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Updated: Aug 13, 2026

Ex Vivo Culture of Chick Cerebellar Slices and Spatially Targeted Electroporation of Granule Cell Precursors
Published on: December 14, 2015
Forskolin prolongs action potential duration and blocks potassium current in embryonic chick sensory neurons
Abstract:
To determine if alterations in internal cyclic adenosine monophosphate (cAMP) play a role in modulation of voltage-dependent channels in embryonic chick sensory neurons in vitro, forskolin (a direct activator of adenylate cyclase) was tested on the cells. Forskolin, in concentrations between 1 and 100 microM, produced dose-dependent, reversible increases in action potential duration. This effect of forskolin was blocked by incubation of the neurons in 1 mM 2',5'-dideoxyadenosine, an inhibitor of forskolin-induced activation of cyclase in other cells. This suggests that the increase in action potential duration is likely to be mediated by activation of adenylate cyclase. Cholera toxin, another cyclase activator, also increased action potential duration when applied to the sensory neurons in a concentration of 10 micrograms/ml. Forskolin applied to voltage-clamped neurons decreased a voltage-dependent outward current, a result consistent with its effect on the action potential. These effects of forskolin are mimicked by capsaicin, but are in marked contrast to those previously reported for norepinephrine on the action potential and membrane currents (Dunlap and Fischbach 1981). Furthermore, forskolin does not block (or attenuate) the effects of norepinephrine, suggesting that increases in adenylate cyclase activity are most likely not involved in norepinephrine's action on the calcium channel.
Insights
Forskolin, a cyclic adenosine monophosphate (cAMP) activator, increases action potential duration in chick sensory neurons by activating adenylate cyclase. This effect is distinct from norepinephrine
Area of Science:
- Neuroscience
- Cellular Biology
- Pharmacology
Background:
- Voltage-dependent ion channels are crucial for neuronal function.
- Internal cyclic adenosine monophosphate (cAMP) levels can modulate these channels.
- Embryonic chick sensory neurons provide a model for studying neuronal excitability.
Purpose of the Study:
- To investigate the role of internal cyclic adenosine monophosphate (cAMP) in modulating voltage-dependent channels.
- To determine if forskolin, an adenylate cyclase activator, affects neuronal action potential duration.
- To compare the effects of forskolin with other modulators like capsaicin and norepinephrine.
Main Methods:
- Application of forskolin and cholera toxin to embryonic chick sensory neurons in vitro.
- Measurement of action potential duration and voltage-dependent outward currents.
- Use of 2',5'-dideoxyadenosine to inhibit adenylate cyclase activity.
- Voltage-clamp techniques to analyze membrane currents.
Main Results:
- Forskolin caused dose-dependent, reversible increases in action potential duration.
- The forskolin-induced effect was blocked by 2',5'-dideoxyadenosine, indicating adenylate cyclase involvement.
- Cholera toxin also increased action potential duration.
- Forskolin decreased voltage-dependent outward current in voltage-clamped neurons.
- Forskolin's effects mimicked capsaicin but contrasted with norepinephrine's previously reported actions.
Conclusions:
- Internal cAMP modulation, via adenylate cyclase activation, significantly impacts action potential duration in these neurons.
- Forskolin's actions on voltage-dependent channels are distinct from those of norepinephrine.
- Adenylate cyclase activation is likely not involved in norepinephrine's modulation of calcium channels.
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