The Parietal Eye (Pineal and Parietal Organs) of Lower Vertebrates

Author(s):  
Eberhard Dodt
1960 ◽  
Vol XXXIII (II) ◽  
pp. 255-260 ◽  
Author(s):  
L. S. Ramaswami ◽  
A. B. Lakshman

ABSTRACT By using enzymes, the gonadotrophic factors in the skipper-frog pituitary glands have been selectively inactivated or destroyed. By incubating a known number of pituitary gland homogenate with ptyalin in a constant temperature bath for 5–6 h the follicle-stimulating factor is inactivated; with trypsin or pepsin, the luteinizing factor is inactivated. Bioassay on gravid skipper-frogs indicate that the ptyalin digested homogenate brings about profuse spawning while the trypsin or pepsin digested homogenates do not. When a combination of ptyalin digested and trypsin digested homogenates is injected into fresh gravid skipper-frogs, poor spawning is brought about. These experiments show that the luteinizing factor alone brings about more profuse spawning than when it is combined with the follicle-stimulating factor. It is likely, therefore, that in the lower vertebrates the luteinizing factor of the pituitary gland plays a more predominant role. The exact proportions in which the different dosages for the control and test animals are administered are also tabulated.


2015 ◽  
Vol 282 (1821) ◽  
pp. 20152147 ◽  
Author(s):  
Teresa Kennedy-Lydon ◽  
Nadia Rosenthal

The hearts of lower vertebrates such as fish and salamanders display scarless regeneration following injury, although this feature is lost in adult mammals. The remarkable capacity of the neonatal mammalian heart to regenerate suggests that the underlying machinery required for the regenerative process is evolutionarily retained. Recent studies highlight the epicardial covering of the heart as an important source of the signalling factors required for the repair process. The developing epicardium is also a major source of cardiac fibroblasts, smooth muscle, endothelial cells and stem cells. Here, we examine animal models that are capable of scarless regeneration, the role of the epicardium as a source of cells, signalling mechanisms implicated in the regenerative process and how these mechanisms influence cardiomyocyte proliferation. We also discuss recent advances in cardiac stem cell research and potential therapeutic targets arising from these studies.


Nature ◽  
1970 ◽  
Vol 228 (5275) ◽  
pp. 991-992 ◽  
Author(s):  
RONALD T. ACTON ◽  
PETER F. WEINHEIMER ◽  
MICHAEL WOLCOTT ◽  
E. EDWARD EVANS ◽  
J. C. BENNETT

2006 ◽  
Vol 86 (2) ◽  
pp. 316-353 ◽  
Author(s):  
J. Leloup ◽  
M. Fontaine

2002 ◽  
Vol 69 (2) ◽  
pp. 97-102
Author(s):  
Livia Lucentini ◽  
Antonella Angiolillo ◽  
Emanuela Varasano ◽  
Fausto Panara

2010 ◽  
Vol 17 (4) ◽  
pp. 498-505 ◽  
Author(s):  
Antonin Bukovsky

AbstractAt the beginning of the last century, reproductive biologists have discussed whether in mammalian species the fetal oocytes persist or are replaced by neo-oogenesis during adulthood. Currently the prevailing view is that neo-oogenesis is functional in lower vertebrates but not in mammalian species. However, contrary to the evolutionary rules, this suggests that females of lower vertebrates have a better opportunity to provide healthy offspring compared to mammals with oocytes subjected to environmental threats for up to several decades. During the last 15 years, a new effort has been made to determine whether the oocyte pool in adult mammals is renewed as well. Most recently, Ji Wu and colleagues reported a production of offspring from female germline stem cells derived from neonatal and adult mouse ovaries. This indicates that both neonatal and adult mouse ovaries carry stem cells capable of producing functional oocytes. However, it is unclear whether neo-oogenesis from ovarian somatic stem cells is physiologically involved in follicular renewal and why menopause occurs. Here we review observations that indicate an involvement of immunoregulation in physiological neo-oogenesis and follicular renewal from ovarian stem cells during the prime reproductive period and propose why menopause occurs in spite of persisting ovarian stem cells.


2001 ◽  
Vol 18 (4) ◽  
pp. 549-558 ◽  
Author(s):  
A. KURAS ◽  
N. GUTMANIENĖ

Nicotinic acetylcholine receptors are localized on retinotectal axons' terminals in lower vertebrates. The effects of activation of these receptors by endogenous acetylcholine were observed under stimulation of mass optic fibers. This study was designed to determine whether endogenous acetylcholine facilitates frog retinotectal transmission, provided only the synapses of an individual optic axon are activated, and to evaluate the feasible extent of nicotinic facilitation in these synapses by applied agonist. To this end, the effects of cholinergic drugs on the extracellular action and synaptic potentials recorded from the terminal arborization of a separate retinotectal fiber (in layer F of the tectum) were investigated in vivo. Glutamatergic nature of retinotectal synapses was reexamined by treatment with kynurenic acid. Both kynurenic acid (0.25–1 mM) and d-tubocurarine chloride (10–15 μM) significantly depressed the synaptic potentials. Carbamylcholine chloride (50–150 μM) evoked a large augmentation of the synaptic potentials and a slight but statistically significant decrease of the action potentials. D-tubocurarine reduced the effect of carbamylcholine. Pilocarpine hydrochloride (50 μM) had only a weak effect. The paired-pulse facilitation of the synaptic potentials changed significantly under the action of carbamylcholine and d-tubocurarine. The obtained results suggest that the glutamate release from activated synapses of individual retinotectal axons is facilitated by endogenous acetylcholine via presynaptic nicotinic receptors. Under used stimulation conditions, this modulation mechanism was employed only partially since its activation by applied carbamylcholine could enhance synaptic transmission up to 2.8 times.


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