Hormonal Control of Cell Death in a Sexually Dimorphic Song Nucleus in the Zebra Finch

2007 ◽  
pp. 173-185 ◽  
Author(s):  
Masakazu Konishi ◽  
Eugene Akutagawa
Keyword(s):  
Cell Death ◽  
Zebra Finch ◽  
Hormonal Control ◽  
Sexually Dimorphic

scholarly journals Hormonal control of programmed cell death/apoptosis

1998 ◽  
pp. 482-491 ◽  
Author(s):  
W Kiess ◽  
B Gallaher
Keyword(s):  
Cell Death ◽  
Mammary Gland ◽  
Growth Factors ◽  
Growth Factor ◽  
Programmed Cell Death ◽  
Cell Types ◽  
Hormonal Control ◽  
Endocrine Glands ◽  
Survival Factors ◽  
Endocrine Tissues

Apoptosis or programmed cell death is a physiological form of cell death that occurs in embryonic development and during involution of organs. It is characterized by distinct biochemical and morphological changes such as DNA fragmentation, plasma membrane blebbing and cell volume shrinkage. Many hormones, cytokines and growth factors are known to act as general and/or tissue-specific survival factors preventing the onset of apoptosis. In addition, many hormones and growth factors are also capable of inducing or facilitating programmed cell death under physiological or pathological conditions, or both. Steroid hormones are potent regulators of apoptosis in steroid-dependent cell types and tissues such as the mammary gland, the prostate, the ovary and the testis. Growth factors such as epidermal growth factor, nerve growth factor, platelet-derived growth factor (PDGF) and insulin-like growth factor-I act as survival factors and inhibit apoptosis in a number of cell types such as haematopoietic cells, preovulatory follicles, the mammary gland, phaeochromocytoma cells and neurones. Conversely, apoptosis modulates the functioning and the functional integrity of many endocrine glands and of many cells that are capable of synthesizing and secreting hormones. In addition, exaggeration of the primarily natural process of apoptosis has a key role in the pathogenesis of diseases involving endocrine tissues. Most importantly, in autoimmune diseases such as autoimmune thyroid disease and type 1 diabetes mellitus, new data suggest that the immune system itself may not carry the final act of organ injury: rather, the target cells (i.e. thyrocytes and beta cells of the islets) commit suicide through apoptosis. The understanding of how hormones influence programmed cell death and, conversely, of how apoptosis affects endocrine glands, is central to further design strategies to prevent and treat diseases that affect endocrine tissues. This short review summarizes the available evidence showing where and how hormones control apoptosis and where and how programmed cell death exerts modulating effects upon hormonally active tissues.

scholarly journals Neural and Hormonal Control of Sexual Behavior

Endocrinology ◽  
2020 ◽  
Vol 161 (10) ◽  
Author(s):  
Kimberly J Jennings ◽  
Luis de Lecea
Keyword(s):  
Sexual Behavior ◽  
Neural Circuits ◽  
Sexual Motivation ◽  
Gonadal Hormones ◽  
Hormonal Control ◽  
Sexually Dimorphic ◽  
Neural Patterning ◽  
Ideal System ◽  
Brain And Behavior ◽  
And Behavior

Abstract Gonadal hormones contribute to the sexual differentiation of brain and behavior throughout the lifespan, from initial neural patterning to “activation” of adult circuits. Sexual behavior is an ideal system in which to investigate the mechanisms underlying hormonal activation of neural circuits. Sexual behavior is a hormonally regulated, innate social behavior found across species. Although both sexes seek out and engage in sexual behavior, the specific actions involved in mating are sexually dimorphic. Thus, the neural circuits mediating sexual motivation and behavior in males and females are overlapping yet distinct. Furthermore, sexual behavior is strongly dependent on circulating gonadal hormones in both sexes. There has been significant recent progress on elucidating how gonadal hormones modulate physiological properties within sexual behavior circuits with consequences for behavior. Therefore, in this mini-review we review the neural circuits of male and female sexual motivation and behavior, from initial sensory detection of pheromones to the extended amygdala and on to medial hypothalamic nuclei and reward systems. We also discuss how gonadal hormones impact the physiology and functioning of each node within these circuits. By better understanding the myriad of ways in which gonadal hormones impact sexual behavior circuits, we can gain a richer and more complete appreciation for the neural substrates of complex behavior.

Neuronal growth, atrophy and death in a sexually dimorphic song nucleus in the zebra finch brain

Nature ◽  
1985 ◽  
Vol 315 (6015) ◽  
pp. 145-147 ◽  
Author(s):  
Masakazu Konishi ◽  
Eugene Akutagawa
Keyword(s):  
Zebra Finch ◽  
Sexually Dimorphic ◽  
Neuronal Growth

Hormonal Control of “Tissue” Transglutaminase Induction during Programmed Cell Death in Frog Liver

1999 ◽  
Vol 247 (2) ◽  
pp. 339-346 ◽  
Author(s):  
Loredana Assisi ◽  
Francesco Autuori ◽  
Virgilio Botte ◽  
Maria Grazia Farrace ◽  
Mauro Piacentini
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Tissue Transglutaminase ◽  
Hormonal Control

Capacitation mechanisms, and the role of capacitation as seen in eutherian mammals

1996 ◽  
Vol 8 (4) ◽  
pp. 581 ◽  
Author(s):  
RA Harrison
Keyword(s):  
Cell Death ◽  
Reproductive Tract ◽  
Physiological State ◽  
Hormonal Control ◽  
Female Reproductive Tract ◽  
Functional Heterogeneity ◽  
Vitro Fertilization ◽  
Range Of Functions

Capacitation, the process whereby spermatozoa are rendered capable of interacting with and fertilizing the egg, was discovered more than 40 years ago. However, our understanding of it is still far from satisfactory. Several factors conspire to obfuscate studies of capacitation mechanisms: the inherent functional heterogeneity of sperm populations, the range of functions used as parameters of capacitation (whence the endpoint of the process has become conceptually uncertain), and the several profound differences between model in vitro fertilization (IVF) systems and the situation in vivo in the female reproductive tract. Recent investigations in the author's laboratory have shown that bicarbonate/CO2, an essential component for successful IVF, causes rapid changes in lipid architecture of the sperm plasma membrane and slower changes in surface coating. These changes are accompanied by membrane destabilization and cell death. Evidence suggests that bicarbonate's actions are mediated through cyclic nucleotide signalling. Of particular note is the heterogeneity in rate of response to bicarbonate shown by individual cells in the sperm populations. Taken together with other observations, the findings suggest that capacitation is a series of positive destabilizing events that eventually lead to cell death. The 'capacitated' state would then be a window of destabilization within which spermatozoa can undergo a zona-induced acrosome reaction and display hyperactivated motility. Further along the destabilization pathway, spontaneous acrosome reactions would occur before total membrane degeneration. In vivo, capacitation would be a conflict between destabilization and sperm survival. Concentrations of bicarbonate are maintained low in the cauda epididymidis, where sperm survive for long periods, and one may speculate that hormonal control of local bicarbonate/CO2 in oviducal 'storage' sites in the female tract could allow 'safe' sequestering of live spermatozoa until around the time of ovulation; the environment may then change to produce a 'capacitating' effect, whence, due to the inherent functional heterogeneity of the sequestered population, small numbers of capacitated spermatozoa are released sequentially. In this way, a succession of spermatozoa in the correct physiological state may be provided for the freshly ovulated egg.

Hormonal control of morphogenetic cell death of the wing hypodermis in Lucilia cuprina

1975 ◽  
Vol 7 (2) ◽  
pp. 281-296 ◽  
Author(s):  
I.M. Seligman ◽  
B.K. Filshie ◽  
F.A. Doy ◽  
A.C. Crossley
Keyword(s):  
Cell Death ◽  
Hormonal Control ◽  
Lucilia Cuprina
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