Immunoreactive Substance P and LH-RH Content in Median Eminence and Pituitary Gland during Proestrus, Oestrus, Lactation and after Anterior Hypothalamic Deafferentation

A dramatic example of neuronal and physiological plasticity in adult mammals occurs during the transition from a non-maternal to a maternal, lactating state. In this study we compared gene expression within a large continuous region of the CNS involved in maternal behaviors (hypothalamus, preoptic regions, and nucleus accumbens) between lactating (L) (postpartum Day 7) and randomly cycling virgin (V) outbred mice. Using high density oligonucleotide arrays representing 11,904 genes, two statistical algorithms were used to identify significant differences in gene expression: robust multi array (p < 0.001) (n = 92 genes) and significance analysis of microarrays using a 10% false discover rate (n = 114 genes). 27 common genes were identified as significant using both techniques. A subset of genes (n = 5) were selected and examined by real-time PCR. Our findings were consistent with previous published work. For example, neuropeptide Y (NPY) and proenkephalin were elevated in L mice, whereas POMC was decreased. Increased levels of NPY Y2 receptor and polo-like kinase and decreased levels of endothelin receptor type b in L mice are examples of novel gene expression changes not previously identified. Expression differences occurred in broad classes. Together, our findings provide possible new material on gene expression changes that may support maternal behaviors. The advantages and drawbacks of sampling large CNS regions using arrays are discussed.

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Effect of Hypothalamic Deafferentation on the Pulsatile Secretion of Luteinizing Hormone in Ovariectomized Lactating Rats*

Tsukamura

Maeda

Ohkura

et al. 1990

J Neuroendocrinology

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The pulsatile luteinizing hormone (LH) secretion in ovariectomized lactating rats bearing complete (CD), anterior (AD), anterolateral (ALD), posterior (PD), or roof (RD) deafferentation of the hypothalamus was determined. All lactating rats were ovariectomized on Day 2 of lactation (Day 0, day of parturition). The deafferentation of nerve fibres to the mediobasal hypothalamus was performed on Day 6 or 7 of lactation. Twenty-four h after the surgery, blood samples were taken through the indwelling atrial catheter every 6 min for 3 h. Plasma concentrations of LH and prolactin (PRL) were measured by radioimmunoassay. The loss of LH pulses associated with lactation was still apparent following AD, PD and sham-deafferentation (SD); pulsatile LH secretion was, however, present in rats with CD, ALD and RD despite continued suckling. The only significant difference in plasma PRL concentrations among the various groups was a reduction in the PRL level in rats with RD in comparison to those with SD. We conclude that the neural signal responsible for the inhibition of pulsatile LH release by suckling is conveyed through the dorsal part of the hypothalamus and PRL does not mediate the suppression of LH pulses in mid-lactationWe reported previously that the suckling stimulus is able to suppress pulsatile luteinizing hormone (LH) secretion in the absence of the negative feedback of steroids in ovariectomized lactating rats (I, 2). It has also been reported that the hypothalamic LH-releasing hormone (LHRH) content in lactating rats is comparable to that of cyclic rats at dioestrus (3,4) and that daily LH surges occur in ovariectomized lactating rats implanted with oestradiol (5). These results suggest that the suckling stimulus suppresses LH release principally by inhibiting pulsatile LHRH release rather than LHRH production.The putative pulse generator regulating pulsatile LHRH release has been thought to be located in the mediobasal hypothalamus (MBH), since pulsatile LH secretion has been observed in either cyclic or ovariectomized rats with complete deafferentation of the MBH (6, 7), and since LHRH has been reported to be released in a pulsatile manner from the MBH in vitro (8). However, the possibility that subchiasmatic LHRH fibres (9), which might be spared by the deafferentation in vivo, maintained the pulsatile secretory pattern could not be ignored.Tindal(l0) has identified the central pathways which convey the suckling stimulus for oxytocin and prolactin (PRL) release in the rabbit. Little is known, however, about the final neural pathway in the hypothalamus for suppressing LH pulses in lactating rats. In the present study, we have made various hypothalamic deafferentations in ovariectomized lactating rats to determine the neural pathway which conveys the inhibitory signal of the suckling stimulus for pulsatile LH secretion. ResultsThe suckling behaviour of the litter of ovariectomized lactating rats with the various hypothalamic deafferentations was similar to that of rats with sham-deafferentation (SD). Th...

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Immunoreactive Substance P and LH-RH Content in Median Eminence and Pituitary Gland during Proestrus, Oestrus, Lactation and after Anterior Hypothalamic Deafferentation

Cited by 6 publications

References 8 publications

Suppression of Noradrenaline-Induced Ovulation by Administration of Substance P into the Third Cerebral Ventricle in Pseudo-Pregnant Rats

Suppression of Noradrenaline-Induced Ovulation by Administration of Substance P into the Third Cerebral Ventricle in Pseudo-Pregnant Rats

Gene array profiling of large hypothalamic CNS regions in lactating and randomly cycling virgin mice

Effect of Hypothalamic Deafferentation on the Pulsatile Secretion of Luteinizing Hormone in Ovariectomized Lactating Rats*

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