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Published on: June 17, 2011
Dopamine modulates Ih in a motor axon
Aleksander W Ballo1, Jennifer C Keene, Patricia J Troy
1The Whitney Laboratory for Marine Bioscience, University of Florida, St. Augustine, Florida 32080, USA.
Summary
Dopamine (DA) triggers nerve impulses in lobster axons by modulating a specific ion channel. This mechanism, involving D(1)-type receptors and cyclic AMP, enables peripheral spike initiation independent of central nervous system signals.
Area of Science:
- Neuroscience
- Neurophysiology
- Ion Channel Modulation
Background:
- Axons of pyloric dilator neurons in lobster stomatogastric nervous system.
- Dopamine (DA) induces peripheral spike initiation in motor nerves.
- This effect is dependent on hyperpolarization-activated inward current (I(h)).
Purpose of the Study:
- Investigate the mechanism of DA-induced peripheral spike initiation.
- Determine the role of D(1)-type receptors and cyclic AMP (cAMP).
- Directly study DA's effect on I(h) using voltage clamp.
Main Methods:
- Two-electrode voltage clamp of lobster axons.
- Application of dopamine (DA), D(1)-type receptor agonists, and cAMP-increasing drugs.
- Inhibition of I(h) and protein kinase A (PKA).
- Computer modeling of axonal properties.
Main Results:
- DA, D(1) agonists, and cAMP-increasing drugs elicited peripheral spike initiation.
- DA decreased maximal I(h) conductance but increased it at relevant potentials by shifting activation.
- DA's effects on I(h) were independent of PKA and potentially direct cAMP modulation.
- Computer models confirmed findings were robust to space-clamp issues.
Conclusions:
- DA modulates I(h) via a D(1)-type receptor mechanism, leading to peripheral spike initiation.
- cAMP directly affects hyperpolarization-activated cyclic nucleotide-gated channels in a phosphorylation-independent manner.
- This study reveals a novel mechanism for neuronal excitability control in peripheral axons.
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