Cyclic Adenosine Monophosphate Signal Transduction Research Articles

A pH-powered mechanochemical engine regulates the buoyancy of Chaoborus midge larvae

The freshwater aquatic larvae of the Chaoborus midge are the world's only truly planktonic insects, regulating their buoyancy using two pairs of internal air-filled sacs, one in the thorax and the other in the seventh abdominal segment. In 1911, August Krogh demonstrated the larvae's ability to control their buoyancy by exposing them to an increase in hydrostatic pressure.1 However, how these insects control the volume of their air-sacs has remained a mystery. Gas is not secreted into the air-sacs, as the luminal gas composition is always the same as that dissolved in the surrounding water.1,2 Instead, the air-sac wall was thought to play some role.3-6 Here we reveal that bands of resilin in the air-sac's wall are responsible for the changes in volume. These bands expand and contract in response to changes in pH generated by an endothelium that envelops the air-sac. Vacuolar type H+ V-ATPase (VHA) in the endothelium acidifies and shrinks the air-sac, while alkalinization and expansion are regulated by the cyclic adenosine monophosphate signal transduction pathway. Thus, Chaoborus air-sacs function as mechanochemical engines, transforming pH changes into mechanical work against hydrostatic pressure. As the resilin bands interlaminate with bands of cuticle, changes in resilin volume are constrained to a single direction along the air-sac's longitudinal axis. This makes the air-sac functionally equivalent to a cross-striated pH muscle and demonstrates a unique biological role for resilin as an active structural element.

Evolution of the techniques used in studying associative olfactory learning and memory in adult Drosophila in vivo: a historical and technical perspective

Drosophila melanogaster behavioral mutants have been isolated in which the ability to form associative olfactory memories has been disrupted primarily by altering cyclic adenosine monophosphate signal transduction. Unfortunately, the small size of the fruit fly and its neurons has made the application of neurobiological techniques typically used to investigate the physiology underlying these behaviors daunting. However, the realization that adult fruit flies could tolerate a window in the head capsule allowing access to the central structures thought to be involved plus the development of genetically expressed reporters of neuronal function has allowed a meteoric expansion of this field over the last decade. This review attempts to summarize the evolution of the techniques involved from the first use of a window to access these brain areas thought to be involved in associative olfactory learning and memory, the mushroom bodies and antennal lobes, to the current refinements which allow both high-resolution multiphoton imaging and patch clamping of identified neurons while applying the stimuli used in the behavioral protocols. This area of research now appears poised to reveal some very exciting mechanisms underlying behavior.

Cordyceps sinensis and its fractions stimulate MA-10 mouse Leydig tumor cell steroidogenesis.

The effects of Cordyceps sinensis (CS) and its extracted fractions on steroidogenesis in MA-10 cells were determined. Different concentrations of CS and 3 fractions of CS (F1, a water-soluble polysaccharide; F2, a water-soluble protein; and F3, a poorly water-soluble polysaccharide and protein) were added to MA-10 mouse Leydig tumor cells with or without human chorionic gonadotropin (hCG), and the production of steroid and the expression of steroidogenic acute regulatory protein (StAR) were examined. The results showed that CS alone (2-10 mg/mL) stimulated MA-10 cell progesterone production in a dose-dependent relationship. Fractions F1 and F3 (2-10 mg/mL) also had significant (P < .05) stimulatory effects on MA-10 cell steroidogenesis with a dose-dependent relationship. However, fraction F2 did not have an effect on MA-10 cells. CS and F3, but not F1, significantly induced more steroid production in hCG-stimulated MA-10 cells (P < .05). As a temporal relationship, F1 and F3 (2 mg/mL) maximally stimulated progesterone production between 1 and 3 hours after stimulation in MA-10 cells. In addition, CS and F3 significantly enhanced MA-10 cell StAR protein expression, which indicates that CS and F3 may use a cyclic adenosine monophosphate signal transduction pathway to activate MA-10 Leydig cell steroidogenesis in a manner to that of luteinizing hormone.

Influence of adenosine or adrenergic agonists on growth hormone stimulated lipolysis by chicken adipose tissue in vitro

In vitro lipolysis by chicken adipose explants was stimulated by growth hormone (GH) or glucagon. Adenosine or the adenosine agonist, N 6-phenylisopropyladenosine (PIA), inhibited GH stimulated lipolysis, the effect of adenosine not being observed in the presence or adenosine deaminase. Glucagon induced lipolysis was also reduced by PIA. It is suggested that adenosine may act by G i linked to either adenylate cyclase (for glucagon) or the signal transduction mechanism for GH. Lipolysis was not stimulated by GH in the presence of phenylephrine (α 1 adrenergic agonist), isoproterenol (β adrenergic agonist), adrenaline or glucagon. Although the presence of p-amino clonidine (α 2 adrenergic agonist) depressed basal lipolysis, a response to GH was still present. Either glucagon or β-adrenergic agonists (isoproterenol, adrenaline) stimulated lipolysis. In both cases, GH attenuated the lipolytic response to these hormones, which act via a cyclic adenosine monophosphate signal transduction mechanism.