Participation of angiotensin II in learning and memory. III. Interactions of angiotensin II with GABAergic drugs

The experiments were carried out on male albino rats trained and tested for retention (24 hr later) in a shuttle-box. Angiotensin II (AT II) 0.10 micrograms intracerebroventricularly (i.c.v.), gamma-aminobutyric acid (GABA) 100 micrograms i.c.v., bicuculline 0.5 and 1.0 mg/kg intraperitoneally (i.p.), and picrotoxin 0.5 and 1.0 mg/kg i.p. administered independently or in combinations immediately after training. AT II was found to improve retention. GABA also facilitated retention. Combination of AT II + GABA potentiated the memory-improving effect of AT II. Bicuculline and picrotoxin at a dose of 0.5 mg/kg did not affect retention, while at a dose of 1.0 mg/kg they improved it. Combinations of AT II + bicuculline (0.5 mg/kg) and AT II + picrotoxin (0.5 mg/kg) abolished the retention-improving effect of AT II. Bicuculline (0.5 mg/kg) or picrotoxin (0.5 mg/kg) abolished the retention-facilitating effect of the combination of AT II + GABA as well as the potentiating action of GABA on the memory effect of AT II. These results suggest the participation of GABAergic transmission in the CNS in the mechanisms of the long-term memory-improving effect of AT II.     

Statistical analysis of clinical, radiographic, and histologic features of temporomandibular arthropathy

For a variety of reasons, the past few years have brought about a tremendous emphasis on conditions affecting the temporomandibular joint and associated structures. Although important advances are being made relative to the diagnosis and treatment of these conditions, a myriad of problems remain for the practitioner who tries to sort through the literature or who attends courses in order to determine a means for properly diagnosing and treating these patients. This article attempts to develop correlations between certain clinical and radiographic findings documented by histologic evaluation as a beginning guide to more sound diagnosis.     

Clinical and hormonal effects of chronic gonadotropin-releasing hormone agonist treatment in polycystic ovarian disease

Previously, we reported that short term administration of a highly potent GnRH agonist (GnRHa) for 1 month to patients with polycystic ovarian disease (PCO) resulted in complete suppression of ovarian steroidogenesis without measurable effects on adrenal steroid production. This new study was designed to evaluate the effects of long term GnRHa administration in PCO patients with respect to their hormone secretion patterns and clinical responses. Eight PCO patients and 10 ovulatory women with endometriosis were treated daily with sc injections of [D-His6-(imBzl]),Pro9-NEt]GnRH (GnRHa; 100 micrograms) for 6 months. Their results were compared to hormone values in 8 women who had undergone bilateral oophorectomies. In response to GnRHa, PCO and ovulatory women had rises of serum LH at 1 month, after which it gradually declined to baseline. In both groups FSH secretion was suppressed throughout treatment. Serum estradiol, estrone, progesterone, 17-hydroxyprogesterone, androstenedione, and testosterone levels markedly decreased to values found in oophorectomized women by 1 month and remained low thereafter. In contrast, serum pregnenolone and 17-hydroxypregnenolone were partially suppressed, and dehydroepiandrosterone, dehydroepiandrosterone sulfate, and cortisol levels did not change. Clinically, hyperplastic endometrial histology in three PCO patients reverted to an inactive pattern, and proliferative endometrium in two other PCO patients became inactive in one and did not change in the other. Regression of proliferative endometrial histology occurred in all ovulatory women. Vaginal bleeding occurred in all women studied during the first month of GnRHa administration, after which all but one PCO patient became amenorrheic. Hot flashes were noted by all ovulatory women and by four of eight PCO patients. All PCO patients noted subjective reduction of skin oiliness, and five had decreased hair growth. We conclude that in premenopausal women: 1) chronic GnRHa administration results in apparently complete persistent suppression of ovarian steroid secretion; 2) adrenal steroid secretion is not influenced directly or indirectly; and 3) its use may be helpful in the treatment of endometrial hyperplasia and ovarian androgen excess in women with PCO.     

Effects of dexamethasone on central and peripheral ACTH systems in the rat

To investigate the simultaneous effects of dexamethasone on peripheral and central adrenocorticotropic hormone (ACTH) systems, rats were treated with dexamethasone or saline for 4 days. Pituitary, plasma, hypothalamus and cerebrospinal fluid (CSF) were then collected and analyzed for ACTH immunoreactivity. Additionally, hypothalamic tissue extracts were analyzed for corticotropin-releasing hormone (CRH) immunoreactivity. Dexamethasone significantly lowered peripheral levels of ACTH as measured in pituitary and plasma. Hypothalamic ACTH content significantly increased while CSF ACTH significantly decreased with dexamethasone treatment. Hypothalamic CRH concentrations showed a small but statistically insignificant decrease. These results suggest that prolonged exposure to dexamethasone affects central as well as peripheral ACTH activity, corroborate our previous findings in rhesus monkeys of decreased CSF ACTH in response to prolonged dexamethasone treatment, suggest that dexamethasone may inhibit the release of ACTH from hypothalamic neurons into the CSF, and provide evidence that the effect of dexamethasone on pituitary ACTH content is of greater magnitude than its effect on hypothalamic CRH.