Kv1.1 Deletion Augments the Afferent Hypoxic Chemosensory Pathway and Respiration

Kline, David D.; Buniel, Maria C.; Glazebrook, Patricia A.; Peng, Ying; Ramirez‐Navarro, Angelina; Prabhakar, Nanduri R.; Kunze, Diana L.

doi:10.1523/jneurosci.4556-04.2005

Cited by 41 publications

(47 citation statements)

References 55 publications

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“…The magnitude and prolonged time period of asynchronous release dramatically potentiates the relative synaptic strength. This additional glutamate release may be upregulated under different physiological or pathophysiological states (Kline et al, 2005). Processes which target TRPV1 activity, either endogenous or exogenous, will have profound effects on information transfer across the synapse.…”

Section: Discussionmentioning

confidence: 99%

Primary Afferent Activation of Thermosensitive TRPV1 Triggers Asynchronous Glutamate Release at Central Neurons

Peters

McDougall

Fawley

et al. 2010

Neuron

165

250

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SUMMARY TRPV1 receptors feature prominently in nociception of spinal primary afferents but are also expressed in unmyelinated cranial visceral primary afferents linked to homeostatic regulation. Cranial visceral afferents enter the brain at the solitary tract nucleus (NTS) to control the heart, lungs and other vital organs. Here we identify a novel role for central TRPV1 in the activity-dependent facilitation of glutamatergic transmission from solitary tract (ST) afferents. Fast, synchronous ST-NTS transmission from capsaicin sensitive (TRPV1+) and insensitive (TRPV1−) afferents was similar. However, afferent activation triggered long lasting asynchronous glutamate release only from TRPV1+ synapses. Asynchronous release was proportional to synchronous EPSC amplitude, activity, and calcium entry. TRPV1 antagonists and low temperature blocked asynchronous release but not evoked EPSCs. At physiological afferent frequencies, asynchronous release strongly potentiated the duration of postsynaptic spiking. This activity dependent TPRV1-mediated facilitation is a novel form of synaptic plasticity that brings a unique central integrative feature to the CNS and autonomic regulation.

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Section: Discussionmentioning

confidence: 99%

Primary Afferent Activation of Thermosensitive TRPV1 Triggers Asynchronous Glutamate Release at Central Neurons

Peters

McDougall

Fawley

et al. 2010

Neuron

165

250

View full text Add to dashboard Cite

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“…Indeed an unusually long delay of offset responding that lasted for several seconds has been seen in Kcna1 −/− cells of the caudal nucleus of the solitary tract with in vitro recording in mice (Kline et al 2005), but comparable effects not been examined with acoustic stimuli.…”

Section: Introductionmentioning

confidence: 94%

Deficits in Responding to Brief Noise Offsets in Kcna1 −/− Mice Reveal a Contribution of This Gene to Precise Temporal Processing Seen Previously Only for Stimulus Onsets

Ison

Allen

2012

JARO

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The voltage-gated potassium channel subunit Kv1.1 encoded by the Kcna1 gene is expressed in many brainstem nuclei, and electrophysiological studies of Kcna1-null mutant (-/-) single neurons suggest that channels containing this subunit are critical for precise processing of rapid acoustic perturbations. We tested the hypothesis that brief offsets of a background noise are behaviorally less salient for Kcna1 -/- mice, measured by changes in noise offset inhibition of acoustic startle reflexes (ASR). In experiment 1, noise offset was followed by ASR-eliciting sound bursts either after 1-10 ms quiet intervals or after the return of noise for 10-290 ms following 10-ms quiet gaps. ASR inhibition to offset and gaps was initially higher in +/+ mice but persisted longer in -/- mice. Experiment 2 contrasted brief abrupt offsets with ramped offsets of the same duration up to 10 ms, the ramps intended to simulate progressively slower internal decays of afferent processing. Both groups had greater inhibition for abrupt offsets at asymptote, and this difference was evident at the 1-ms interval in +/+ but not -/- mice. Further, the asymptotic effect of ramped offsets in +/+ mice was equal to that produced by abrupt offsets in null mutants, suggesting more perseveration of internal afferent activity following noise offset in -/- mice. Overall, these data are consistent with prior electrophysiological studies showing that the neural mechanisms for processing acoustic transients are less effective in Kcna1 -/- mice and support previous proposals that Kv1.1 contributes to the perception of animal vocalizations and human speech.

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“…In conscious, unrestrained rats, ventilation was assessed by whole body plethysmography (24,27). One DSAP-and one IgG-treated rat were placed in adjoining whole body plethysmography chambers and experiments run simultaneously using the same gas sources.…”

Section: Plethysmography For Ventilatory Assessmentmentioning

confidence: 99%

Catecholaminergic neurons projecting to the paraventricular nucleus of the hypothalamus are essential for cardiorespiratory adjustments to hypoxia

King

Ruyle

Kline

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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King TL, Ruyle BC, Kline DD, Heesch CM, Hasser EM. Catecholaminergic neurons projecting to the paraventricular nucleus of the hypothalamus are essential for cardiorespiratory adjustments to hypoxia. Am J Physiol Regul Integr Comp Physiol 309: R721-R731, 2015. First published July 8, 2015 doi:10.1152/ajpregu.00540.2014.-Brainstem catecholamine neurons modulate sensory information and participate in control of cardiorespiratory function. These neurons have multiple projections, including to the paraventricular nucleus (PVN), which contributes to cardiorespiratory and neuroendocrine responses to hypoxia. We have shown that PVN-projecting catecholaminergic neurons are activated by hypoxia, but the function of these neurons is not known. To test the hypothesis that PVN-projecting catecholamine neurons participate in responses to respiratory challenges, we injected IgG saporin (control; n ϭ 6) or anti-dopamine ␤-hydroxylase saporin (DSAP; n ϭ 6) into the PVN to retrogradely lesion catecholamine neurons projecting to the PVN. After 2 wk, respiratory measurements (plethysmography) were made in awake rats during normoxia, increasing intensities of hypoxia (12, 10, and 8% O 2) and hypercapnia (5% CO 2-95% O2). DSAP decreased the number of tyrosine hydroxylase-immunoreactive terminals in PVN and cells counted in ventrolateral medulla (VLM; Ϫ37%) and nucleus tractus solitarii (nTS; Ϫ36%). DSAP produced a small but significant decrease in respiratory rate at baseline (during normoxia) and at all intensities of hypoxia. Tidal volume and minute ventilation (V E) index also were impaired at higher hypoxic intensities (10-8% O 2; e.g., VE at 8% O2: IgG ϭ 181 Ϯ 22, DSAP ϭ 91 Ϯ 4 arbitrary units). Depressed ventilation in DSAP rats was associated with significantly lower arterial O 2 saturation at all hypoxic intensities. PVN DSAP also reduced ventilatory responses to 5% CO 2 (VE: IgG ϭ 176 Ϯ 21 and DSAP ϭ 84 Ϯ 5 arbitrary units). Data indicate that catecholamine neurons projecting to the PVN are important for peripheral and central chemoreflex respiratory responses and for maintenance of arterial oxygen levels during hypoxic stimuli.chemoreflex; blood pressure; ventilation; anti-dopamine ␤-hydroxylase saporin; brainstem PERIPHERAL CHEMOREFLEX ACTIVATION by systemic hypoxia produces highly integrated respiratory, autonomic, behavioral, and endocrine responses (15,17). Together these responses are critical for homeostasis, serving to restore and maintain tissue oxygenation. The central nervous system pathways involved in responses to acute hypoxia are complex. Peripheral chemoreceptor afferent nerves from the carotid bodies project onto neurons located in the nucleus tractus solitarii (nTS) (40, 51), where chemoreceptor afferent input is modulated and integrated. The nTS sends projections to the rostral ventrolateral medulla (RVLM) (28,30), and this projection is considered the primary pathway mediating cardiorespiratory chemoreflex responses.The hypothalamic paraventricular nucleus (PVN) is also important in the integrated respo...

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Kv1.1 Deletion Augments the Afferent Hypoxic Chemosensory Pathway and Respiration

Cited by 41 publications

References 55 publications

Primary Afferent Activation of Thermosensitive TRPV1 Triggers Asynchronous Glutamate Release at Central Neurons

Primary Afferent Activation of Thermosensitive TRPV1 Triggers Asynchronous Glutamate Release at Central Neurons

Deficits in Responding to Brief Noise Offsets in Kcna1 −/− Mice Reveal a Contribution of This Gene to Precise Temporal Processing Seen Previously Only for Stimulus Onsets

Catecholaminergic neurons projecting to the paraventricular nucleus of the hypothalamus are essential for cardiorespiratory adjustments to hypoxia

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