Effects of epinephrine, glucagon and vasoactive intestinal polypeptide on chloride secretion by teleost opercular membrane

1982 ◽  
Vol 146 (1) ◽  
pp. 27-34 ◽  
Author(s):  
J. Kevin Foskett ◽  
Guylaine M. Hubbard ◽  
Terry E. Machen ◽  
Howard A. Bern
Keyword(s):  
Vasoactive Intestinal Polypeptide ◽  
Chloride Secretion ◽  
Intestinal Polypeptide

Antagonists of epithelial chloride channels inhibit cAMP synthesis

1991 ◽  
Vol 69 (4) ◽  
pp. 501-506 ◽  
Author(s):  
S. Heisler
Keyword(s):  
Vasoactive Intestinal Polypeptide ◽  
Chloride Channels ◽  
Chloride Transport ◽  
Chloride Secretion ◽  
Channel Blockers ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Camp Synthesis ◽  
Camp Formation ◽  
Intestinal Polypeptide

In past studies we observed that the chloride channel blocker, diphenylamine-2-carboxylate (DPC) and chemically related drugs (Hoechst compounds 131, 143, 144) inhibited cAMP formation in mouse pituitary tumor cells. The object of this study was to determine whether these drugs inhibited chloride transport in human T-84 colonic carcinoma cells through an effect on cAMP metabolism. Chloride secretion (measured as 125I efflux from isotope-preloaded cells) was stimulated in a concentration-dependent manner by vasoactive intestinal polypeptide (VIP) (EC50 = 1.5 × 10−10 M) which similarly increased cAMP synthesis (EC50 = 1.6 × 10−8 M). The cAMP response to VIP was inhibited 17, 52, 55, and 78% maximally by DPC and compounds 144, 143, and 131, respectively. In untreated T-84 cells, 125I secretion fell by 66% after 3 min; VIP (10−7 M) increased secretion about fivefold over the same period. Both basal and VIP-stimulated 125I secretion were inhibited up to 60% by compound 131. Pretreatment of cells with pertussis toxin did not attenuate the inhibitory effect of channel blockers on either VIP-stimulated cAMP synthesis or 125I secretion. The cationophore, A-23187, which had no effect on cAMP formation, and 8-Br-cAMP both stimulated 125I secretion from T-84 cells. These secretory responses were inhibited by compound 131. The mechanism by which phenylanthranilic acids antagonize cAMP synthesis and its significance is not known; however, the data suggest that this family of drugs may inhibit chloride transport by both cAMP-dependent and independent mechanisms.Key words: T-84 cells, chloride secretion, vasoactive intestinal polypeptide, diphenylamine-2-carboxylate, inhibition of cyclic AMP synthesis.

VASOACTIVE INTESTINAL POLYPEPTIDE STIMULATES ADENYLATE CYCLASE AND SEROTONIN N-ACETYLTRANSFERASE ACTIVITIES IN RAT PINEAL IN VITRO

1980 ◽  
Vol 1 (1) ◽  
pp. 84-87 ◽  
Author(s):  
TOSHIO KANEKO ◽  
PO-YUAN CHENG ◽  
HIROSHI OKA ◽  
TOSHITSUGU ODA ◽  
NOBORU YANAIHARA ◽  
...  
Keyword(s):  
Adenylate Cyclase ◽  
Vasoactive Intestinal Polypeptide ◽  
Intestinal Polypeptide

scholarly journals Development-Dependent Plasticity in Vasoactive Intestinal Polypeptide Neurons in the Infralimbic Cortex

2021 ◽  
Vol 2 (1) ◽  
Author(s):  
Stuart A Collins ◽  
Ipe Ninan
Keyword(s):  
Sex Differences ◽  
Anxiety Disorders ◽  
Vasoactive Intestinal Polypeptide ◽  
Cortical Plasticity ◽  
Male Mice ◽  
Infralimbic Cortex ◽  
Membrane Excitability ◽  
Gabaergic Transmission ◽  
Intestinal Polypeptide

Abstract The onset of several neuropsychiatric disorders including anxiety disorders coincides with adolescence. Consistently, threat extinction, which plays a key role in the regulation of anxiety-related behaviors, is diminished during adolescence. Furthermore, this attenuated threat extinction during adolescence is associated with an altered synaptic plasticity in the infralimbic medial prefrontal cortex (IL-mPFC), a brain region critical for threat extinction. However, the mechanism underlying the altered plasticity in the IL-mPFC during adolescence is unclear. Given the purported role of vasoactive intestinal polypeptide expressing interneurons (VIPINs) in disinhibition and hence their potential to affect cortical plasticity, we examined whether VIPINs exhibit an adolescence-specific plasticity in the IL-mPFC. We observed an increase in GABAergic transmission and a decrease in excitability in VIPINs during adolescence. Male mice show a significantly higher VIPIN-pyramidal neuron GABAergic transmission compared with female mice. The observed increase in GABAergic transmission and a decrease in membrane excitability in VIPINs during adolescence could play a role in the altered plasticity in the adolescent IL-mPFC. Furthermore, the suppression of VIPIN-mediated GABAergic transmission in females might be relevant to sex differences in anxiety disorders.

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