Calcium channel upregulation in response to activation of neurotrophin and surrogate neurotrophin receptor tyrosine kinases

Black, Melony J.; Woo, Yeunkyung; Rane, Stanley G.

doi:10.1002/jnr.10748

Cited by 9 publications

(12 citation statements)

References 58 publications

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“…The average, maximal, and range of peak heights were all markedly higher in NGF-differentiated cells. Higher [Ca 2+ ] cyt peaks might be expected from the greater surface-to-volume ratio of differentiated cells and from a reported increase in Ca 2+ current (Black et al, 2003). …”

Section: Resultsmentioning

confidence: 99%

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Calcium Transport Mechanisms of PC12 Cells

Duman

Chen

Hille

2008

The Journal of General Physiology

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Many studies of Ca2+ signaling use PC12 cells, yet the balance of Ca2+ clearance mechanisms in these cells is unknown. We used pharmacological inhibition of Ca2+ transporters to characterize Ca2+ clearance after depolarizations in both undifferentiated and nerve growth factor-differentiated PC12 cells. Sarco-endoplasmic reticulum Ca2+ ATPase (SERCA), plasma membrane Ca2+ ATPase (PMCA), and Na+/Ca2+ exchanger (NCX) account for almost all Ca2+ clearance in both cell states, with NCX and PMCA making the greatest contributions. Any contribution of mitochondrial uniporters is small. The ATP pool in differentiated cells was much more labile than that of undifferentiated cells in the presence of agents that dissipated mitochondrial proton gradients. Differentiated PC12 cells have a small component of Ca2+ clearance possessing pharmacological characteristics consistent with secretory pathway Ca2+ ATPase (SPCA), potentially residing on Golgi and/or secretory granules. Undifferentiated and differentiated cells are similar in overall Ca2+ transport and in the small transport due to SERCA, but they differ in the fraction of transport by PMCA and NCX. Transport in neurites of differentiated PC12 cells was qualitatively similar to that in the somata, except that the ER stores in neurites sometimes released Ca2+ instead of clearing it after depolarization. We formulated a mathematical model to simulate the observed Ca2+ clearance and to describe the differences between these undifferentiated and NGF-differentiated states quantitatively. The model required a value for the endogenous Ca2+ binding ratio of PC12 cell cytoplasm, which we measured to be 268 ± 85. Our results indicate that Ca2+ transport in undifferentiated PC12 cells is quite unlike transport in adrenal chromaffin cells, for which they often are considered models. Transport in both cell states more closely resembles that of sympathetic neurons, for which differentiated PC12 cells often are considered models. Comparison with other cell types shows that different cells emphasize different Ca2+ transport mechanisms.

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Section: Resultsmentioning

confidence: 99%

“…NGF increases the N- and P/Q-type Ca 2+ current (as well as Na + current) in PC12 cells (Black et al, 2003); Ba 2+ currents are tripled. There is an increased transcription of N-type but not of P/Q-type channel genes (Colston et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Calcium Transport Mechanisms of PC12 Cells

Duman

Chen

Hille

2008

The Journal of General Physiology

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“…It is now well established that loss of neurotrophins results in neural degeneration, and exposure to either endogenous or exogenous neurotrophins promotes neuronal survival1. Whilst there is growing evidence that neurotrophins can also modulate ion channel activity and expression234567, the details of which channels are affected, and how this influences neural communication is still being resolved.…”

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confidence: 99%

Firing frequency and entrainment maintained in primary auditory neurons in the presence of combined BDNF and NT3

Wright

Gillespie

O’Leary

et al. 2016

Sci Rep

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Primary auditory neurons rely on neurotrophic factors for development and survival. We previously determined that exposure to brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT3) alters the activity of hyperpolarization-activated currents (Ih) in this neuronal population. Since potassium channels are sensitive to neurotrophins, and changes in Ih are often accompanied by a shift in voltage-gated potassium currents (IK), this study examined IK with exposure to both BDNF and NT3 and the impact on firing entrainment during high frequency pulse trains. Whole-cell patch-clamp recordings revealed significant changes in action potential latency and duration, but no change in firing adaptation or total outward IK. Dendrotoxin-I (DTX-I), targeting voltage-gated potassium channel subunits KV1.1 and KV1.2, uncovered an increase in the contribution of DTX-I sensitive currents with exposure to neurotrophins. No difference in Phrixotoxin-1 (PaTX-1) sensitive currents, mediated by KV4.2 and KV4.3 subunits, was observed. Further, no difference was seen in firing entrainment. These results show that combined BDNF and NT3 exposure influences the contribution of KV1.1 and KV1.2 to the low voltage-activated potassium current (IKL). Whilst this is accompanied by a shift in spike latency and duration, both firing frequency and entrainment to high frequency pulse trains are preserved.

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“…For example, opioids increase while PDGFR-β decreases current amplitudes of voltage-sensitive calcium channels and voltage-activated potassium channels 15–17 . Conversely, opioids decrease, while PDGFR-β increases the non-selective cation current 17,18 .…”

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confidence: 99%