Serotonin enhances a low-voltage-activated calcium current in rat spinal motoneurons

Berger, Albert J.; Takahashi, Tomoyuki

doi:10.1523/jneurosci.10-06-01922.1990

Cited by 102 publications

(70 citation statements)

References 28 publications

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“…Although some neurotransmitters have been documented to inhibit T-type currents, presumably via G-protein-mediated processes (Formenti and Sansone, 1991), serotonin has been reported to enhance rather than inhibit T-type currents in CNS neurons (Berger and Takahashi, 1990;Fraser and MacVicar, 1991). In contrast to this, we found that serotonin reversibly inhibited T-type currents in R-B neurons.…”

Section: Modulation Of the T-type Currentscontrasting

confidence: 98%

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Serotonergic Inhibition of the T-Type and High Voltage-Activated Ca²⁺Currents in the Primary Sensory Neurons ofXenopusLarvae

Sun

Dale

1997

J. Neurosci.

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The primary sensory Rohon-Beard (R-B) neurons of Xenopus larvae are highly analogous to the C fibers of the mammalian pain pathway. We explored the actions of 5-HT by studying the modulation of Ca 2ϩ currents. In ϳ80% of the acutely isolated R-B neurons, 5-HT inhibited the high voltage-activated (HVA) currents by 16% (n ϭ 29) and the T-type currents by 24% (n ϭ 41). The modulation of the T-type and the HVA currents was mimicked by selective 5-HT 1A and 5-HT 1D agonists: 8-OH-DPAT and L-694,247. The effects of the agonists were blocked by their respective 5-HT 1A or 5-HT 1D antagonists: p-MPPI and GR127935, suggesting that both 5-HT 1A and 5-HT 1D receptors were involved. Approximately 70% of the actions of 5-HT on HVA currents was occluded by -conotoxin-GVIA (N-type channel blocker), whereas the rest of the modulation (ϳ30%) was occluded by Ͻ100 nM -agatoxin-TK (P/Q-type channel blocker). This suggests that 5-HT acts on N-and P/Q-type Ca 2ϩ channels. Neither the modulation of the T-type nor that of the HVA currents was accompanied by changes in their voltage-dependent kinetics. Cell-attached patch-clamp recordings suggest that the modulation of the T-type channel occurs through a membrane-delimited second messenger. We have studied the functional consequences of the modulation of T-type Ca 2ϩ channels and have found that these channels play a role in spike initiation in R-B neurons. Modulation of T-type channels by 5-HT therefore could modulate the sensitivity of this sensory pathway by increasing the thresholds of R-B neurons. This is a new and potentially important locus for modulation of sensory pathways in vertebrates.

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Section: Modulation Of the T-type Currentscontrasting

confidence: 98%

“…The effects of 5-HT on T -type channels are variable. In some CNS neurons 5-HT has no action on T-type channels (e.g., motoneurons; Bayliss et al, 1995), whereas in others it acts to increase the T-type current (Berger and Takahashi, 1990;Fraser and MacVicar, 1991).…”

mentioning

confidence: 99%

Serotonergic Inhibition of the T-Type and High Voltage-Activated Ca²⁺Currents in the Primary Sensory Neurons ofXenopusLarvae

Sun

Dale

1997

J. Neurosci.

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“…Methods in preparing viable spinal slices were adapted from the methods of Berger and Takahashi (1990) as previously described ). Briefly, a laminectomy was performed in young rats (12-17 d old) anesthetized with halothane.…”

Section: Methodsmentioning

confidence: 99%

Primary Afferent NMDA Receptors Increase Dorsal Horn Excitation and Mediate Opiate Tolerance in Neonatal Rats

Zeng¹,

Thomson²,

Aicher³

et al. 2006

J. Neurosci.

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EPSC (mEPSC) frequency in contrast to a decrease in mEPSC frequency produced by NMDA in opiate-naive slices. Finally, NMDAR antagonists inhibit the expression of opiate tolerance both in inhibiting EPSCs in spinal slices and in inhibiting behavioral nociceptive responses to heat.NMDAR antagonists have been reported in many studies to inhibit morphine analgesic tolerance. Our studies suggest that an increase in primary afferent NMDAR expression and activity mediates a hypersensitivity to noxious stimuli and causes the inhibition of opiate efficacy, which defines tolerance.

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“…Lack of the burst firing of thalamocortical relay neurons and resistance to absence seizures in mice lacking ␣1G T-type Ca 2ϩ channels. Neuron 31: [35][36][37][38][39][40][41][42][43][44][45]2001, with permission from Elsevier Science.) Ca 2ϩ conductance; it is not observed in Ca 2ϩ -free external solutions, and it can be blocked by divalent cations such as Co 2ϩ and Ni 2ϩ .…”

Section: A Low-threshold Calcium Spikesmentioning

confidence: 99%

“…One of the first studies showed that 10 M serotonin could stimulate rat spinal motoneuron T-type currents by 66% in a slice preparation (36). Also in a slice preparation, dorsal horn neurons were found to be stimulated by substance P (1 M), although some neurons were inhibited (347).…”

Section: B Hormonal Stimulationmentioning

confidence: 99%

Molecular Physiology of Low-Voltage-Activated T-type Calcium Channels

Perez‐Reyes

2003

Physiological Reviews

1,488

1,446

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T-type Ca2+ channels were originally called low-voltage-activated (LVA) channels because they can be activated by small depolarizations of the plasma membrane. In many neurons Ca2+ influx through LVA channels triggers low-threshold spikes, which in turn triggers a burst of action potentials mediated by Na+ channels. Burst firing is thought to play an important role in the synchronized activity of the thalamus observed in absence epilepsy, but may also underlie a wider range of thalamocortical dysrhythmias. In addition to a pacemaker role, Ca2+ entry via T-type channels can directly regulate intracellular Ca2+ concentrations, which is an important second messenger for a variety of cellular processes. Molecular cloning revealed the existence of three T-type channel genes. The deduced amino acid sequence shows a similar four-repeat structure to that found in high-voltage-activated (HVA) Ca2+ channels, and Na+ channels, indicating that they are evolutionarily related. Hence, the α1-subunits of T-type channels are now designated Cav3. Although mRNAs for all three Cav3 subtypes are expressed in brain, they vary in terms of their peripheral expression, with Cav3.2 showing the widest expression. The electrophysiological activities of recombinant Cav3 channels are very similar to native T-type currents and can be differentiated from HVA channels by their activation at lower voltages, faster inactivation, slower deactivation, and smaller conductance of Ba2+. The Cav3 subtypes can be differentiated by their kinetics and sensitivity to block by Ni2+. The goal of this review is to provide a comprehensive description of T-type currents, their distribution, regulation, pharmacology, and cloning.

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Serotonin enhances a low-voltage-activated calcium current in rat spinal motoneurons

Cited by 102 publications

References 28 publications

Serotonergic Inhibition of the T-Type and High Voltage-Activated Ca²⁺Currents in the Primary Sensory Neurons ofXenopusLarvae

Serotonergic Inhibition of the T-Type and High Voltage-Activated Ca²⁺Currents in the Primary Sensory Neurons ofXenopusLarvae

Primary Afferent NMDA Receptors Increase Dorsal Horn Excitation and Mediate Opiate Tolerance in Neonatal Rats

Molecular Physiology of Low-Voltage-Activated T-type Calcium Channels

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Serotonin enhances a low-voltage-activated calcium current in rat spinal motoneurons

Cited by 102 publications

References 28 publications

Serotonergic Inhibition of the T-Type and High Voltage-Activated Ca2+Currents in the Primary Sensory Neurons ofXenopusLarvae

Serotonergic Inhibition of the T-Type and High Voltage-Activated Ca2+Currents in the Primary Sensory Neurons ofXenopusLarvae

Primary Afferent NMDA Receptors Increase Dorsal Horn Excitation and Mediate Opiate Tolerance in Neonatal Rats

Molecular Physiology of Low-Voltage-Activated T-type Calcium Channels

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Serotonergic Inhibition of the T-Type and High Voltage-Activated Ca²⁺Currents in the Primary Sensory Neurons ofXenopusLarvae

Serotonergic Inhibition of the T-Type and High Voltage-Activated Ca²⁺Currents in the Primary Sensory Neurons ofXenopusLarvae