The technique of intracranial microdialysis was used to monitor changes in the outflow of the catecholamines, noradrenaline, adrenaline and dopamine and the inhibitory amino-acid y-arninobutyric acid (GABA) in the preopticlseptal area of the conscious ewe during an oestradiol-induced surge of luteinizing hormone (LH). The s a m e animals were sampled twice from an identical brain site, once in the presence of oestradiol and once in its absence, when no surge occurred and LH levels remained low. Changes in the outflow of GABA, noradrenaline and adrenaline (but not dopamine) were related to changes in LH secretion. Specifically, GABA outflow was maximal in the h o u r s following oestradiol administration but began a sustained fall some 10 h before the surge began, to level off just before the first increment in LH secretion. Low GABA concentrations were maintained until after gonadotrophin levels had once more returned to baseline. The release of all three catecholamines was pulsatile. Noradrenergic activity was greater in the presence of oestradiol although activity did not alter over t h e 20 h of sampling. The pulse frequency of adrenaline was maximal in the h o u r s immediately prior to the LH surge and minimal in the hours following its initiation. These data suggest that a decrease in GABAergic transmission in t h e vicinity of t h e LH-releasing hormone cell bodies is a necessary component of the neural mechanism by which the oestradiol-induced surge of LH is generated. A general increase in noradrenergic activity coupled with changes in the release of adrenaline at t h e time of the surge may be additional prerequisites for successful ovulation.The hormonal events which are required to elicit the massive increment in luteinizing hormone (LH) secretion necessary to cause ovulation are relatively well understood and allow us, to some degree, to manipulate both our own fertility and that of other species ( I , 2). In contrast, the neural events which are a prerequisite for the LH surge remain largely enigmatic.Our knowledge has recently been extended by data demonstrating conclusively that the oestradiol-induced LH surge in the ewe results from a massive increase in the secretion of LH-releasing hormone (LHRH) into the portal vessels from nerve terminals located in the median eminence (3, 4). The cell bodies of these LHRH neurons are located in the preoptic and septa1 areas (POA/S) of the ovine brain ( 5 ) but as these cells d o not themselves possess oestrogen receptors (6), other steroid-sensitive neural elements must mediate oestrogen effects on LH. In relation to this, the POA is innervated by neurons containing the catecholamine neurotransmitters noradrenaline (NA; 7, 8) adrenaline (A; 9) and dopamine (DA; 10) and the inhibitory amino-acid y-aminobutyric acid (GABA; 1 I , 12). NA and GABA neurons have been shown to concentrate oestrogen (1 3-1 5 ) and all four neuroactive substances have been implicated in mediating the actions of gonadal steroids on LH secretion (16,17). This study sought to d...