scholarly journals NaV1.5 sodium channel window currents contribute to spontaneous firing in olfactory sensory neurons

2014 ◽  
Vol 112 (5) ◽  
pp. 1091-1104 ◽  
Author(s):  
Christopher T. Frenz ◽  
Anne Hansen ◽  
Nicholas D. Dupuis ◽  
Nicole Shultz ◽  
Simon R. Levinson ◽  
...  
Keyword(s):  
Spontaneous Activity ◽  
Sensory Neurons ◽  
Immunohistochemical Analysis ◽  
Resting Potential ◽  
Olfactory Sensory Neurons ◽  
Spontaneous Firing ◽  
Whole Cell Patch Clamp ◽  
Window Current ◽  
Olfactory Tissue ◽  
Α Subunits

Olfactory sensory neurons (OSNs) fire spontaneously as well as in response to odor; both forms of firing are physiologically important. We studied voltage-gated Na+ channels in OSNs to assess their role in spontaneous activity. Whole cell patch-clamp recordings from OSNs demonstrated both tetrodotoxin-sensitive and tetrodotoxin-resistant components of Na+ current. RT-PCR showed mRNAs for five of the nine different Na+ channel α-subunits in olfactory tissue; only one was tetrodotoxin resistant, the so-called cardiac subtype NaV1.5. Immunohistochemical analysis indicated that NaV1.5 is present in the apical knob of OSN dendrites but not in the axon. The NaV1.5 channels in OSNs exhibited two important features: 1) a half-inactivation potential near −100 mV, well below the resting potential, and 2) a window current centered near the resting potential. The negative half-inactivation potential renders most NaV1.5 channels in OSNs inactivated at the resting potential, while the window current indicates that the minor fraction of noninactivated NaV1.5 channels have a small probability of opening spontaneously at the resting potential. When the tetrodotoxin-sensitive Na+ channels were blocked by nanomolar tetrodotoxin at the resting potential, spontaneous firing was suppressed as expected. Furthermore, selectively blocking NaV1.5 channels with Zn2+ in the absence of tetrodotoxin also suppressed spontaneous firing, indicating that NaV1.5 channels are required for spontaneous activity despite resting inactivation. We propose that window currents produced by noninactivated NaV1.5 channels are one source of the generator potentials that trigger spontaneous firing, while the upstroke and propagation of action potentials in OSNs are borne by the tetrodotoxin-sensitive Na+ channel subtypes.

scholarly journals Spontaneously active NaV1.5 sodium channels may underlie odor sensitivity

2016 ◽  
Vol 116 (2) ◽  
pp. 776-783 ◽  
Author(s):  
Vincent E. Dionne
Keyword(s):  
Membrane Potential ◽  
Sodium Channels ◽  
Sensory Neurons ◽  
Olfactory System ◽  
Cellular Response ◽  
Olfactory Sensory Neurons ◽  
Spontaneous Firing ◽  
Channel Activity ◽  
Recent Account ◽  
Odor Sensitivity

The olfactory system is remarkably sensitive to airborne odor molecules, but precisely how very low odor concentrations bordering on just a few molecules per olfactory sensory neuron can trigger graded changes in firing is not clear. This report reexamines signaling in olfactory sensory neurons in light of the recent account of NaV1.5 sodium channel-mediated spontaneous firing. Using a model of spontaneous channel activity, the study shows how even submillivolt changes in membrane potential elicited by odor are expected to cause meaningful changes in NaV1.5-dependent firing. The results suggest that the random window currents of NaV1.5 channels may underpin not only spontaneous firing in olfactory sensory neurons but the cellular response to odor as well, thereby ensuring the robustness and sensitivity of signaling that is especially important for low odor concentrations.

scholarly journals Modulation of Spontaneous and Odorant-Evoked Activity of Rat Olfactory Sensory Neurons by Two Anorectic Peptides, Insulin and Leptin

2009 ◽  
Vol 101 (6) ◽  
pp. 2898-2906 ◽  
Author(s):  
Agnès Savigner ◽  
Patricia Duchamp-Viret ◽  
Xavier Grosmaitre ◽  
Michel Chaput ◽  
Samuel Garcia ◽  
...  
Keyword(s):  
Patch Clamp ◽  
Spontaneous Activity ◽  
Sensory Neurons ◽  
Olfactory Epithelium ◽  
Signal To Noise Ratio ◽  
Isoamyl Acetate ◽  
Firing Frequency ◽  
Olfactory Sensory Neurons ◽  
Underlying Mechanisms

In mammals, the sense of smell is modulated by the status of satiety, which is mainly signaled by blood-circulating peptide hormones. However, the underlying mechanisms linking olfaction and food intake are poorly understood. Here we investigated the effects of two anorectic peptides, insulin and leptin, on the functional properties of olfactory sensory neurons (OSNs). Using patch-clamp recordings, we analyzed the spontaneous activity of rat OSNs in an in vitro intact epithelium preparation. Bath perfusion of insulin and leptin significantly increased the spontaneous firing frequency in 91.7% ( n = 24) and 75.0% ( n = 24) of the cells, respectively. When the activity was electrically evoked, both peptides shortened the latency to the first action potential by ∼25% and decreased the interspike intervals by ∼13%. While insulin and leptin enhanced the electrical excitability of OSNs in the absence of odorants, they surprisingly reduced the odorant-induced activity in the olfactory epithelium. Insulin and leptin decreased the peak amplitudes of isoamyl acetate-induced electroolfactogram (EOG) signals to 46 and 38%, respectively. When measured in individual cells by patch-clamp recordings, insulin and leptin decreased odorant-induced transduction currents and receptor potentials. Therefore by increasing the spontaneous activity but reducing the odorant-induced activity of OSNs, an elevated insulin and leptin level (such as after a meal) may result in a decreased global signal-to-noise ratio in the olfactory epithelium, which matches the smell ability to the satiety status.

scholarly journals 108 Neuropathic Pain and Ectopic Spontaneous Action Potential Activity of Human Primary Sensory Neurons

Neurosurgery ◽  
2017 ◽  
Vol 64 (CN_suppl_1) ◽  
pp. 222-222
Author(s):  
Robert Y North ◽  
Laurence D Rhines ◽  
Claudio E Tatsui ◽  
Ganesh Rao ◽  
Patrick M Dougherty
Keyword(s):  
Neuropathic Pain ◽  
Patch Clamp ◽  
Spontaneous Activity ◽  
Sensory Neurons ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Membrane Properties ◽  
Primary Sensory Neurons ◽  
Whole Cell Patch Clamp ◽  
Intrinsic Membrane Properties

Abstract INTRODUCTION Hyperexcitability of primary sensory neurons and its most extreme form, spontaneous activity, are key cellular-level drivers of neuropathic pain. Though extensively studied in animal models of neuropathic pain and established as a phenomenon occurring in human primary sensory neurons, this altered electrophysiology has not been rigorously studied for human primary sensory neurons nor has its relationship to clinical symptoms of neuropathic pain been established. METHODS The study was approved by the M.D. Anderson IRB. Written informed consent for participation was obtained from each tissue donor. Human dorsal root ganglia and medical histories were obtained from patients undergoing oncological spine surgery that necessitated sacrifice of spinal nerve roots as part of standard of care. Clinical data regarding presence of radicular/neuropathic pain was obtained through retrospective review of medical records or collected at time of study enrollment. Neurons were dissociated from surrounding tissue, briefly maintained in cell-culture (24-72 hours), and examined with whole-cell patch clamp techniques. RESULTS >Electrophysiological recordings were obtained from a total of 110 neurons, dissociated from 23 dorsal root ganglia, donated by 13 patients. Spontaneous activity was noted in 15% (12/79) of neurons from ganglia with pain in a corresponding dermatome vs 0% (0/31) of neurons from pain free ganglia (P < 0.05) Compared to neurons without spontaneous activity, human sensory neurons with spontaneous activity had significantly altered intrinsic membrane properties; depolarized resting membrane potential, hyperexcitability, and altered action potential kinetics (all P < 0.05). CONCLUSION Utilizing whole-cell patch clamp of dissociated human primary sensory neurons from patients both with and without neuropathic pain this study presents two important new findings: 1) first demonstration of a statistically significant association between in vitro spontaneous activity of dissociated human primary sensory neurons and neuropathic pain 2) the first characterization of the altered intrinsic membrane properties associated with spontaneous activity in human primary sensory neurons.

scholarly journals Aldehyde-specific responses of olfactory sensory neurons in the praying mantis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kota Ezaki ◽  
Takashi Yamashita ◽  
Thomas Carle ◽  
Hidehiro Watanabe ◽  
Fumio Yokohari ◽  
...  
Keyword(s):  
Sensory Neurons ◽  
Activity Patterns ◽  
Critical Role ◽  
Response Spectra ◽  
Olfactory Cues ◽  
Olfactory Sensory Neurons ◽  
Praying Mantis ◽  
Pheromonal Communication ◽  
Class B ◽  
Excitatory Responses

AbstractAlthough praying mantises rely mainly on vision for predatory behaviours, olfaction also plays a critical role in feeding and mating behaviours. However, the receptive processes underlying olfactory signals remain unclear. Here, we identified olfactory sensory neurons (OSNs) that are highly tuned to detect aldehydes in the mantis Tenodera aridifolia. In extracellular recordings from OSNs in basiconic sensilla on the antennae, we observed three different spike shapes, indicating that at least three OSNs are housed in a single basiconic sensillum. Unexpectedly, one of the three OSNs exhibited strong excitatory responses to a set of aldehydes. Based on the similarities of the response spectra to 15 different aldehydes, the aldehyde-specific OSNs were classified into three classes: B, S, and M. Class B broadly responded to most aldehydes used as stimulants; class S responded to short-chain aldehydes (C3–C7); and class M responded to middle-length chain aldehydes (C6–C9). Thus, aldehyde molecules can be finely discriminated based on the activity patterns of a population of OSNs. Because many insects emit aldehydes for pheromonal communication, mantises might use aldehydes as olfactory cues for locating prey habitat.

Sign in / Sign up

Export Citation Format

Share Document