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Opioid‐mediated modulation of calcium currents in striatal and pallidal neurons following reserpine treatment: Focus on kappa response
Author(s) -
Spadoni Francesca,
Martella Giuseppina,
Martorana Alessandro,
Lavaroni Franco,
D'Angelo Vincenza,
Bernardi Giorgio,
Stefani Alessandro
Publication year - 2003
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.10294
Subject(s) - globus pallidus , dynorphin , chemistry , endocrinology , medicine , κ opioid receptor , reserpine , damgo , striatum , enkephalin , basal ganglia , neuroscience , dopamine , agonist , receptor , opioid , opioid peptide , biology , biochemistry , central nervous system
Previous work has shown that enkephalins target N‐type calcium (Ca 2+ ) channels in striatal and globus pallidus (GP) neurons, principally through activation of μ‐like receptors. Here, we examined the effects of selective μ, δ, and κ agonists on Ca 2+ currents in striatal and GP neurons isolated from either control or reserpine‐treated rats. In cells from control rats DAMGO and dynorphin (DYN) inhibited high‐voltage‐activated (HVA) Ca 2+ currents preferentially in “medium‐to‐small” GP cells (likely to correspond to parvalbumin‐negative cells). The κ response was elicited by several agonists (DYN 17, DYN 13, BRL, U50‐488‐H), U50‐488‐H being the most effective (>30% maximal inhibition). U50‐488‐H affected both ω‐CgTxGVIA‐sensitive and nimodipine‐sensitive Ca 2+ conductances. The κ‐mediated effect (but not the μ response) was slow and blocked by chelerythrine, supporting the involvement of protein kinase C. In neurons from reserpinized rats we observed modest changes in the μ‐inhibited fraction in small GP cells and a dramatic reduction of the κ‐sensitive fraction in principal striatal cells. These data imply that aminergic depletion alters opiate transmission differentially in the indirect and direct pathways. The suppression of the κ response only in striatum reinforces the notion of an imbalance of endogenous opiates as relevant in extrapyramidal motor dysfunctions. Synapse 51:194–205, 2004. © 2003 Wiley‐Liss, Inc.