90 min (p < 0.0 1), and GAB
A turnover was estimated as the slope of the line formed by increased
GABA concentration versus time, determined by linear regression. There
was considerable regional variation both in the initial steady-state
concentrations of GABA and in the rates of GABA turnover. Of 10 discre
te brain structures, GABA turnover was highest in the medial preoptic
nucleus and lowest in the caudate nucleus. Turnover times in the termi
nal fields of known GABAergic projection neurons ranged sevenfold, fro
m 2.6 h in the substantia nigra to 0.4 h in the lateral vestibular nuc
leus. The effect of castration on GABA turnover in 13 microdissected b
rain regions was investigated by measuring regional GABA concentration
s before and 30 min after injection of aminooxyacetic acid in intact r
ats or 2 or 6 days postcastration. Following castration, steady-state
GABA concentrations were increased, and GABA turnover decreased in the
diagonal band of Broca, the medial preoptic area, and the median emin
ence. GABA turnover increased in the medial septal nucleus and was una
ffected in the cortex, striatum, and hindbrain. These results are cons
istent with the hypothesis that testosterone negative-feedback control
of luteinizing hormone-releasing hormone involves steroid-sensitive G
ABAergic neurons in the rostral and medial basal hypothalamus.