title: P-type Ca2+ channels mediate excitatory and inhibitory synaptic transmitter release in crayfish muscle.
abstract: The toxin fraction (FTX) and peptide omega-Aga-IVA from the venom of the funnel-web spider Agelenopsis aperta, as well as a synthetic analogue of FTX, specifically block the P-type voltage-dependent Ca2+ channel (VDCC). The effects of these toxins on synaptic transmission were studied in the neuromuscular synapses of the crayfish opener muscle, which has a single excitatory and a single inhibitory motoneuron. FTX selectively and reversibly blocked excitatory and inhibitory postsynaptic currents and potentials in a dose-dependent manner. FTX had no effect on (i) resting and postsynaptic membrane conductance, (ii) postsynaptic L-type VDCC, and (iii) both glutamate- and gamma-aminobutyric acid-induced postsynaptic responses. Mean amplitude and frequency of miniature postsynaptic potentials were unchanged by FTX. The postsynaptic VDCC was inhibited by nifedipine, a selective dihydropyridine antagonist of L-type VDCC, whereas synaptic transmission was unaffected. Transmission was also undisturbed by omega-conotoxin, suggesting that N-type VDCCs are not involved. The peptide omega-Aga-IVA blocked excitatory and inhibitory transmission without affecting postsynaptic VDCC. Synaptic transmission was also blocked by synthetic FTX. We conclude that presynaptic P-type VDCCs are involved in both evoked excitatory and inhibitory transmitter release in crayfish neuromuscular synapses.
authors.affiliation: Instituto Cajal Consejo Superior de Investigaciones Cientificas, Madrid, Spain.
authors.forename: A
authors.initials: A
authors.lastname: Araque
authors.forename: F
authors.initials: F
authors.lastname: Clarac
authors.forename: W
authors.initials: W
authors.lastname: Buño
mesh_terms: D000818:Animals; D003400:Astacoidea; D002121:Calcium Channel Blockers / Q000633:toxicity*; D015220:Calcium Channels / Q000502:physiology*; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology; D005971:Glutamates / Q000633:toxicity; D018698:Glutamic Acid; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000502:physiology; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology*; D009132:Muscles / Q000294:innervation / Q000502:physiology*; D009469:Neuromuscular Junction / Q000187:drug effects / Q000502:physiology*; D009498:Neurotoxins / Q000633:toxicity; D009543:Nifedipine / Q000494:pharmacology; D011073:Polyamines / Q000633:toxicity*; D013111:Spider Venoms / Q000494:pharmacology / Q000633:toxicity; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology*; D020867:omega-Agatoxin IVA
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; C071920:FTX, spider toxin; D005971:Glutamates; D009498:Neurotoxins; D011073:Polyamines; D013111:Spider Venoms; D013757:Tetraethylammonium Compounds; D020867:omega-Agatoxin IVA; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D019789:Tetraethylammonium; D009543:Nifedipine