High intracellular calcium levels during and after electrical discharges in molluscan peptidergic neurons

Kits, Karel S.; Dreijer, A.M.C.; Lodder, J.C.; Borgdorff, Aren J.; Wadman, Wytse J.

doi:10.1016/s0306-4522(96)00651-3

Cited by 18 publications

(12 citation statements)

References 35 publications

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“…It is known that action potentials evoked from the caudodorsal cells of Lymnaea (which are homologous to the bag cell neurons of Aplysia) become less sensitive to calcium channel blockers during the refractory period (Kits and Bos, 1982). At this time, spike trains do not evoke a detectable rise in intracellular calcium (Kits et al, 1997). These observations could be partly explained if refractory neurons showed less spike broadening and reduced calcium influx.…”

Section: Discussionmentioning

confidence: 99%

Heterologous Expression of the K_v3.1 Potassium Channel Eliminates Spike Broadening and the Induction of a Depolarizing Afterpotential in the Peptidergic Bag Cell Neurons

Whim

Kaczmarek

1998

J. Neurosci.

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The bag cell neurons of Aplysia are a cluster of cells that control egg laying behavior. After brief synaptic stimulation, they depolarize and fire spontaneously for up to 30 min. During the first few seconds of this afterdischarge, the action potentials of the bag cell neurons undergo pronounced broadening. Single bag cell neurons in culture also show spike broadening in response to repeated depolarizations. This broadening is frequencydependent and associated with the induction of a depolarizing afterpotential lasting minutes. In some neurons the depolarizing afterpotential is sufficient to trigger spontaneous firing. To test the possibility that spike broadening during stimulation is required to trigger the depolarizing afterpotential, we eliminated frequency-dependent broadening by heterologous expression of the Kv3.1 potassium channel. This channel has rapid activation and deactivation kinetics and no use-dependent inactivation. Expression of Kv3.1 prevented spike broadening and also eliminated the depolarizing afterpotential. Measurements of the integral of calcium current during voltage commands, which simulated the action potentials of the control neurons and those expressing Kv3.1, indicate that spike broadening produces up to a fivefold increase in calcium entry. Manipulations that limit calcium entry during action potentials or chelation of intracellular calcium using BAPTA AM prevented the induction of the depolarizing afterpotential. We conclude that spike broadening is essential for the induction of the depolarizing afterpotential probably by regulating calcium influx and suggest that one of the physiological roles of spike broadening may be to regulate long-term changes in neuronal excitability.

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Section: Discussionmentioning

confidence: 99%

Heterologous Expression of the K_v3.1 Potassium Channel Eliminates Spike Broadening and the Induction of a Depolarizing Afterpotential in the Peptidergic Bag Cell Neurons

Whim

Kaczmarek

1998

J. Neurosci.

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“…Rather, sustained action potential trains are required for Ca 2+ inside terminals to reach overall levels sufficient to trigger release. Among the consequences of the existence of selective mechanisms of release for coexisting peptides and classical transmitters is the possibility that long-lasting intracellular Ca 2+ elevation may cause the release of neuropeptides to outlast the duration of electrical activity, thus uncoupling release from spiking (Kits et al, 1997).…”

Section: Neuropeptide Releasementioning

confidence: 99%

Neuromodulatory function of neuropeptides in the normal CNS

Merighi

Salio

Ferrini

et al. 2011

Journal of Chemical Neuroanatomy

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“…Among the consequence of the existence of selective mechanisms of release for coexisting peptides and classical transmitters is the possibility that long-lasting intracellular Ca 2+ elevation may cause the release of neuropeptides to outlast the duration of electrical activity, thus uncoupling release from spiking (Kits et al 1997). Therefore, in terminals with both types of vesicles, a focal increase in Ca 2+ at the synaptic membrane tends to discharge SSVs, whereas a more diffuse elevation of Ca 2+ inside the terminal favors the release of LGVs (Verhage et al 1991).…”

Section: Co-existence Of Neuropeptides and Fast-acting Neurotransmittersmentioning

confidence: 99%

Neuropeptides as synaptic transmitters

Salio¹,

Lossi²,

Ferrini³

et al. 2006

Cell Tissue Res

154

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Neuropeptides are small protein molecules (composed of 3-100 amino-acid residues) that have been localized to discrete cell populations of central and peripheral neurons. In most instances, they coexist with low-molecular-weight neurotransmitters within the same neurons. At the subcellular level, neuropeptides are selectively stored, singularly or more frequently in combinations, within large granular vesicles. Release occurs through mechanisms different from classical calcium-dependent exocytosis at the synaptic cleft, and thus they account for slow synaptic and/or non-synaptic communication in neurons. Neuropeptide co-storage and coexistence can be observed throughout the central nervous system and are responsible for a series of functional interactions that occur at both pre- and post-synaptic levels. Thus, the subcellular site(s) of storage and sorting mechanisms into different neuronal compartments are crucial to the mode of release and the function of neuropeptides as neuronal messengers.

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High intracellular calcium levels during and after electrical discharges in molluscan peptidergic neurons

Cited by 18 publications

References 35 publications

Heterologous Expression of the K_v3.1 Potassium Channel Eliminates Spike Broadening and the Induction of a Depolarizing Afterpotential in the Peptidergic Bag Cell Neurons

Heterologous Expression of the K_v3.1 Potassium Channel Eliminates Spike Broadening and the Induction of a Depolarizing Afterpotential in the Peptidergic Bag Cell Neurons

Neuromodulatory function of neuropeptides in the normal CNS

Neuropeptides as synaptic transmitters

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High intracellular calcium levels during and after electrical discharges in molluscan peptidergic neurons

Cited by 18 publications

References 35 publications

Heterologous Expression of the Kv3.1 Potassium Channel Eliminates Spike Broadening and the Induction of a Depolarizing Afterpotential in the Peptidergic Bag Cell Neurons

Heterologous Expression of the Kv3.1 Potassium Channel Eliminates Spike Broadening and the Induction of a Depolarizing Afterpotential in the Peptidergic Bag Cell Neurons

Neuromodulatory function of neuropeptides in the normal CNS

Neuropeptides as synaptic transmitters

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Product

Resources

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Heterologous Expression of the K_v3.1 Potassium Channel Eliminates Spike Broadening and the Induction of a Depolarizing Afterpotential in the Peptidergic Bag Cell Neurons

Heterologous Expression of the K_v3.1 Potassium Channel Eliminates Spike Broadening and the Induction of a Depolarizing Afterpotential in the Peptidergic Bag Cell Neurons