Tachykinins cause inward current through NK1 receptors in bullfrog sensory neurons

Akasu, Takashi; Ishimatsu, Masaru; Yamada, Kei

doi:10.1016/0006-8993(95)01506-x

Cited by 29 publications

(36 citation statements)

References 39 publications

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“…However, whether NK-1 receptors are also expressed in primary sensory neurons and the involvement of this expression in pain sensitization are still obscure. Since Dray and Pinnock (1982) first reported that SP induced depolarization of rat DRG neurons, similar results have been shown in bullfrog and cat DRG neurons as well as in guinea pig trigeminal ganglion neurons by intracellular or whole-cell patch recordings (Inoue et al, 1995;Akasu et al, 1996;Li and Zhao, 1998). Together, the results suggest an existence of functional NK-1 receptors in primary sensory neurons.…”

Section: Introductionsupporting

confidence: 76%

“…The relevant evidence is limited and contradictory (Malcangio and Bowery, 1999). Several electrophysiological studies showed that SP activates DRG neurons in vitro and in vivo, suggesting an existence of NK-1 in primary sensory neurons (Dray and Pinnock, 1982;Inoue et al, 1995;Akasu et al, 1996;Li and Zhao, 1998;Szucs et al, 1999). Reverse transcription-PCR and in situ hybridization have detected NK-1 mRNA in the DRGs of cat, rat, and mouse.…”

Section: Discussionmentioning

confidence: 99%

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Neurokinin-1 Receptor Enhances TRPV1 Activity in Primary Sensory Neurons via PKCε: A Novel Pathway for Heat Hyperalgesia

Zhang¹,

Cang²,

Kawasaki³

et al. 2007

J. Neurosci.

173

160

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The neuropeptide substance P (SP) is expressed in unmyelinated primary sensory neurons and represents the best known "pain" neurotransmitter. It is generally believed that SP regulates pain transmission and sensitization by acting on neurokinin-1 receptor (NK-1), which is expressed in postsynaptic dorsal horn neurons. However, the expression and role of NK-1 in primary sensory neurons are not clearly characterized. Our data showed that NK-1 was expressed in both intact and dissociated dorsal root ganglion (

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Section: Introductionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Neurokinin-1 Receptor Enhances TRPV1 Activity in Primary Sensory Neurons via PKCε: A Novel Pathway for Heat Hyperalgesia

Zhang¹,

Cang²,

Kawasaki³

et al. 2007

J. Neurosci.

173

160

View full text Add to dashboard Cite

show abstract

“…Since the first report that SP depolarizes rat DRG neurons (Dray and Pinnock, 1982), many studies have focused on the actions of neurokinins on sensory neurons (Spigelman and Puil, 1990;Inoue et al, 1995;Akasu et al, 1996;Li and Zhao, 1998;Abdulla et al, 2001) and on firing in bladder afferent nerves (Morrison, 1999). In general, SP elicits excitatory actions including membrane depolarization (Spigelman and Puil, 1990;Li and Zhao, 1998), inward current (Inoue et al, 1995;Akasu et al, 1996;Yang et al, 2003), or enhanced excitability in the absence of a membrane potential change (Abdulla et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

“…In general, SP elicits excitatory actions including membrane depolarization (Spigelman and Puil, 1990;Li and Zhao, 1998), inward current (Inoue et al, 1995;Akasu et al, 1996;Yang et al, 2003), or enhanced excitability in the absence of a membrane potential change (Abdulla et al, 2001). However, the effects have been variable.…”

Section: Discussionmentioning

confidence: 99%

Activation of Neurokinin-1 Receptors Increases the Excitability of Guinea Pig Dorsal Root Ganglion Cells

Zhang

Pietra

Lovati

et al. 2012

J Pharmacol Exp Ther

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The suppression of overactive bladder symptoms in patients and overactive bladder reflexes in animal models by neurokinin (NK)-1 receptor antagonists raises the possibility that these drugs target sensory neurons. This mechanism was evaluated by examining the interactions between a specific NK-1 agonist, [Sar 9 ,Met(O 2 )(11)]-substance P (Sar-Met-SP), and a potent NK-1 antagonist, netupitant (NTP), on small size (20 -30 m) dissociated L6 and S1 dorsal root ganglion (DRG) neurons from female guinea pigs. Current-clamp recording revealed that SarMet-SP (1 M) elicited membrane depolarization (average 8.05 Ϯ 1.38 mV) in 27% (18 of 65) of DRG neurons. In 74% of the remaining neurons (35 of 47) Sar-Met-SP decreased the rheobase for action potential (AP) generation and increased the response to a suprathreshold stimulus (3 times rheobase) without changing the membrane potential. Sar-Met-SP also induced changes in the action potential (AP) wave form, including 1) an increase in overshoot (average 5 mV, n ϭ 35 neurons), 2) a prolongation of AP duration (from 4.64 to 5.29 ms, n ϭ 34), and 3) a reduction in the maximal rate of AP repolarization. NTP (200 nM) reversed the Sar-Met-SP-induced changes. Ca 2ϩ imaging showed that application of Sar-Met-SP (1 M) decreased the tachyphylaxis induced by repeated application of capsaicin (0.5 M), an effect blocked by pretreatment with NTP (200 nM). These results raise the possibility that activation of NK-1 receptors in primary sensory neurons plays a role in the generation of overactive bladder and that block of NK-1 receptors in these neurons may contribute to efficacy of NK-1 antagonists in the treatment of overactive bladder symptoms.

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“…SP activates voltage-dependent Ca 2ϩ channels, voltage-dependent K ϩ conductances, Cl Ϫ currents, Ih currents, voltage-dependent Na ϩ channels, and nonselective cationic channels (Adams et al, 1983;Stanfield et al, 1985;Bley and Tsien, 1990;Shen and North, 1992;Bertrand and Galligan, 1994;Aosaki and Kawaguchi, 1996). In most neurons, SP depolarizes membrane potential by decreasing resting K ϩ conductances (Akasu et al, 1996;Lepre et al, 1996;Ptak et al, 2000;Yasuda et al, 2001). This seems not to be the case for respiratory neurons because the slow depolarization persisted after blocking K ϩ channels with TEA externally or cesium internally.…”

Section: Discussionmentioning

confidence: 99%

Substance P-Mediated Modulation of Pacemaker Properties in the Mammalian Respiratory Network

Peña¹,

Ramirez²

2004

J. Neurosci.

142

144

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Neuromodulators are integral parts of a neuronal network, and unraveling how these substances alter neuronal activity is critical for understanding how networks generate patterned activity and, ultimately, behavior. In this study, we examined the cellular mechanisms underlying the excitatory action of substance P (SP) on the respiratory network isolated in spontaneously active transverse slice preparation of mice. SP produced a slow depolarization in all recorded inspiratory pacemaker and non-pacemaker neurons. Ion exchange experiments and blockers for different ion channels suggest that the slow depolarization is caused by the activation of a low-threshold TTX-insensitive cationic current that carries mostly Na ϩ . The SP-induced slow depolarization increased tonic discharge in nonpacemaker neurons and primarily enhanced the frequency of bursting in Cd 2ϩ -insensitive pacemaker neurons. In the Cd 2ϩ -sensitive pacemaker neuron, the burst frequency was not significantly affected, whereas burst duration and amplitude were more enhanced than in Cd 2ϩ -insensitive pacemaker neurons. In a subset of non-pacemaker neurons that produced NMDA-dependent subthreshold oscillations, SP caused the production of bursts of action potentials. We conclude that the degree of pacemaker activity in the respiratory network is not fixed but dynamically regulated by neuromodulators such as SP. This finding may have clinical implications for Rett syndrome in which SP levels along with other neuromodulators are decreased in the brainstem.

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Tachykinins cause inward current through NK1 receptors in bullfrog sensory neurons

Cited by 29 publications

References 39 publications

Neurokinin-1 Receptor Enhances TRPV1 Activity in Primary Sensory Neurons via PKCε: A Novel Pathway for Heat Hyperalgesia

Neurokinin-1 Receptor Enhances TRPV1 Activity in Primary Sensory Neurons via PKCε: A Novel Pathway for Heat Hyperalgesia

Activation of Neurokinin-1 Receptors Increases the Excitability of Guinea Pig Dorsal Root Ganglion Cells

Substance P-Mediated Modulation of Pacemaker Properties in the Mammalian Respiratory Network

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