The effect of Ac-LHRH5-10, an LHRH fragment capable of facilitating lordosis, and LHRH on the firing rate of mediobasal hypothalamic neurons receiving input from the septal area, (a site containing the majority of LHRH perikarya) was studied via conventional extracellular recording techniques. A multibarrelled glass electrode assembly was lowered through the dorsomedial and ventromedial hypothalamus to detect single units responsive to septal area stimulation, and to iontophoretically apply Ac-LHRH5-10 and LHRH. Ovariectomized rats were primed with estradiol benzoate (EB; n=21) or left untreated (n=34) to determine if the neuronal responsiveness to septal area stimulation and/or to the two peptides was subject to estrogenic modulation.
Of the total number of 228 neurons recorded in the study, 51 units (22.4%) were orthodromically responsive to septal area stimulation. The orthodromic responses in EBprimed animals (n = 20) were characterized by a short-latency, short-duration increase in membrane excitability. When spontaneous activity was sufficiently high, the excitatory response was followed by, or superimposed upon, an inhibitory response of longer duration. Similar orthodromic excitatory and inhibitory response characteristics were observed in 21 of the 31 neurons recorded in nonprimed animals. In the remaining ten neurons, however, the excitatory component was absent.
Iontophoretic application of both Ac-LHRH5-I0 and LHRH was found to produce predominantly an inhibitory effect on cell firing. Most neurons responded to the two peptides in a similar manner (i.e., inhibited by both peptides, excited by both peptides, or not effected by either peptide). However, 39.5% of the neurons exhibited a different response to the two agents. Responsiveness to Ac-LHRH5-10, but not to LHRH, was enhanced by estrogen priming. Iontophoretically applied Ac-LHRH5-10 was found to mimic the inhibitory component of the orthodromic response in 21 of the 30 neurons tested. The same was true for LHRH in 15 of the 27 neurons tested.
Taken together, these results indicate that the septal-stimulation-evoked inhibition of mediobasal hypothalamic neurons may be mediated by the LHRH fragment and/or LHRH and that this input is subject to estrogenic modulation. Furthermore, the results suggest that Ac-LHRH5-10 may act to facilitate lordotic responding by inhibiting the firing rate of mediobasal hypothalamic neurons.