NMDA receptor-mediated control of GABA release from neurointermediate lobes of female and male rats.

The effect of glutamate (GLUT) and its ionotropic receptor agonists on K(+)-evoked GABA release from the neurointermediate lobe (NIL) was investigated in diestrus, ovariectomized, ovariectomized-estrogenized female rats and intact male rats. GLUT and N-methyl-D-aspartate (NMDA) increased K(+)-evoked GABA release from the NIL in all the experimental groups. This stimulatory effect of NMDA was blocked by specific NMDA receptor antagonists but not by non-NMDA receptor antagonists. However, kainate did not modify evoked GABA release from the NIL in any of these groups. Neither GLUT nor NMDA modified nitric oxide synthase activity. These results indicate that GLUT, acting through NMDA receptors, stimulates evoked GABA release from the NIL of female and male rats. This effect is not influenced by gonadal status and does not appear to be mediated by nitric oxide production.

Identification and neuroanatomical distribution of immunoreactivity for mammalian gonadotropin-releasing hormone (mGnRH) in the brain and neural hypophyseal lobe of the toad Bufo arenarum.

The presence and distribution of gonadotropin-releasing hormone (GnRH) in sexually mature specimens of Bufo arenarum was studied by reverse phase/high performance liquid chromatography (RP-HPLC) combined with radioimmunoassay and immunocytochemistry. The analysis of brain extracts with RP-HPLC followed by radioimmunoassay with PBL#45 antiserum showed the presence of only one peak with immunoreactivity for GnRH (ir-GnRH) having the chromatographic and immunological characteristics of mammalian GnRH (mGnRH). This peak was further analyzed with two mGnRH-specific antisera, EL-15 and m1076, yielding serial dilution displacement curves parallel to those obtained with the mGnRH synthetic standard. Immunocytochemical results with the monoclonal antibody LRH13 showed the presence of a terminal nerve-septo-preoptic system with neurons and fibers distributed from the olfactory bulb, septal area, and anterior preoptic area toward the hypothalamus and hypophyseal neural lobe. The main group of ir-GnRH fibers and neurons was identified in the anterior preoptic area. These neurons appear to be the origin of fibers that, after surrounding the preoptic recess, border the dorsal surface of the optic chiasma, extend through the infundibulum, traverse the external layer of the median eminence, and end in the pars nervosa.

Pathology of the neurohypophysis.

Neurohypophysis is composed of nerve fibers and has an intimate morphologic and functional contact with the hypothalamus. Pathology of the posterior lobe of the pituitary gland may develop several clinical features such as diabetes insipidus, which is caused by infections, vascular events, surgical complications and benign and malignant tumors as well as metastasis. Inappropriate secretion of vasopressin (Schwartzbartter syndrome) is due to excessive vasopressin release from the posterior pituitary or the ectopic production by various tumors, mainly carcinoid of the lung.

Effect of salt depletion on sodium concentration in serum and urine of Bufo chilensis. Evidences for increased levels of neurohypophysial principles in their plasma.

Salt-depleted toads Bufo chilensis were compared with animals maintained in NaCl solution and a control group with respect to Na+ content in serum and urine. Plasma hydro-osmotic activity of the animals was measured by increased water transfer across the isolated urinary bladder of the frog (Caudiverbera caudiverbera). Sodium in serum is not affected by pre-adaptation in distilled water. Urine Na+ is markedly reduced. Plasma from depleted animals increases water transfer across the isolated urinary bladder. Immersion in NaCl solution did not have this effect. An increase in neurohypophysial hormones in the blood of the animals is postulated.

Evidences against a primary role for the pituitary neural lobe in the development and maintenance of DOC-salt hypertension.

The role of the antidiuretic hormone (ADH) in the development and maintenance of the hypertensive state produced by deoxycorticosterone (DOC) and salt in rats is a matter of controversy. The effects of neural lobe lesions that would prevent the release of the hormone to the systemic circulation without affecting the hypothetical release from the hypothalamic nuclei to other areas of the central nervous system was tested. A diabetes insipidus-like syndrome was obtained. But, neither the delay in the onset nor the development of DOC-salt hypertension was modified. This lesion made in rats at 3-4 weeks post DOC-salt did not alter the hypertension during the following 3 more weeks of treatment. These results suggest that the neural lobe would not be essential for the development and maintenance of DOC-salt hypertension in rats.

Evidences against a primary role for the pituitary neural lobe in the development and maintenance of Doc-salt hipertension

El papel de la hormona antidiurètica(ADH) en el desarrollo y mantenimiento de la hipertensión producida por la desoxicorticosterona y la sal en las ratas está sujeto a discusión. Por ello se estudió el efecto de la lesión del lóbulo neural, la cual prevendria la descarga de la hormona a la circulación, sin modificar la hipotètica descarga desde los nucleos hipotalamicos a otras àreas del sistema nervioso central, sobre la presión arterial de las ratas tratadas con DOC-sal. Se obtuvo un sindrome similar al producido por la diabetes insipida (ausencia de ADH circulante). No obstante, la lesión no modifica ni el intervalo hasta la manifestación de la hipertensión ni su desarrollo. La lesión hecha en animales previamente tratados durante 3-4 semanas con DOC-sal no modificó la hipertensión mantenida al continuar el tratamiento 3 semanas mas. Estos resultados sugieren que en la rata el lóbulo neural no seria esencial para el desarrollo y mantenimiento de la hipertensión por DOC-sal

Evidences against a primary role for the pituitary neural lobe in the development and maintenance of Doc-salt hipertension

El papel de la hormona antidiurÞtica(ADH) en el desarrollo y mantenimiento de la hipertensión producida por la desoxicorticosterona y la sal en las ratas está sujeto a discusión. Por ello se estudió el efecto de la lesión del lóbulo neural, la cual prevendria la descarga de la hormona a la circulación, sin modificar la hipotÞtica descarga desde los nucleos hipotalamicos a otras Oreas del sistema nervioso central, sobre la presión arterial de las ratas tratadas con DOC-sal. Se obtuvo un sindrome similar al producido por la diabetes insipida (ausencia de ADH circulante). No obstante, la lesión no modifica ni el intervalo hasta la manifestación de la hipertensión ni su desarrollo. La lesión hecha en animales previamente tratados durante 3-4 semanas con DOC-sal no modificó la hipertensión mantenida al continuar el tratamiento 3 semanas mas. Estos resultados sugieren que en la rata el lóbulo neural no seria esencial para el desarrollo y mantenimiento de la hipertensión por DOC-sal (AU)

Ultrastructure and electrical activity of the rat neurohypophysis.

Ultrastructural and electrophysiological studies of the rat neurohypophysis was carried out following stimulation to cause vasopressin release. Unit activity was investigated with microelectrodes, filtered, integrated, and recorded simultaneously with blood pressure in a polygraph. The basal unit activity was challenged by perfusing the hypothalamus and pituitary gland with hypertonic, hypotonic, and isotonic solutions through the internal carotid and by bleeding. Posterior lobes were fixed in osmium tetroxide and stained with uranyl acetate for electron microscopy. Single unit activity from the neural lobe showed mostly a continuous pattern of activity with a rate of discharge (RD) of 7 to 30 pulses per 10 s during control periods. Following hypertonic stimulation, out of 20 units studied, 35% increased, 10% decreased, and 55% did not change their RD. The effect of bleeding was studied in 34 units. Following the withdrawal of 1 ml of blood from the jugular vein, 29% increased, 32% decreased, and 38% did not change their RD. It is concluded that the existence in the neurohypophysis of fibers which are excited or inhibited by stimuli known to cause vasopressin release supports the hypothesis of the existence of a modulatory mechanism for neuropeptide release in the neural lobe.

Evidence for the control of prolactin secretion by hypophysial posterior lobe extracts.

The effect of posterior lobe extracts on prolactin secretion in vitro was compared with that of median eminence, hypothalamic (with and without median eminence) and cortex extracts. The posterior lobe extract clearly inhibited adenohypophysial prolactin secretion, showing a similar effect to that of the hypothalamic extracts. The median eminence extract showed inconstant inhibitory effects, while the cerebral cortex extracts showed no effect. The removal of the median eminence did not modify the hypothalamic inhibitory effect. Although the median eminence has always been considered to be the final common pathway for the control of adenohypophysial secretion, these results suggest that the posterior lobe may also play a physiological role in this control.