PMID- 1652000
OWN - NLM
STAT- MEDLINE
DCOM- 19910926
LR  - 20191210
IS  - 0022-3077 (Print)
IS  - 0022-3077 (Linking)
VI  - 65
IP  - 6
DP  - 1991 Jun
TI  - The neuropeptide FMRFa both inhibits and enhances the Ca2+ current in dissociated 
      Helix neurons via independent mechanisms.
PG  - 1517-27
AB  - 1. The modulation of the voltage-activated Ca2+ current by the neuropeptide 
      Phe-Met-Arg-Phe-NH2 (FMRFa) was investigated in dissociated central neurons from 
      Helix aspersa using whole-cell voltage-clamp recording techniques. External Ba2+ 
      was always used as the charge carrier in this study, and the intracellular Ca2+ 
      concentration was buffered to 20 nM with ethylene glycol-bis(beta-aminoethyl 
      ether)-N,N,N',N'-tetraacetic acid (EGTA). 2. Run-down of the Ca2+ currents was 
      not a problem as long as the neurons were dialyzed with a patch electrode filling 
      solution containing ATP (1 or 2 mM). In ATP-dialyzed neurons, the rate of 
      inactivation of the calcium current increased with time without any significant 
      change in the rate of activation. However, when neurons were dialyzed with 
      guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S; 100 microM; with ATP), the rate 
      of inactivation decreased with time. There was no effect of GTP gamma S on the 
      rate of activation of the Ca2+ current. This suggests that guanosine 
      5'-triphosphate (GTP)-binding proteins (G proteins) are able to modulate the rate 
      of inactivation of the Ca2+ current in Helix neurons. 3. FMRFa both decreased and 
      enhanced the amplitude of the Ca2+ current in these neurons. This inhibition was 
      observed in most neurons, while the enhancement was observed in 20% of the 
      neurons. Although the enhancement usually was preceded by the inhibitory 
      response, sometimes the enhancement was observed separately. 4. The FMRFa-induced 
      inhibition of the Ca2+ current usually consisted of a decrease in both the 
      amplitude and the rate of inactivation of this current, effects that were reduced 
      as the membrane potential was stepped to more depolarized potentials. A pertussis 
      toxin (PTX)-sensitive G protein mediated this response, whereas no evidence was 
      found to suggest the involvement of any known intracellular messenger. Therefore 
      this inhibition may have resulted from a direct coupling between the FMRFa 
      receptor and the Ca2+ channels via a PTX-sensitive G protein. 5. Arachidonic acid 
      (100 microM) irreversibly reduced the amplitude of the Ca2+ current, but it did 
      not alter the relative inhibition of this current by FMRFa. 6. The FMRFa-induced 
      enhancement of the Ca2+ current was difficult to study because it was observed 
      infrequently, and was rarely observed independently of the FMRFa-induced 
      inhibitory response. In addition, the ability of FMRFa to enhance this current 
      usually disappeared with time.(ABSTRACT TRUNCATED AT 400 WORDS)
FAU - Yakel, J L
AU  - Yakel JL
AD  - Laboratoire de Neurobiologie, Ecole Normale Superieure, Paris, France.
LA  - eng
GR  - 1 F06 TW01401-01/TW/FIC NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurophysiol
JT  - Journal of neurophysiology
JID - 0375404
RN  - 0 (Arachidonic Acids)
RN  - 0 (Calcium Channels)
RN  - 0 (Neuropeptides)
RN  - 0 (Virulence Factors, Bordetella)
RN  - 0U46U6E8UK (NAD)
RN  - 27YG812J1I (Arachidonic Acid)
RN  - 37589-80-3 (Guanosine 5'-O-(3-Thiotriphosphate))
RN  - 64190-70-1 (FMRFamide)
RN  - EC 2.4.2.31 (Pertussis Toxin)
RN  - EC 3.6.1.- (GTP-Binding Proteins)
SB  - IM
MH  - Animals
MH  - Arachidonic Acid
MH  - Arachidonic Acids/pharmacology
MH  - Calcium Channels/*drug effects
MH  - Electrodes
MH  - Electrophysiology
MH  - FMRFamide
MH  - GTP-Binding Proteins/metabolism
MH  - Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology
MH  - Helix, Snails/*physiology
MH  - NAD/physiology
MH  - Neurons/drug effects/*metabolism
MH  - Neuropeptides/*pharmacology
MH  - Pertussis Toxin
MH  - Synapses/physiology
MH  - Synaptic Transmission/drug effects
MH  - Virulence Factors, Bordetella/pharmacology
EDAT- 1991/06/01 00:00
MHDA- 1991/06/01 00:01
CRDT- 1991/06/01 00:00
PHST- 1991/06/01 00:00 [pubmed]
PHST- 1991/06/01 00:01 [medline]
PHST- 1991/06/01 00:00 [entrez]
AID - 10.1152/jn.1991.65.6.1517 [doi]
PST - ppublish
SO  - J Neurophysiol. 1991 Jun;65(6):1517-27. doi: 10.1152/jn.1991.65.6.1517.