Interplay between low threshold voltage-gated K(+) channels and synaptic inhibition in neurons of the chicken nucleus laminaris along its frequency axis.
Animals; IPSC; Chick Embryo; Patch-Clamp Techniques; Neurons/*physiology; Auditory Pathways/*physiology; GABAergic inhibition; Inhibitory Postsynaptic Potentials/*physiology; interaural time difference; IPSP; Sound Localization/physiology; Synaptic Transmission/*physiology; tonotopy; voltage-gated low-threshold potassium current; whole-cell patch; Potassium Channels; Voltage-Gated/*physiology
Central auditory neurons that localize sound in horizontal space have specialized intrinsic and synaptic cellular mechanisms to tightly control the threshold and timing for action potential generation. However, the critical interplay between intrinsic voltage-gated conductances and extrinsic synaptic conductances in determining neuronal output are not well understood. In chicken, neurons in the nucleus laminaris (NL) encode sound location using interaural time difference (ITD) as a cue. Along the tonotopic axis of NL, there exist robust differences among low, middle, and high frequency (LF, MF, and HF, respectively) neurons in a variety of neuronal properties such as low threshold voltage-gated K(+) (LTK) channels and depolarizing inhibition. This establishes NL as an ideal model to examine the interactions between LTK currents and synaptic inhibition across the tonotopic axis. Using whole-cell patch clamp recordings prepared from chicken embryos (E17-E18), we found that LTK currents were larger in MF and HF neurons than in LF neurons. Kinetic analysis revealed that LTK currents in MF neurons activated at lower voltages than in LF and HF neurons, whereas the inactivation of the currents was similar across the tonotopic axis. Surprisingly, blockade of LTK currents using dendrotoxin-I (DTX) tended to broaden the duration and increase the amplitude of the depolarizing inhibitory postsynaptic potentials (IPSPs) in NL neurons without dependence on coding frequency regions. Analyses of the effects of DTX on inhibitory postsynaptic currents led us to interpret this unexpected observation as a result of primarily postsynaptic effects of LTK currents on MF and HF neurons, and combined presynaptic and postsynaptic effects in LF neurons. Furthermore, DTX transferred subthreshold IPSPs to spikes. Taken together, the results suggest a critical role for LTK currents in regulating inhibitory synaptic strength in ITD-coding neurons at various frequencies.
Hamlet William R; Liu Yu-Wei; Tang Zheng-Quan; Lu Yong
Frontiers in neural circuits
2014
1905-07
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.3389/fncir.2014.00051" target="_blank" rel="noreferrer noopener">10.3389/fncir.2014.00051</a>
Coronary microvascular Kv1 channels as regulatory sensors of intracellular pyridine nucleotide redox potential.
* NADH; *endothelium; *ion channels; *vascular smooth muscle; *vasodilation; Animals; Coronary Vessels/chemistry; Humans; Microcirculation; Oxidation-Reduction; Potassium Channels; Pyrimidine Nucleotides/*metabolism; Reactive Nitrogen Species/metabolism; Reactive Oxygen Species/metabolism; Voltage-Gated/*physiology
Smooth muscle voltage-gated potassium (Kv) channels are important regulators of microvascular tone and tissue perfusion. Recent studies indicate that Kv1 channels represent a key component of the physiological coupling between coronary blood flow and myocardial oxygen demand. While the mechanisms by which metabolic changes in the heart are transduced to alter coronary Kv1 channel gating and promote vasodilation are unclear, a growing body of evidence underscores a pivotal role of Kv1 channels in sensing the cellular redox status. Here, we discuss current knowledge of mechanisms of Kv channel redox regulation with respect to pyridine nucleotide modulation of Kv1 function via ancillary Kvbeta proteins as well as direct modulation of channel activity via reactive oxygen and nitrogen species. We identify areas of additional research to address the integration of regulatory processes under altered physiological and pathophysiological conditions that may reveal insights into novel treatment strategies for conditions in which the matching of coronary blood supply and myocardial oxygen demand is compromised.
Dwenger Marc M; Ohanyan Vahagn; Navedo Manuel F; Nystoriak Matthew A
Microcirculation (New York, N.Y. : 1994)
2018
2018-01
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1111/micc.12426" target="_blank" rel="noreferrer noopener">10.1111/micc.12426</a>