On the receptors which mediate the hyperpolarization of salivary gland cells of Nauphoeta cinerea Olivier.

Krach

Arch Insect Biochem Physiol

et al. 2006

The acinar salivary glands of cockroaches receive a dual innervation from the subesophageal ganglion and the stomatogastric nervous system. Acinar cells are surrounded by a plexus of dopaminergic and serotonergic varicose fibers. In addition, serotonergic terminals lie deep in the extracellular spaces between acinar cells. Excitation-secretion coupling in cockroach salivary glands is stimulated by both dopamine and serotonin. These monoamines cause increases in the intracellular concentrations of cAMP and Ca(2+). Stimulation of the glands by serotonin results in the production of a protein-rich saliva, whereas stimulation by dopamine results in saliva that is protein-free. Thus, two elementary secretory processes, namely electrolyte/water secretion and protein secretion, are triggered by different aminergic transmitters. Because of its simplicity and experimental accessibility, cockroach salivary glands have been used extensively as a model system to study the cellular actions of biogenic amines and to examine the pharmacological properties of biogenic amine receptors. In this review, we summarize current knowledge concerning the aminergic control of cockroach salivary glands and discuss our efforts to characterize Periplaneta biogenic amine receptors molecularly.

Section: +supporting

confidence: 55%

The aminergic control of cockroach salivary glands

Krach

Arch Insect Biochem Physiol

et al. 2006

“…Secondly, the effects of dopamine and ADTN were not antagonized by haloperidol (10 gM), methysergide (10 gM), fluphenazine (1 gM) or a-flupenthixol (1 gM). (These are potent antagonists of dopamine at other sites: Seeman, Lau Wong, Tedesco & Wong, 1975;Dray, Gonye & Oakley, 1976;Burt, Creese & Snyder, 1976;Ginsborg, House & Silinsky, 1976.) Control responses to phenylephrine or noradrenaline were also unaffected by these drugs.…”

Section: Dopamine Receptors?mentioning

confidence: 99%

HYPERPOLARIZING ‘α₂’‐ADRENOCEPTORS IN RAT SYMPATHETIC GANGLIA

Brown

Caulfield

1979

British J Pharmacology

147

1 Receptors mediating catecholamine-induced hyperpolarization of isolated superior cervical sympathetic ganglia of the rat have been characterized by means of an extracellular recording method. 2 (-)-Noradrenaline (EC50, 1.7 + 0.6 tM) produced an immediate low-amplitude (<40 V) hyperpolarization. The hyperpolarization was increased on removal of external Ca 2+ or on reduction of external K+ from 6 to 2 mm. Hyperpolarization was unaffected by changing the temperature from 250 to 37°C. [3H]{-)-noradrenaline uptake.6 Clonidine (0.01 to 1 giM), oxymetazoline (0.01 to 1 gM) and ergometrine (0.1 to 10 gM) produced a persistent, low-amplitude hyperpolarization, as though they were partial agonists. Responses to the agonists were blocked by yohimbine (1 gM) but not be prazosin (1 gM).7 It is concluded that the adrenergic cell bodies in the ganglion were hyperpolarized through activation of the same type of a-receptor as those present at adrenergic nerve terminals.

“…Finally, phentolamine reversibly blocked the secretory response to exogenous cyclic AMP or IBMX. Previously it had been shown that phentolamine is a competitive antagonist of the dopamine-evoked hyperpolarization of acinar cells and fluid secretion by the gland (Ginsborg, House & Silinsky, 1976;Bowser-Riley, et al 1978). Now it is also evident that phentolamine might act within the acinar cells at a stage after cyclic AMP synthesis.…”

Section: Cyclic Amp As a Mediatormentioning

confidence: 99%

Cyclic Amp as a Possible Mediator of Dopamine Stimulation of Cockroach Gland Cells

Gray¹,

Ginsborg²,

House

1984

Exp Physiol

Isolated salivary glands of the cockroach Nauphoeta cinerea Olivier secrete fluid in response to nerve stimulation or application of dopamine, the acinar cells undergoing a hyperpolarization during secretion. The aim of the present work was to examine whether cyclic AMP acts as a second messenger in the acinar cells to cause the secretory and electrical responses to the transmitter dopamine. Cyclic AMP (10-500 microM) in the bathing solution of isolated glands caused a dose-dependent secretory response but no change in the membrane potential of acinar cells. The time courses and magnitudes of the secretory responses to cyclic AMP resembled those features of responses to dopamine. Forskolin, an adenylate cyclase activator, caused fluid secretion but the responses were small and irregular. The phosphodiesterase inhibitor, 3-isobutyl-l-methylxanthine (IBMX)(1-1000 microM) produced fluid secretion in a dose-dependent manner, the maximal response being equal to that of dopamine. Maintained responses to cyclic AMP or IBMX required the presence of extracellular calcium ions. An inhibitor (MDL 12,330A) of adenylate cyclase suppressed the secretory responses to dopamine, cyclic AMP, IBMX, the ionophore A23817 or the readmission of calcium ions to the bathing solution; this inhibitor did not block the acinar hyperpolarization caused by nerve stimulation. Cyclic AMP stimulation of glands, bathed in chloride-free solution to prevent fluid secretion, produced a change in the gland cells which outlasted the period of exogenous cyclic AMP stimulation and expressed itself as a transient secretion upon return of the normal bathing solution. It was concluded that stimulus-secretion coupling in this gland involves a calcium-dependent second messenger system and that cyclic AMP is probably the second messenger. The evidence did not support the idea that cyclic AMP is also a second messenger for the acinar cell hyperpolarization evoked by nerve stimulation.