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Updated: Jul 18, 2026

Preparation of Acute Brain Slices Using an Optimized N-Methyl-D-glucamine Protective Recovery Method
Published on: February 26, 2018
Delta opioids reduce the neurotransmitter release probability by enhancing transient (KV4) K+-currents in
Xochitl Jose1, Juan Carlos Pineda, Cynthia Rodriguez
1Neurociencias, FES Iztacala, Universidad Nacional Autónoma de México, Mexico.
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.
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