We measured the peripheral-type benzodiazepine receptors (PBRs), a marker of gliosis, in 26 brain areas (cerebral cortex, thalamus and extrapyramidal system) of the postmortem brains of 13 chronic schizophrenics and 10 controls, using [3H] PK 11195 as a ligand for the receptor assay. The specific [3H] PK 11195 binding was significantly decreased in three brain areas (superior parietal cortex, primary visual area and putamen) of schizophrenics, although there were no changes in the binding in the other brain areas. Scatchard analysis revealed that there were decreases in both the Bmax and Kd of [3H] PK 11195 binding in the brain areas. These results were almost in accordance with a number of neuropathological studies reporting that there was no change or reduction in glial cells in the brain regions of schizophrenics and suggested that the decreased density of PBRs in the brain may be involved in the pathophysiology of schizophrenia, associated with reduced production of neurosteroids coupled to PBRs.

Regulation of prolactin secretion in pituitary is considered to be mostly carried with the action of prolactin inhibiting factor in hypothalamus. We have investigated on the subject of prolactin releasing factor in the hypothalamus of rats in last stage of pregnancy using puerperal and ovariectomized rats as recipients. After prepared the cell-free system of pregnant rat hypothalamus with sonic oscillator, supernatant was produced by ultracentrifuge (25,000 X g, 30 min.) and utilized for the experiments. When the extract was injected intramuscularly to puerperal rats (48-60 hours after delivery), serum prolactin values increased gradually to 3 times of control values, but pituitary prolactin values showed the variation with decrease and recovery. The control values were obtained by determination after injection of cerebral cortical extract to puerperal rats. After administration of a extract of non-pregnant rat hypothalamus to puerperal rats, serum prolactin values decreased and pituitary prolactin values increased antagonistically. In the ovariectomized rats pretreated with estradiol and progesterone, serum prolactin values increased in 1 hour after administration of the extract of pregnant rat hypothalamus, but pituitary prolactin values did not show any variation. The present experiment suggests that the prolactin secretion promoting factor exists in the hypothalamus of pregnant rats and predominates over as compared with PIF in last stage of pregnancy.

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The present study attempted to elucidate stimulatory factor(s) in the rat hypothalamus which controls prolactin secretion from the anterior pituitary.Rat serum prolactin was elevated so much in late pregnancy that we prepared the hypothalamic extract of late pregnant rats. Prolactin levels in serum and pituitary were determined by radioimmunoassay. After injection of this extract into a lactating rat 43-60 hr after delivery, the serum prolactin level was elevated significantly one to four hr later and the pitui tary prolactin level declined two hr later. On the other hand, the hypothalamic extract of normal female rats prepared in a similar manner inhibited prolactin secretion from the anterior pituitary in the lactating rat as described by other authors.These data indicate that the prolactin releasing factor may consist in the hypothalamus of late pregnant rat, and be predominant over the prolactin inhibiting factor during late pregnancy. Prolactin secretion was also investigated in lactating and non-lactating puerperium rats. Prolactin in serum and pituitary declined with days after delivery in non-lactating rats, but not in lactating rats. The presumed factor for such prolactin release in lactating rats is considered to be the prolactin releasing factor. prolactin; prolactin releasing factor; hy pothalamus; lactation and pregnancyThe predominantly inhibitory influence of the hypothalamus on prolactin secretion from the pituitary has been well established.The stimulatory factor, however, was recently reported.The participation of serotonergic neurons appears to be important in the neuronal events leading to this hypothalamic stimulation of prolactin release (Lu and Meites 1973;Krulich 1975). In addition, oral admin istration of 5-hydroxytryptophan, a precursor of serotonin, significantly increases plasma prolactin (Kato et al. 1974).Although evidence of the hypothalamic regulation of prolactin secretion is generally accepted, there has been no establishment of hypothalamic control during pregnancy when prolactin secretion increases. In the present study, the prolactin releasing factor (PRF) in the hypothalamus was investigated using late pregnant

Tohoku J. exp. Med., 1978, 126 (1), 77-84 -Pregnant rat hypothalamic fragments were extracted with 30 mM Tris-HCl buffer at pH 7.8, subjected to enzymatic digestion, and applied to gel filtration on Sephadex G-25 for purification of the prolactin releasing factor.Effect of the eluted fractions on the release of prolactin were tested by the determination of serum and pituitary prolactin after the injection in lactating rats.Prolactin was estimated by radioimmunoassay.One fraction (tube number 61-73) eluted later than synthetic ACTH enhanced release of prolactin 30min after injection, but other fractions had no effect on the release of prolactin.Prolactin releasing factor would be quan titatively predominant over prolactin inhibiting factor in pregnant rat. prolactin; prolactin releasing factor; hypothalamus; lactation and pregnancy