Acetylcholine enhances excitability by lowering the threshold of spike generation in olfactory receptor cells

2013 ◽  
Vol 110 (9) ◽  
pp. 2082-2089 ◽  
Author(s):  
Mahito Ohkuma ◽  
Fusao Kawai ◽  
Ei-ichi Miyachi

Olfactory perception is influenced by behavioral states, presumably via efferent regulation. Using the whole cell version of patch-clamp recording technique, we discovered that acetylcholine, which is released from efferent fibers in the olfactory mucosa, can directly affect the signal encoding in newt olfactory receptor cells (ORCs). Under current-clamp conditions, application of carbachol, an acetylcholine receptor agonist, increased the spike frequency of ORCs and lowered their spike threshold. When a 3-pA current to induce near-threshold depolarization was injected into ORCs, 0.0 spikes/s were generated in control solution and 0.5 spikes/s in the presence of carbachol. By strong stimuli of injection of a 13-pA current into ORCs, 9.1 and 11.0 spikes/s were generated in control and carbachol solutions, respectively. A similar result was observed by bath application of 50 μM acetylcholine. Under voltage-clamp conditions, carbachol increased the peak amplitude of a voltage-gated sodium current by 32% and T-type calcium current by 39%. Atropine, the specific muscarinic receptor antagonist, blocked the enhancement by carbachol of the voltage-gated sodium current and T-type calcium current, suggesting that carbachol increases those currents via the muscarinic receptor rather than via the nicotinic receptor. In contrast, carbachol did not significantly change the amplitude of the L-type calcium current or the delayed rectifier potassium current in the ORCs. Because T-type calcium current is known to lower the threshold in ORCs, we suggest that acetylcholine enhance excitability by lowering the threshold of spike generation in ORCs via the muscarinic receptor.

1997 ◽  
Vol 109 (2) ◽  
pp. 265-272 ◽  
Author(s):  
Fusao Kawai ◽  
Takashi Kurahashi ◽  
Akimichi Kaneko

Effects of odorants on voltage-gated ionic channels were investigated in isolated newt olfactory receptor cells by using the whole cell version of the patch–clamp technique. Under voltage clamp, membrane depolarization to voltages between −90 mV and +40 mV from a holding potential (Vh) of −100 mV generated time- and voltage-dependent current responses; a rapidly (< 15 ms) decaying initial inward current and a late outward current. When odorants (1 mM amyl acetate, 1 mM acetophenone, and 1 mM limonene) were applied to the recorded cell, the voltage-gated currents were significantly reduced. The dose-suppression relations of amyl acetate for individual current components (Na+ current: INa, T-type Ca2+ current: ICa,T, L-type Ca2+ current: ICa,L, delayed rectifier K+ current: IKv and Ca2+-activated K+ current: IK(Ca)) could be fitted by the Hill equation. Half-blocking concentrations for each current were 0.11 mM (INa), 0.15 mM (ICa,T), 0.14 mM (ICa,L), 1.7 mM (IKv), and 0.17 mM (IK(Ca)), and Hill coefficient was 1.4 (INa), 1.0 (ICa,T), 1.1 (ICa,L), 1.0 (IKv), and 1.1 (IK(Ca)), suggesting that the inward current is affected more strongly than the outward current. The activation curve of INa was not changed significantly by amyl acetate, while the inactivation curve was shifted to negative voltages; half-activation voltages were −53 mV at control, −66 mV at 0.01 mM, and −84 mV at 0.1 mM. These phenomena are similar to the suppressive effects of local anesthetics (lidocaine and benzocaine) on INa in various preparations, suggesting that both types of suppression are caused by the same mechanism. The nonselective blockage of ionic channels observed here is consistent with the previous notion that the suppression of the transduction current by odorants is due to the direst blockage of transduction channels.


1989 ◽  
Vol 61 (5) ◽  
pp. 994-1000 ◽  
Author(s):  
I. Schmiedel-Jakob ◽  
P. A. Anderson ◽  
B. W. Ache

1. The basic electrical properties of olfactory (antennule) receptor cells were studied in an in situ preparation of the spiny lobster using whole cell patch-clamp recording. 2. The current-voltage relationship of the cells was linear for membrane potentials between -150 and -40 mV and rectified at more positive membrane potentials. The input resistance at rest averaged 508 M omega. The cells displayed two time constants, with mean values of 29.8 and 8.2 ms. 3. Depolarizing current steps elicited fast, overshooting action potentials at a mean threshold of -32 mV from an imposed resting membrane potential of -65 mV. The action potentials were tetrodotoxin (TTX) and tetraethylammonium (TEA) sensitive, suggesting they are typical sodium/potassium action potentials. 4. Odor stimulation evoked slow, dose-dependent, depolarizing receptor potentials up to 50 mV in amplitude. In approximately 30% of cells tested, these led to repetitive spiking when the cells were depolarized beyond -45 to -30 mV. The amplitude of the receptor potential was graded as a linear function of the logarithm of the odor concentration. 5. The amplitude of the receptor potential varied linearly with the membrane potential between -70 and -30 mV. Extrapolated reversal potentials appeared to be normally distributed around a mean value of -3.6 mV. 6. The results collectively indicate that lobster olfactory receptor cells have electrical properties similar to, but not necessarily identical with, those currently envisaged for olfactory receptor cells in other species.


2013 ◽  
Vol 40 (1) ◽  
pp. 66-70 ◽  
Author(s):  
Kengo Tamari ◽  
Hiroko Takeuchi ◽  
Masayoshi Kobayashi ◽  
Takashi Kurahashi ◽  
Tetsuro Yamamoto

Author(s):  
Bert Ph. M. Menco

Vertebrate olfactory receptor cells are specialized neurons that have numerous long tapering cilia. The distal parts of these cilia line the interface between the external odorous environment and the luminal surface of the olfactory epithelium. The length and number of these cilia results in a large surface area that presumably increases the chance that an odor molecule will meet a receptor cell. Advanced methods of cryoprepration and immuno-gold labeling were particularly useful to preserve the delicate ultrastructural and immunocytochemical features of olfactory cilia required for localization of molecules involved in olfactory signal-transduction. We subjected olfactory tissues to freeze-substitution in acetone (unfixed tissues) or methanol (fixed tissues) followed by low temperature embedding in Lowicryl K11M for that purpose. Tissue sections were immunoreacted with several antibodies against proteins that are presumably important in olfactory signal-transduction.


1998 ◽  
Vol 80 (2) ◽  
pp. 1011-1015 ◽  
Author(s):  
Matt Wachowiak ◽  
Lawrence B. Cohen

Wachowiak, Matt and Lawrence B. Cohen. Presynaptic afferent inhibition of lobster olfactory receptor cells: reduced action-potential propagation into axon terminals. J. Neurophysiol. 80: 1011–1015, 1998. Action-potential propagation into the axon terminals of olfactory receptor cells was measured with the use of voltage-sensitive dye imaging in the isolated spiny lobster brain. Conditioning shocks to the olfactory nerve, known to cause long-lasting suppression of olfactory lobe neurons, allowed the selective imaging of activity in receptor cell axon terminals. In normal saline the optical signal from axon terminals evoked by a test stimulus was brief (40 ms) and small in amplitude. In the presence of low-Ca2+/high-Mg2+ saline designed to reduce synaptic transmission, the test response was unchanged in time course but increased significantly in amplitude (57 ± 16%, means ± SE). This increase suggests that propagation into receptor cell axon terminals is normally suppressed after a conditioning shock; this suppression is presumably synaptically mediated. Thus our results show that presynaptic inhibition occurs at the first synapse in the olfactory pathway and that the inhibition is mediated, at least in part, via suppression of action-potential propagation into the presynaptic terminal.


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