Modulation by APGW-amide, an Achatina endogenous inhibitory tetrapeptide, of currents induced by neuroactive compounds on Achatina neurons: peptides.
1. Modulatory effects of APGW-amide (Ala-Pro-Gly-Trp-NH2), proposed as an inhibitory neurotransmitter of Achatina neurons, perfused at 3 x 10(-6) M on the currents induced by neuroactive peptides, ejected by brief pressure, were examined by using Achatina giant neuron types, v-RCDN (ventral-right cerebral distinct neuron) and PON (periodically oscillating neuron), under voltage clamp. 2. Outward current (Iout) caused by FMRFamide (Phe-Met-Arg-Phe-NH2) on v-RCDN, which was probably K+ dependent, was inhibited with membrane conductance (g) increase by APGW-amide. From the dose (pressure duration)-response curves of FMRFamide and a Lineweaver-Burk plot of these data, the inhibition caused by APGW-amide was mainly in an uncompetitive manner. 3. Iout caused by APGW-amide on v-RCDN, which was probably K+ dependent, was inhibited with g increase by APGW-amide. The inhibition caused by APGW-amide was partly in a competitive manner and partly in a noncompetitive manner. 4. Iout caused by [Ser2]-Mytilus inhibitory peptide, [Ser2]-MIP (Gly-Ser-Pro-Met-Phe-Val-NH2) on v-RCDN, which was probably K+ dependent, was inhibited with g increase by APGW-amide. Because the modulation of this current was not so marked, a dose-response study of this compound was not carried out. Iin induced by oxytocin on PON was not affected by APGW-amide. 5. From the dose-response curves of APGW-amide, perfused consecutively, the inhibitory effects of APGW-amide on the Iout caused by APGW-amide were stronger than those on the Iout caused by FMRFamide. 6. The inhibition of the APGW-amide-induced Iout on v-RCDN by APGW-amide was partly due to the competition in the receptor sites and partly to the g increase. The inhibition by APGW-amide on the Iout induced by FMRFamide and [Ser2]-MIP would be partly due to the g increase. In addition, we consider that APGW-amide affects intracellular signal transduction systems or ionic channels, thus modulating these currents. 7. The currents modulated by APGW-amide were different from those modulated by achatin-1, another Achatina endogenous neuroexcitatory peptide. We consider that the mechanisms underlying the modulatory effects of APGW-amide are different from those of achatin-I.
Han
X Y
XY
Department of Physiology, Gifu University School of Medicine, Japan.
Salunga
T L
TL
Zhang
W
W
Takeuchi
H
H
Matsunami
K
K
D000818:Animals; D019835:FMRFamide / Q000494:pharmacology; D066298:In Vitro Techniques; D009474:Neurons / Q000187:drug effects*; D009479:Neuropeptides / Q000494:pharmacology*; D018377:Neurotransmitter Agents / Q000494:pharmacology*; D009842:Oligopeptides / Q000494:pharmacology; D010121:Oxytocin / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D012908:Snails; D009435:Synaptic Transmission / Q000187:drug effects*
C055988:Mytilus inhibitory peptide; D009479:Neuropeptides; D018377:Neurotransmitter Agents; D009842:Oligopeptides; C063193:alanyl-prolyl-glycyl-tryptophanamide; D010121:Oxytocin; D019835:FMRFamide