Abstract：
:Midbrain dopamine neurons are pacemakers in vitro, but in vivo they fire less regularly and occasionally in bursts that can lead to a temporary cessation in firing produced by depolarization block. The therapeutic efficacy of antipsychotic drugs used to treat the positive symptoms of schizophrenia has been attributed to their ability to induce depolarization block within a subpopulation of dopamine neurons. We summarize the results of experiments characterizing the physiological mechanisms underlying the ability of these neurons to enter depolarization block in vitro, and our computational simulations of those experiments. We suggest that the inactivation of voltage-dependent Na(+) channels, and, in particular, the slower component of this inactivation, is critical in controlling entry into depolarization block. In addition, an ether-a-go-related gene (ERG) K(+) current also appears to be involved by delaying entry into and speeding recovery from depolarization block. Since many antipsychotic drugs share the ability to block this current, ERG channels may contribute to the therapeutic effects of these drugs.
journal_name
Prog Mol Biol Transl Scijournal_title
Progress in molecular biology and translational scienceauthors
Yu N,Tucker KR,Levitan ES,Shepard PD,Canavier CCdoi
10.1016/B978-0-12-397897-4.00011-5subject
Has Abstractpub_date
2014-01-01 00:00:00pages
53-82eissn
1877-1173issn
1878-0814pii
B978-0-12-397897-4.00011-5journal_volume
123pub_type
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