title: Delta opioids reduce the neurotransmitter release probability by enhancing transient (KV4) K+-currents in corticostriatal synapses as evaluated by the paired pulse protocol.
abstract: Field recordings were used to determine the influence of delta-opioid receptor activation on corticostriatal synaptic transmission. Application of the selective delta-opioid receptor agonist, [Tyr-D-Pen-Gly-Phe-D-Pen]-enkephalin (DPDPE, 1 microM), decreased the amplitude of the field-excitatory synaptic potential and at the same time increased the paired pulse ratio (PPR) suggesting a presynaptic site of action. This response reversed rapidly when DPDPE was washed and blocked by 1 nM of the selective delta-receptor antagonist naltrindole. Neither omega-conotoxin GVIA (1 microM) nor omega-agatoxin TK (400 nM), blockers of N- and P/Q-type Ca2+-channels, respectively, nor TEA (1 mM), blocker of some classes of K+-channels, occluded the effects of DPDPE. Instead, 1 mM 4-AP or 400 microM Ba2+ occluded completely the effects of DPDPE. Therefore, the results suggest that the modulation by delta opioids at corticostriatal terminals is mediated by transient (KV4) K+-conductances.
authors.affiliation: Neurociencias, FES Iztacala, Universidad Nacional Autónoma de México, Mexico.
authors.forename: Xochitl
authors.initials: X
authors.lastname: Jose
authors.forename: Juan Carlos
authors.initials: JC
authors.lastname: Pineda
authors.forename: Cynthia
authors.initials: C
authors.lastname: Rodriguez
authors.forename: Ernesto
authors.initials: E
authors.lastname: Mendoza
authors.forename: Elvira
authors.initials: E
authors.lastname: Galarraga
authors.forename: José
authors.initials: J
authors.lastname: Bargas
authors.forename: Jaime
authors.initials: J
authors.lastname: Barral
mesh_terms: D000701:Analgesics, Opioid / Q000494:pharmacology; D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism*; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism*; D004558:Electric Stimulation; D020881:Enkephalin, D-Penicillamine (2,5)- / Q000494:pharmacology*; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D008297:Male; D009292:Narcotic Antagonists / Q000494:pharmacology; D009434:Neural Pathways / Q000187:drug effects / Q000378:metabolism*; D018377:Neurotransmitter Agents / Q000378:metabolism*; D018847:Opioid Peptides / Q000378:metabolism; D009924:Organ Culture Techniques; D026902:Potassium Channel Blockers / Q000494:pharmacology; D017729:Presynaptic Terminals / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D017465:Receptors, Opioid, delta / Q000819:agonists* / Q000037:antagonists & inhibitors / Q000378:metabolism; D051672:Shal Potassium Channels / Q000819:agonists* / Q000037:antagonists & inhibitors / Q000378:metabolism; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology
chemical_list: D000701:Analgesics, Opioid; D002121:Calcium Channel Blockers; D009292:Narcotic Antagonists; D018377:Neurotransmitter Agents; D018847:Opioid Peptides; D026902:Potassium Channel Blockers; D017465:Receptors, Opioid, delta; D051672:Shal Potassium Channels; D020881:Enkephalin, D-Penicillamine (2,5)-