RESUMO

The present investigation was designed to investigate the fate of the large pool of neurohypophyseal hormones that is never released into the blood. Normal Sprague-Dawley and taiep mutant rats were investigated under normal water balance, after dehydration and after dehydration-rehydration. Lectin histochemistry and light- and electron-microscopic immunocytochemistry using antibodies against vasopressin, oxytocin, and neurophysins used at low (1:1,000) and high (1:15,000) dilutions allowed to distinguish (1) recently packed immature granules, as those located in the perikaryon; (2) mature; and (3) aged granules. The distribution of these granules within the different domains of the neurosecretory axons located in the neural lobe, namely, undilated segments, swellings, terminals, and Herring bodies, and the response of these compartments to dehydration and dehydration-rehydration allowed to roughly follow the routing of the granules through such axonal domains. It is suggested that granules may move backward and forward between the terminals and the swellings. At variance, aged granules located in Herring body are retained in this compartment and would finally become degraded. Herring bodies displayed distinct lectin binding and immunocytochemical properties, allowing to distinguish them from axonal swellings. After a dehydration-rehydration cycle, immunocytochemistry and electron microscopy revealed that Herring bodies were no longer present in the neural lobe and that several terminals had degenerated. It is concluded that (1) the neurophysin axons may undergo remodeling under appropriate stimuli and (2) Herring bodies are a specialized and plastic domain of the magnocellular neurosecretory neuron involved in the disposal of aged neurosecretory granules. No differences were detected at the neural lobe level between normal and mutant rats subjected to the same experimental conditions.

Assuntos

RESUMO

The mouse neurohypophysis was studied at different ages of development in order to analyse the ultrastructural changes that lead to the maturation of the neurogliohemal complex and to determine the existence of permeability between the blood capillaries and the neurohypophysial channels. In all the studies ages, two groups of 5 animals each were intravenously injected with different tracer solutions: to one group, 10 microliters of cationized ferritin were used and to the other, 10 microliters of ferrous fumarate were applied. For the ultrastructural studies the tissue samples were processed using the conventional techniques for electron microscopy. At day 17 of prenatal age, some hypothalamic axons (10 axonic profiles/20 microns2) were already seen within the neurohypophysis, increasing threefold (26 to 30 axonic profiles/20 microns2) at prenatal day 19. In these axons terminals, the first neurosecretory vesicles began to appear. At this early age, the glial cells formed few prolongations. Between postnatal days 1 and 9, numerous axon terminals containing dense neurosecretory vesicles composed the neuropile areas. After day 9, there was a broadening of the intercellular space, which we have termed as neurohypophysial channels; these were actually expansions of the existing extracellular space in the neurohypophysis. Between days 9 and 21, the population of axon terminals showing a higher density of neurosecretory vesicles continued to increase in number. Some of these axon terminals were separated by irregular neurohypophysial channels. The glial cells showed scarce cytoplasm and formed numerous lamellar prolongations, which became increasingly finer surrounding bundles of individual axons.(ABSTRACT TRUNCATED AT 250 WORDS)

Assuntos

RESUMO

L-3H-fucose was injected into the lateral cerebral ventricle of vasopressin-deficient Brattleboro and control Long-Evans rats which were subsequently killed at several time intervals after the injection. The hypothalamus and the neurohypophysis were processed for light- and electronmicroscopic radioautography. Other complementary experiments using immunocytochemical and enzyme-histochemical techniques were also undertaken. L-3H-fucose was incorporated into newly synthesized glycoproteins in the Golgi apparatus of supraoptic and paraventricular neurons, and later on labelled glycoproteins migrated to lysosomes and the plasma membrane surrounding the perikaryon. The Golgi apparatus of the vasopressin-deficient neurons remained heavily labelled as long as 3 days after injection, in sharp contrast with the normal neurons in which there was a remarkable decrease of label in the Golgi region between 4 and 24 h after the isotope administration. Labelled glycoproteins also migrated to the neurohypophysis and were mainly found in the axonal plasma membrane, vesicles and axoplasm. The renewal of glycoproteins in the neurohypophysis of Brattleboro rats was faster than in the normal rats and this was attributed to the lack of formation of products which are normally packaged in secretory granules in the perikaryon and released at the axon terminal in the neurohypophysis. Colchicine caused a disturbance in the topography of the organelles of the perikaryon and the most striking features were the displacement of Golgi stacks to the periphery of the perikaryon and an accumulation of mitochondria in this neuronal region. No secretory granules were observed in the vasopressin-deficient neurons of untreated or colchicine-treated Brattleboro rats. By contrast, secretory granules (most of them labelled with 3H-fucose) were concentrated in the perikaryon of colchicine-treated Long-Evans rats. In these rats, colchicine caused a severe block in the migration of 3H-fucose-labelled glycoproteins to the neurohypophysis, but this did not occur in the Brattleboro rats. The results of the experiments were interpreted in the light of the genetic defect known to occur in Brattleboro rats which causes the inability to produce vasopressin and also remarkable morphological and physiological changes in the affected neurons.

Assuntos

RESUMO

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.

Assuntos

Assuntos