Responses of medullary reticulospinal and other reticular neurons to somatosensory and brainstem stimulation in anesthetized or freely-moving ovariectomized rats with or without estrogen treatment.

Abstract

The medical medullary reticular formation (mMRF) is probably involved in controlling lordosis, a feminine mating reflex which requires both estrogen priming and appropriate somatosensory input(s). We have recorded single-unit activity of antidromically identified reticulospinal (RS) and unidentified (UI) neurons in mMRF of ovariectomized rats with or without estrogen treatment to investigate neurohormonal mechanisms regulating lordosis. The units were recorded in both acute and chronic preparations, the latter involving implanted "floating" wire electrodes to allow the influence of estrogen on a particular unit to be followed for several days. A substantial number of RS and UI units in both acute and chronic preparations were either excited or inhibited by a lordosis-eliciting somatosensory stimulation, indicating that the lordosis-eliciting sensory inputs did reach mMRF. The majority of these units responded promptly to the stimulation, and could participate in triggering the short-latency lordosis reflex. Electrical stimulation of several brainstem locations revealed that there was an extensive and specific convergence on mMRF neurons between inputs from the lordosis-eliciting stimulation and mesencephalic central gray, which has been shown to relay lordosis-inducing estrogen influence from hypothalamus to lower brainstem. Therefore, mMRF neurons can receive both the estrogen influence and the lordosis-eliciting inputs and integrate them. Although no apparent estrogen influence was detected in chronic preparations, statistical comparisons of results from acute preparations with or without estrogen treatment suggest that estrogen can increase the proportion of the neurons excited by the lordosis-eliciting stimulation and facilitate neuronal excitability. Both effects are consistent with the prevailing notion that the net lordosis-inducing influence of estrogen is facilitatory, and they may be mechanisms for making lordosis elicitable.