| First Author | Bender KJ | Year | 2010 |
| Journal | Neuron | Volume | 68 |
| Issue | 3 | Pages | 500-11 |
| PubMed ID | 21040850 | Mgi Jnum | J:252969 |
| Mgi Id | MGI:6100565 | Doi | 10.1016/j.neuron.2010.09.026 |
| Citation | Bender KJ, et al. (2010) Dopaminergic modulation of axon initial segment calcium channels regulates action potential initiation. Neuron 68(3):500-11 |
| abstractText | Action potentials initiate in the axon initial segment (AIS), a specialized compartment enriched with Na(+) and K(+) channels. Recently, we found that T- and R-type Ca(2+) channels are concentrated in the AIS, where they contribute to local subthreshold membrane depolarization and thereby influence action potential initiation. While periods of high-frequency activity can alter availability of AIS voltage-gated channels, mechanisms for long-term modulation of AIS channel function remain unknown. Here, we examined the regulatory pathways that control AIS Ca(2+) channel activity in brainstem interneurons. T-type Ca(2+) channels were downregulated by dopamine receptor activation acting via protein kinase C, which in turn reduced neuronal output. These effects occurred without altering AIS Na(+) or somatodendritic T-type channel activity and could be mediated by endogenous dopamine sources present in the auditory brainstem. This pathway represents a new mechanism to inhibit neurons by specifically regulating Ca(2+) channels directly involved in action potential initiation. |
