The hypogonadal (HPG) mouse is a mutant that lacks a functional
gonadotropin-releasing hormone (
GnRH) gene. In this study, female HPG mice received bilateral intrahypothalamic implants of an immortalized
GnRH-secreting cell line (GT1-7). Nine mice were tested 42- 65 days after implantation to determine whether these cells could support spontaneous and/or N/-methyl-d,
l-aspartic acid (
NMDA)-stimulated
luteinizing hormone (LH) secretion. When sampled via intravenous
catheters, four mice had measurable LH secretion. Three of these mice responded to
NMDA challenges with significant increases in circulating LH.
GnRH immunocytochemistry revealed that GT1-7 cells were present in these four mice and three others in which LH values were not detectable. There were about 1200
GnRH cells dispersed within the piriform cortex and olfactory tubercle, and no
tumor found in one of the HPG mice that responded to
NMDA, whereas the other
NMDA responders had large bilateral
hypothalamic tumors. The presence or absence of such
tumors did not predict the capacity to respond to the
NMDA challenge with alterations in LH secretion. This study provides the first evidence that intrahypothalamic GT1-7 cells can support LH release in the HPG mouse, and that this secretion can be modified by pharmacological agents.