Continuous ulnar nerve block at the forearm for early active mobilisation following flexor tendon reconstruction.

A 63-year-old woman had sustained a subcutaneous rupture of the flexor digitorum profundus tendon of the little finger due to osteoarthritis of the pisotriquetral joint. She underwent excision of the pisiform bone and reconstruction of the flexor digitorum profundus tendon of the little finger using an autogenous palmaris longus tendon graft. After surgery, a continuous ulnar nerve block was performed at the forearm under ultrasound and nerve stimulator guidance. During rehabilitation, she could not actively extend her little finger independently due to the block; however, she could actively extend it when the dorsum of the metacarpophalangeal joint was pressed by the occupational therapist, resulting in successful early active mobilisation. A continuous ulnar nerve block at the forearm may help to facilitate early active mobilisation after reconstructive surgery for little finger flexor tendon rupture. However, it may restrict the active extension of the little finger because the block does not spare the innervation of the intrinsic muscles responsible for little finger extension.

Effect of Lipopolysaccharide Exposure on Structure and Function of the Carotid Body in Newborn Rats.

Premature infants are vulnerable to infections and have unstable breathing (Di Fiore JM, Martin RJ, Gauda EB, Respir Physiol Neurobiol 189:213-222, 2013). Inflammation adversely modifies carotid body (CB) structure and chemosensitivity in adult animals. We determined the effect of inflammation on CB structure and function in newborn rat pups. Pups were given LPS (0.1 mg/kg; IP) or saline at postnatal day 2 (P2). At P9-10 (1 week after exposure) various studies were done including ventilation, carotid sinus nerve (CSN) activity and histology. Using whole body plethysmography, we found that LPS exposure attenuates the change in interbreath (IBI) interval in response to changes in oxygen tension 1 week after LPS exposure. The response of the CSN to hypoxia was attenuated and delayed in onset in LPS-treated animals as compared to controls. Histological sections of the CB were examined for inflammatory cells at P4 (n = 7) and P9-12 (n = 6). After LPS exposure, only mast cells were seen, often encircling the CB, and clustered within the CSN as it entered the CB. Mast cells per section (mean ± SEM) were higher at P9-12 in LPS (7.4 ± 1.5) vs saline (5.4 ± 1.4) exposed animals (p = 0.04). Surprisingly, more mast cells were seen at 7-10 days vs 48 h after LPS exposure. In a newborn model of inflammation, breathing is altered which is associated with changes in structure and function of the carotid body.

Is the Carotid Body a Metabolic Monitor?

The carotid body is a multi-modal sensor and it has been debated if it senses low glucose. We have hypothesized that the carotid body is modified by some metabolic factors other than glucose and contributes to whole body glucose metabolism. This study examined the roles of insulin, leptin and transient receptor potential (TRP) channels on carotid sinus nerve (CSN) chemoreceptor discharge. In agreement with other studies, CSN activity was not modified by low glucose. Insulin did not affect the CSN hypoxic response. Leptin significantly augmented the CSN response to hypoxia and nonspecific Trp channel blockers (SKF96365, 2-APB) reversed the effect of leptin. Gene expression analysis showed high expression of Trpm3, 6, and 7 channels in the carotid body and petrosal ganglion. The results suggest that the adult mouse carotid body does not sense glucose levels directly. The carotid body may contribute to neural control of glucose metabolism via leptin receptor-mediated TRP channel activation.

Role of BK Channels in Murine Carotid Body Neural Responses in vivo.

The aim of this study was to explore the role of BK channels in the hypoxic sensitivity of the in vivo murine carotid body (CB). Four strains of mice (DBA/2J, A/J, BKα1 knockout and BKα1 wild type - FVB background) were used. The mice were anesthetized, paralyzed and mechanically ventilated (PaCO(2) ~ 35 mmHg, PO(2) > 300 mmHg). We measured carotid sinus nerve (CSN) activity during three gas challenges (F(I)O(2): 0.21, 0.15 and 0.10). CSN activity was analyzed with time-variant spectral analysis with frequency domain conversion (Fast Fourier Transforms). Afferent CSN activity increased with lowering F(I)O(2) in the DBA/2J, BKKO and BKWT mice with the most robust response in 600-800 frequencies. No substantial changes were observed in the A/J mice. Although maximal neural output was similar between the BKKO and BKWT mice, the BKWT had a higher early response compared to BKKO. Thus, BK channels may play a role in the initial response of the CB to hypoxia. The contribution of BKß subunits or the importance of frequency specific responses was unable to be determined by the current study.

Benzodiazepines and GABA-GABAA receptor system in the cat carotid body.

Benzodiazepines (BZs) suppress ventilation possibly by augmenting the GABA(A) receptor activity in the respiratory control system, but precise sites of action are not well understood. The goals of this study were: (1) to identify GABA(A) receptor subunits in the carotid body (CB) and petrosal ganglion (PG); (2) to test if BZs exert their effects through the GABA(A) receptor in the CB chemosensory unit. Tissues were taken from euthanized adult cats. RNA was extracted from the brain, and cDNA sequences of several GABA(A) receptor subunits were determined. Subsequent RT-PCR analysis demonstrated the gene expression of alpha2, alpha3, beta3, and gamma2 subunits in the CB and the PG. Immunoreactivity for GABA and for GABA(A) receptor beta3 and gamma2 subunits was detected in chemosensory glomus cells (GCs) in the CB and neurons in the PG. The functional aspects of the GABA-GABA(A) receptor system in the CB was studied by measuring CB neural output using in vitro perfusion setup. Two BZs, midazolam and diazepam, decreased the CB neural response to hypoxia. With continuous application of bicuculline, a GABA(A) receptor antagonist, the effects of BZs were abolished. In conclusion, the GABA-GABA(A) receptor system is functioning in the CB chemosensory system. BZs inhibit CB neural response to hypoxia by enhancing GABA(A) receptor activity.

Identification of M1 and M2 muscarinic acetylcholine receptors in the cat carotid body chemosensory system.

The carotid body is a major arterial chemoreceptor that senses low O2 tension, high CO2 tension and low pH in the arterial blood. It is generally believed that neurotransmitters, including acetylcholine (ACh), participate in the genesis of afferent neural output from the carotid body and modulate the function of chemoreceptor cells (glomus cells). Previous pharmacological studies suggest that M1 and M2 muscarinic ACh receptors (mAChRs) are involved in these processes. This study was designed to demonstrate the presence and localization of M1 and M2 mAChRs in the carotid body and in the petrosal ganglion of the cat. Since DNA sequences of the cat M1 and M2 mAChRs were not known, we first determined partial DNA sequences. These sequences and deduced amino acid sequences highly resembled those of human and the rat. Subsequent reverse transcription-polymerase chain reaction (RT-PCR)analysis has demonstrated that mRNAs for M1 and M2 mAChRs are present in the carotid body and the petrosal ganglion of the cat. Immunohistochemistry has indicated that the localization of these receptors appears different. Immunoreactivity for M1 mAChR was strong in nerves in the carotid body. Nerve endings positively stained for M1 mAChR appear to innervate glomus cells. Weak staining for M1 mAChRs was seen in glomus cells. On the other hand, M2 receptor protein seems to be present in glomus cells but not on nerve endings. One third of the neurons in the petrosal ganglion showed immunoreactivity for M1 mAChR. Many neurons and nerve fibers in the petrosal ganglion expressed M2 mAChR immunoreactivity. The results were consistent with previous pharmacological studies. Thus, activation of M1 mAChRs on afferent nerve endings may be linked to the increase in neural output during hypoxia. Further, M1 and M2 mAChRs on glomus cells modulate the release of neurotransmitters.

Transient ischemic attack due to dissection of the middle cerebral artery--case report.

A 57-year-old man presented with a transient ischemic attack due to dissection of the middle cerebral artery. He suffered total aphasia and clouding of consciousness for several minutes. On admission, he was alert without neurological deficit. Magnetic resonance (MR) angiography and conventional angiography depicted irregularity and double lumen of the left middle cerebral artery. The diagnosis was dissection of the middle cerebral artery. After 1 month, he left our institute with no neurological deficit. Transient ischemic attack associated with dissection of an intracranial artery is unusual. The source images of MR angiography are useful for the essential follow up of dissection.

Acetylcholine sensitivity of cat petrosal ganglion neurons.

We investigated if neuronal nicotinic acetylcholine receptors (nAChRs) are localized in chemoreceptor afferent neurons in the cat petrosal ganglion (PG) and if acetylcholine (ACh) excites chemoreceptor afferent neurons. Immunocytochemistry revealed that a majority of PG neurons expressed alpha 4 and/or alpha 7 subunits of neuronal nAChRs, and a part of them were tyrosine hydroxylase positive. Excitability of cultured PG neurons was studied with patch clamp techniques (whole cell configuration). ACh and nicotine evoked both inward and outward currents. The inward current was partially blocked by removal of extracellular calcium and by antagonists for alpha 4 beta 2 (dihydro-beta-erythroidine) or alpha 7 nAChRs (methyllycaconitine). Outward current was blocked by 4-aminopyridine (4-AP) and sometimes by atropine. ACh-induced membrane potential changes were well correlated with ACh-induced currents. Depolarization and hyperpolarization occurred in response to ACh. Occasionally depolarization was followed by a train of action potentials. The results suggest that heterogeneous neuronal nAChRs are widely distributed in both chemoreceptor and other PG neurons. In some neurons nAChRs may be functionally coupled with outward K+ channels. Further studies are required to determine whether chemoreceptor neurons have a distinct distribution pattern of nAChRs and K+ channels.

Acetylcholine is released from in vitro cat carotid bodies during hypoxic stimulation.

Previous pharmacological, immunocytochemical, electrophysiological, and microfluorometric studies have suggested that acetylcholine (ACh) is a critically important excitatory transmitter in the chemotransduction of hypoxia by the cat carotid body (CB). With the use of HPLC this study shows that the in vitro cat CB releases ACh under normoxic conditions; this release is increased when the CB is challenged with hypoxia. The preliminary observation that greater amounts of ACh are liberated in the presence of gallamine and AFDX116 suggests the presence of functioning M2 muscarinic receptors on the glomus cells of the CB.

L-DOPA and high oxygen influence release of catecholamines from the cat carotid body.

Current modelling of carotid body (CB) chemotransduction postulates an essential role for neurotransmitters, including dopamine (DA). Catecholamines (CA) released from incubated/superfused cat CBs has often been reported to diminish rapidly over the course of the exposure. The purpose of the first set of experiments was to determine the effects of including L-dihydroxyphenylalanine (L-DOPA), the immediate precursor to DA, in the incubation medium. CBs were removed from deeply anesthetized cats, cleaned of connective tissue, and placed in separate incubation tubes containing Krebs Ringer Bicarbonate solution (KRB) at 37 degrees C. One tube contained 40 microM L-DOPA. Both tubes were bubbled for 2 hr with a normoxic gas mixture (21% O2/6% CO2). This was followed immediately by a 30-minute exposure to a hypoxic gas mixture (4% O2/5% CO2). The mean amounts of DA, dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and norepinephrine (NE) released during 30 min exposures were always greater when L-DOPA was present. The use of gas mixture like the above normoxic gas mixture in incubation studies has often been considered quasi-hypoxic. Hence, in a second set of experiments we tested the effect of high oxygen mixture (95% O2/5% CO2). All other features of these experiments were the same as the above. The high oxygen environment correlated with lower DA release suggesting a reduced excitation/inhibition. The subsequent exposure to hypoxia, however, provoked a much larger release of DA and NE. The data demonstrate the substantial effect of oxygen on the release of CAs and the apparent need of a DA precursor like L-DOPA to allow detection of the changes in CA release from the CBs upon exposure to a hypoxic stimulus.

Acetylcholine release from cat carotid bodies.

Hypoxia, hypercapnia and acidosis stimulate the carotid body (CB) sending increased neural activity via a branch of the glossopharyngeal nerve to nucleus tractus solitarius; this precipitates an impressive array of cardiopulmonary, endocrine and renal reflex responses. However, the cellular mechanisms by which these stimuli generate the increased CB neural output are only poorly understood. Central to the understanding of these mechanisms is the determination of which agents are released within the CB in response to hypoxia, and serve as the stimulating transmitter(s) for chemosensory nerve endings. Acetylcholine (ACh) has been proposed as such an agent from the outset, but this proposal has been, and remains, controversial. The present study tests two hypotheses: (1) The CB releases ACh under normoxic/normocapnic conditions; and (2) The amount released increases during hypoxia and other conditions known to increase neural output from the CB. These hypotheses were tested in 12 experiments in which both CBs were removed from the anesthetized cat and incubated at 37 degrees C in a physiological salt solution while the solution was bubbled with four different concentrations of oxygen and carbon dioxide. The incubation medium was exchanged at 10 min intervals for 30 min (three periods of incubation). The medium was analyzed with high performance liquid chromatography-electrochemical detection for ACh content. Normoxic/normocapnic conditions (21% O2/6% CO2) produced a total of 0.639 +/- 0.106 pmol/150 microl (mean +/- S.E.M.; n = 12). All stimulating conditions produced larger total outputs: 4% O2/2% CO2 produced 1.773 +/- 0.46 pmol/150 microl; 0% O2/5% CO2, 0.868 +/- 0.13 pmol/150 microl; 4% O2/10% CO2, 1.077 +/- 0.21 pmol/150 microl. These three amounts were significantly greater than the normoxic/normocapnic condition, but indistinguishable among themselves. Further, the amount of ACh released did not diminish over the 30 min of stimulation. These data support the concept that during hypoxia ACh functions as a stimulating transmitter in the CB, and are consistent with the earlier reports of cholinergic enzymes and receptors found in the CB.

Roles of ion channels in carotid body chemotransmission of acute hypoxia.

In this review, we have highlighted the roles of ion channels in carotid body chemotransmission of acute hypoxia. With the application of new technologies, significant breakthroughs have been made in the last decade. The discovery of oxygen-sensitive K(+) channels in rabbit glomus cells has generated the membrane model of hypoxic chemotransmission: the inhibition of oxygen-sensitive K(+) channels by hypoxia initiates the depolarization of glomus cells and increases the firing frequency of glomus cells. The depolarization of glomus cells activates voltage-gated Ca(2+) channels, elevating intracellular Ca(2+) which triggers the release of neurotransmitters. The correlation of these events in rabbit glomus cells has been shown. However, a large corpus of data indicates that various mechanisms may be involved in different species. In rats, Ca(2+)-activated K(+) channels are inhibited by hypoxia. The role of this inhibition on rat glomus cell function is controversial, and the contribution of leak-type K(+) channels to rat glomus cell depolarization has recently been proposed. On the other hand, in cats, nicotinic ACh receptors (ligand-gated cation channels) may play a key role in initiating the depolarization of glomus cells and increasing the cytosolic Ca(2+) of glomus cells in response to hypoxia. Hypoxic inhibition of oxygen-sensitive K(+) channels would participate to further depolarize cat glomus cells. Additionally, the activity of Cl(-) channels and the modulation of ion channels by neurotransmitters may influence the excitability of glomus cells. For generating action potentials in chemoreceptor afferent nerves, nicotinic ACh receptors appear to be involved in cats and rats.

Presence of nicotinic acetylcholine receptors in cat carotid body afferent system.

With immunocytochemical techniques using a monoclonal antibody for alpha7 subunits of neuronal nicotinic acetylcholine receptors, we have found these subunits to be exclusively expressed in nerve fibers in the carotid body. Double-immunostaining showed that alpha7 subunit-positive nerve endings enveloped tyrosine hydroxylase-positive glomus cells. Some carotid sinus nerve fibers and tyrosine hydroxylase-positive petrosal ganglion neurons also expressed alpha7 subunits. These data support a role for acetylcholine in carotid body neurotransmission.

Substance P immunoreactive nerve terminals in the dorsolateral nucleus of the tractus solitarius: roles in the baroreceptor reflex.

Physiological and light microscopic evidence suggest that substance P (SP) may be a neurotransmitter contained in first-order sensory baroreceptor afferents; however, ultrastructural support for this hypothesis is lacking. We have traced the central projections of the carotid sinus nerve (CSN) in the cat by utilizing the transganglionic transport of horseradish peroxidase (HRP). The dorsolateral subnucleus of the nucleus tractus solitarius (dlNTS) was processed for the histochemical visualization of transganglionically labeled CSN afferents and for the immunocytochemical visualization of SP by dual labeling light and electron microscopic methods. Either HRP or SP was readily identified in single-labeled unmyelinated axons, myelinated axons, and nerve terminals in the dlNTS. SP immunoreactivity was also identified in unmyelinated axons, myelinated axons, and nerve terminals in the dlNTS, which were simultaneously identified as CSN primary afferents. However, only 15% of CSN terminals in the dlNTS were immunoreactive for SP. Therefore, while the ultrastructural data support the hypothesis that SP immunoreactive first-order neurons are involved in the origination of the baroreceptor reflex, they suggest that only a modest part of the total sensory input conveyed from the carotid sinus baroreceptors to the dlNTS is mediated by SP immunoreactive CSN terminals. Five types of axo-axonic synapses were observed in the dlNTS. SP immunoreactive CSN afferents were very rarely involved in these synapses. Furthermore, SP terminals were never observed to form the presynaptic element in an axo-axonic synapse with a CSN afferent. Therefore, SP does not appear to be involved in the modulation of the baroreceptor reflex in the dlNTS.

Electrophysiological and immunocytological demonstration of cell-type specific responses to hypoxia in the adult cat carotid body.

We have recently shown two types of cat carotid body cells based on the oxygen sensitivity of voltage-gated potassium channels. In the present study, we attempted to determine the correlation between cell types (glomus cells, sheath cells, and subtypes of glomus cells) and oxygen sensitivity of potassium channels. Further, changes in membrane potentials in response to hypoxia were also examined. Carotid body cells harvested from adult cats were cultured, and a whole cell patch clamp method was applied to determine the oxygen sensitivity of outward current. The tested cells were identified by Lucifer Yellow in the patch pipette. Glomus cells and sheath cells were immunocytochemically identified using tyrosine hydroxylase (TH) and glial fibrillary acidic protein (GFAP) as markers. The cells whose outward current was inhibited by hypoxia showed TH-immunoreactivity but not GFAP-immunoreactivity. The cells whose outward current was not sensitive to hypoxia were GFAP-positive or TH-negative. One TH-positive cell had oxygen-insensitive outward current. The resting membrane potentials of the cells having oxygen-sensitive outward current were significantly higher (-55+/-3 mV) than those of the cells having oxygen-insensitive outward current (-35+/-2 mV). The former type of cells was depolarized during hypoxia, but not the latter type of cells. These results suggest that most glomus cells of the adult cat carotid body possess oxygen-sensitive potassium channels and are depolarized in response to hypoxia. On the other hand, sheath cells and possibly a small fraction of glomus cells possess oxygen-insensitive potassium channels and their membrane potential is not affected by hypoxia.

Acetylcholine increases intracellular calcium of arterial chemoreceptor cells of adult cats.

Acetylcholine increases intracellular calcium of arterial chemoreceptor cells of adult cats. J. Neurophysiol. 78: 2388-2395, 1997. Several neurotransmitters have been reported to play important roles in the chemoreception of the carotid body. Among them acetylcholine (ACh) appears to be involved in excitatory processes in the cat carotid body. As one of the steps to elucidate possible roles of ACh in carotid body chemoreception in the cat, we examined the effect of ACh on intracellular calcium concentration ([Ca2+]i) of cultured carotid body cells. The carotid body from adult cats was dissociated and cultured for up to 2 wk. [Ca2+]i was measured from clusters of cells with a microfluorometric technique using Indo-1 AM. Experiments were performed at 37 degrees C, and cells were continuously superfused with modified Krebs solutions equilibrated with 5% CO2-16% O2-79% N2. ACh (100 mu M) caused a marked increase in [Ca2+]i in approximately 70% of clusters, and the responses to 1-300 mu M of ACh were concentration dependent. The magnitude and kinetics of the ACh response were mimicked by the application of nicotine, whereas muscarinic agonists, pilocarpine, and muscarine failed to evoke a similar response. ACh-induced increase in [Ca2+]i was dependent on extracellular Ca2+: it was greatly reduced or completely abolished by a transient removal of extracellular Ca2+. The response was consistently but only partially reduced by caffeine (5 mM) or nifedipine (10 mu M). The effect of mecamylamine (100 mu M) was inhibitory but small. Moreover, the increase in [Ca2+]i in response to ACh was also observed in some clusters that did not respond to high K (100 mM) Krebs. These results suggest that ACh increases [Ca2+]i of cultured carotid body cells by activating neuronal nicotinic ACh receptors, leading to Ca2+ influx via nicotinic channels. In addition, other pathways such as Ca2+ influx through L-type calcium channels, perhaps secondary to membrane depolarization, and Ca2+ release from intracellular stores may participate in increasing [Ca2+]i in response to ACh. Muscarinic receptors appear to play only a small role, if any.

Further cholinergic aspects of carotid body chemotransduction of hypoxia in cats.

From the 1930s into the 1970s, the role of acetylcholine (ACh) in the carotid body's chemotransduction of hypoxia was debated. Since the late 1970s, the issue has been pursued only intermittently or not at all. The purpose of this study was to test again with a new preparation the hypothesis that ACh is an excitatory neurotransmitter in the cat carotid body's chemotransduction of hypoxia. We tested the effect of the specific nicotinic blocker mecamylamine and the muscarinic blocker of all five muscarinic receptors, atropine. We further tested the effects of M1 and M2 muscarinic-receptor blockers. The carotid body region was selectively perfused with hypoxic Krebs-Ringer bicarbonate (KRB) solutions that were blocker free or contained varying doses of the blockers. Both mecamylamine and atropine reduced the response to hypoxic KRB in a dose-related manner. The M2 muscarinic-receptor blockers gallamine and AFDX 116 increased the response to hypoxic KRB, whereas the M1 muscarinic-receptor blocker pirenzepine reduced the response to hypoxic KRB. These data are consistent with an excitatory role for ACh in the carotid body chemotransduction of hypoxia in the cat.

Reflex stimulation of renal sympathetic nerve activity and blood pressure in response to apnea.

The purpose of this study was to examine the role of afferent input in the reflex modulation of renal sympathetic nerve activity (SNA) in response to apnea. Apneas of 20-, 40-, and 60-s duration were induced in the anesthetized, paralyzed cat (n = 7) ventilated with either room air or 100% oxygen. While receiving room air, there were increases (p < 0.005) in renal SNA of 34.5 +/- 4.2%, 53.3 +/- 6.4%, and 59.9 +/- 7.2% of maximum during the 20-, 40-, and 60-s apneas, respectively. There were corresponding increases (p < 0.025) in mean arterial pressure (Pa) of 9 +/- 3, 30 +/- 9, and 45 +/- 12 mm Hg during the 20-, 40-, and 60-s apneas while receiving room air, respectively. The effect of 100% oxygen was to reduce (p < 0.0001) the renal SNA response to apnea, at a matched level of PaCO2, by at least 80%, and to eliminate any increase in Pa. During the first breath of the postapneic period, there was a partial inhibition of renal SNA. During the second and third breaths of the postapneic period, there was a marked fall in renal SNA that was associated with a precipitous decline in directly recorded carotid chemoreceptor activity (n = 2). The magnitude of the fall in renal SNA after apnea was related to the degree of postapneic hypertension. We conclude that hypoxic chemoreceptor stimulation is the predominant factor generating the renal SNA response to apnea, with modulating inputs from thoracic afferents and arterial baroreceptors likely contributing to the marked inhibition of renal SNA immediately after the apnea.

Two types of voltage-gated K channels in carotid body cells of adult cats.

The purpose of this study was to investigate if the oxygen-sensitive K channel is present in the carotid body cells of adult cats, and if all carotid body cells express the oxygen-sensitive K channel. A standard patch-clamp technique with a whole-cell configuration was applied to cultured carotid body cells from adult cats. The cells were continuously perfused with Krebs equilibrated with 5% CO2/air or 5% CO2/argon at room temperature. The results showed that electrophysiologically at least two types of cells existed in cultured cat carotid body cells. One type expressed the oxygen-sensitive K channel and the other expressed the oxygen-insensitive K channel. The oxygen-sensitive K channel was voltage-dependent with a threshold potential of -30 mV. No inactivation was observed during 40 ms of stimulation. The slope of the steady-state current-voltage curve was almost linear in the range from -30 mV to +50 mV. Hypoxia (pO2 = 25 mmHg) reversibly depressed the K current by 22%. The current was inhibited by 4-aminopyridine (10 mM) and tetraethylammonium (4-25 mM), but insensitive to charybdotoxin (100 nM). The oxygen-insensitive K channel showed similar characteristics to that of the oxygen-sensitive K channel in the threshold and the speed of activation, and the shape of I-V curve. The cat is the third species in which the oxygen-sensitive K channel was found in the carotid body. The sensitivity of K channels to oxygen may be a unique feature of chemosensory cells, but the properties of the oxygen-sensitive K channels are different among cats, rats, and rabbits.