NK-3 receptor activation depolarizes and induces an after-depolarization in pyramidal neurons in gerbil cingulate cortex

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NK-3 receptor activation depolarizes and induces an after-depolarization in pyramidal neurons in gerbil cingulate cortex. / Rekling, Jens C.

In: Brain Research Bulletin, Vol. 63, No. 2, 2004, p. 85-90.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Rekling, JC 2004, 'NK-3 receptor activation depolarizes and induces an after-depolarization in pyramidal neurons in gerbil cingulate cortex', Brain Research Bulletin, vol. 63, no. 2, pp. 85-90. https://doi.org/10.1016/j.brainresbull.2004.01.004

APA

Rekling, J. C. (2004). NK-3 receptor activation depolarizes and induces an after-depolarization in pyramidal neurons in gerbil cingulate cortex. Brain Research Bulletin, 63(2), 85-90. https://doi.org/10.1016/j.brainresbull.2004.01.004

Vancouver

Rekling JC. NK-3 receptor activation depolarizes and induces an after-depolarization in pyramidal neurons in gerbil cingulate cortex. Brain Research Bulletin. 2004;63(2):85-90. https://doi.org/10.1016/j.brainresbull.2004.01.004

Author

Rekling, Jens C. / NK-3 receptor activation depolarizes and induces an after-depolarization in pyramidal neurons in gerbil cingulate cortex. In: Brain Research Bulletin. 2004 ; Vol. 63, No. 2. pp. 85-90.

Bibtex

@article{f9546f70cde811dd9473000ea68e967b,
title = "NK-3 receptor activation depolarizes and induces an after-depolarization in pyramidal neurons in gerbil cingulate cortex",
abstract = "The involvement of tachykinins in cortical function is poorly understood. To study the actions of neurokinin-3 (NK3) receptor activation in frontal cortex, whole cell patch clamp recordings were performed from pyramidal neurons in slices of cingulate cortex from juvenile gerbils. Senktide (500nM), a selective NK3 receptor agonist, induced a transient increase in spontaneous EPSPs in layer V pyramidal neurons, accompanied by a small depolarization ( approximately 4 mV). EPSPs during senktide had a larger amplitude and faster 10-90% rise time than during control. Senktide induced a transient depolarization in layer II/III pyramidal neurons, which often reached threshold for spikes. The depolarization ( approximately 6 mV) persisted in TTX, and was accompanied by an increase in input resistance. Senktide also transiently induced a slow after-depolarization, which appeared following a depolarizing pulse. The slow after-depolarization persisted in TTX. These data suggest that activation of NK3 receptors on layer II/III pyramidal neurons induce post-synaptic depolarization and an after-depolarization, which could be mediated by blockade of a leak potassium conductance and a non-selective cation conductance, respectively.",
author = "Rekling, {Jens C}",
note = "Keywords: Animals; Cerebral Cortex; Excitatory Postsynaptic Potentials; Female; Gerbillinae; Gyrus Cinguli; Male; Peptide Fragments; Pyramidal Cells; Receptors, Neurokinin-3; Substance P",
year = "2004",
doi = "10.1016/j.brainresbull.2004.01.004",
language = "English",
volume = "63",
pages = "85--90",
journal = "Brain Research Bulletin",
issn = "0361-9230",
publisher = "Elsevier",
number = "2",

}

RIS

TY - JOUR

T1 - NK-3 receptor activation depolarizes and induces an after-depolarization in pyramidal neurons in gerbil cingulate cortex

AU - Rekling, Jens C

N1 - Keywords: Animals; Cerebral Cortex; Excitatory Postsynaptic Potentials; Female; Gerbillinae; Gyrus Cinguli; Male; Peptide Fragments; Pyramidal Cells; Receptors, Neurokinin-3; Substance P

PY - 2004

Y1 - 2004

N2 - The involvement of tachykinins in cortical function is poorly understood. To study the actions of neurokinin-3 (NK3) receptor activation in frontal cortex, whole cell patch clamp recordings were performed from pyramidal neurons in slices of cingulate cortex from juvenile gerbils. Senktide (500nM), a selective NK3 receptor agonist, induced a transient increase in spontaneous EPSPs in layer V pyramidal neurons, accompanied by a small depolarization ( approximately 4 mV). EPSPs during senktide had a larger amplitude and faster 10-90% rise time than during control. Senktide induced a transient depolarization in layer II/III pyramidal neurons, which often reached threshold for spikes. The depolarization ( approximately 6 mV) persisted in TTX, and was accompanied by an increase in input resistance. Senktide also transiently induced a slow after-depolarization, which appeared following a depolarizing pulse. The slow after-depolarization persisted in TTX. These data suggest that activation of NK3 receptors on layer II/III pyramidal neurons induce post-synaptic depolarization and an after-depolarization, which could be mediated by blockade of a leak potassium conductance and a non-selective cation conductance, respectively.

AB - The involvement of tachykinins in cortical function is poorly understood. To study the actions of neurokinin-3 (NK3) receptor activation in frontal cortex, whole cell patch clamp recordings were performed from pyramidal neurons in slices of cingulate cortex from juvenile gerbils. Senktide (500nM), a selective NK3 receptor agonist, induced a transient increase in spontaneous EPSPs in layer V pyramidal neurons, accompanied by a small depolarization ( approximately 4 mV). EPSPs during senktide had a larger amplitude and faster 10-90% rise time than during control. Senktide induced a transient depolarization in layer II/III pyramidal neurons, which often reached threshold for spikes. The depolarization ( approximately 6 mV) persisted in TTX, and was accompanied by an increase in input resistance. Senktide also transiently induced a slow after-depolarization, which appeared following a depolarizing pulse. The slow after-depolarization persisted in TTX. These data suggest that activation of NK3 receptors on layer II/III pyramidal neurons induce post-synaptic depolarization and an after-depolarization, which could be mediated by blockade of a leak potassium conductance and a non-selective cation conductance, respectively.

U2 - 10.1016/j.brainresbull.2004.01.004

DO - 10.1016/j.brainresbull.2004.01.004

M3 - Journal article

C2 - 15130696

VL - 63

SP - 85

EP - 90

JO - Brain Research Bulletin

JF - Brain Research Bulletin

SN - 0361-9230

IS - 2

ER -

ID: 9255713