Excitotoxic lesions of the medial amygdala differentially disrupt prolactin secretory responses in cycling and mated female rats.
This study examined the role of the posterodorsal medial amygdala (MePD) in the control of prolactin secretion in gonadally intact female rats 20 min after mating, during the oestrous cycle, and during early pregnancy/pseudopregnancy (P/PSP). Cycling females received bilateral infusions of an excitotoxic dose of N-methyl-D-aspartate (NMDA) or vehicle into the MePD. Two to 4 weeks later, they were surgically implanted with intra-atrial catheters for repeated blood sampling and were mated on the evening of proestrus until receiving 5, 10, 15 or 20 intromissions or 15 mounts-without-intromission (MO) from males. The percentages of rats becoming P/PSP increased as a function of numbers of intromissions received. All groups receiving intromissions showed similar approximately four-fold increases in plasma prolactin concentrations 20 min after mating, while MO rats showed no increase at this time. There was no effect of NMDA lesion on this acute secretory response. Among rats that continued cycling, bilateral MePD lesion completely abolished the diurnal preovulatory prolactin surge, while incomplete and sham lesions did not. In rats that subsequently became P/PSP, bilateral lesion of the MePD resulted in dampening of prolactin concentrations at all sampling times 6-7 days after mating, while incomplete or sham lesions did not alter prolactin secretion at these times. These results demonstrate that the MePD is selectively important for the secretion of prolactin on the afternoon of proestrus and that this structure may also modulate prolactin release in P/PSP rats. Activity within MePD neurones does not appear to be required for the acute prolactin response to vaginocervical stimulation which occurs within minutes after mating.
Polston
E K
EK
Division of Neuroscience, Oregon Regional Primate Research Center, Beaverton, OR, USA.
Erskine
M S
MS
D000679:Amygdala / Q000378:metabolism* / Q000473:pathology*; D000818:Animals; D003307:Copulation / Q000502:physiology*; D004971:Estrus / Q000378:metabolism*; D018690:Excitatory Amino Acid Agonists / Q000633:toxicity; D005260:Female; D005498:Follicular Phase / Q000378:metabolism; D016202:N-Methylaspartate / Q000633:toxicity; D009410:Nerve Degeneration / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D009498:Neurotoxins; D011187:Posture / Q000502:physiology; D011374:Progesterone / Q000097:blood; D011388:Prolactin / Q000097:blood / Q000378:metabolism*; D011863:Radioimmunoassay; D051381:Rats; D020318:Rats, Long-Evans
D018690:Excitatory Amino Acid Agonists; D009498:Neurotoxins; D011374:Progesterone; D016202:N-Methylaspartate; D011388:Prolactin