Current and voltage clamp studies of the spike medium afterhyperpolarization of hypoglossal motoneurons in a rat brain stem slice preparation.
(17/392)
Whole-cell patch clamp recordings were performed on hypoglossal motoneurons (HMs) in a brain stem slice preparation from the neonatal rat. The medium afterhyperpolarization (mAHP) was the only afterpotential always present after single or multiple spikes, making it suitable for studying its role in firing behavior. At resting membrane potential (-68.8 +/- 0.7 mV), mAHP (23 +/- 2 ms rise-time and 150 +/- 10 ms decay) had 9.5 +/- 0.7 mV amplitude, was suppressed in Ca(2+)-free medium or by 100 nM apamin, and reversed at -94 mV membrane potential. These observations suggest that mAHP was due to activation of Ca(2+)-dependent, SK-type K(+) channels. Carbachol (10-100 microM) reversibly and dose dependently blocked the mAHP and depolarized HMs (both effects prevented by 10 microM atropine). Similar mAHP block was produced by muscarine (50 microM). In control solution a constant current pulse (1 s) induced HM repetitive firing with small spike frequency adaptation. When the mAHP was blocked by apamin, the same current pulse evoked much higher frequency firing with strong spike frequency adaptation. Carbachol also elicited faster firing and adapting behavior. Voltage clamp experiments demonstrated a slowly deactivating, apamin-sensitive K(+) current (I(AHP)) which could account for the mAHP. I(AHP) reversed at -94 mV membrane potential, was activated by depolarization as short as 1 ms, decayed with a time constant of 154 +/- 9 ms at -50 mV, and was also blocked by 50 microM carbachol. These data suggest that mAHP had an important role in controlling firing behavior as clearly demonstrated after its pharmacological block and was potently modulated by muscarinic receptor activity. (+info)
Time-dependent changes in input resistance of rat hypoglossal motoneurons associated with whole-cell recording.
(18/392)
The effect of cellular dialysis associated with whole-cell recording was studied in 24 developing hypoglossal motoneurons in a rat brainstem slice preparation. In all cases, establishing whole-cell continuity with the electrode solution resulted in an increase in the input resistance measured in current clamp. The mean magnitude of this increase was 39.7% and the time course of the maximum effect was quite variable. There was no correlation found between the time to maximum effect and the magnitude of the increase in resistance. These data indicate that the passive membrane properties are not constant during whole-cell recording in mammalian motoneurons. (+info)
The small GTP-binding protein TC10 promotes nerve elongation in neuronal cells, and its expression is induced during nerve regeneration in rats.
(19/392)
We have made a rat cDNA library using nerve-transected hypoglossal nuclei. Using this library, we performed expressed-sequence tag analysis coupled with in situ hybridization to identify genes whose expression is altered in response to nerve injury. In this gene screening, a member of Rho family GTPases, TC10, which had not yet been characterized in neuronal cells, was identified. TC10 mRNA expression was very low in normal motor neurons; however, axotomy induced its expression dramatically. Other family members such as RhoA, Rac1, and Cdc42 were moderately expressed in normal motor neurons and showed slight upregulation after axotomy. The expression level of TC10 mRNA was low in the embryonic brain and gradually increased with development. However, the expression of TC10 mRNA in the adult brain was lower and more restricted than that of RhoA, Rac1, and Cdc42. Cultured dorsal root ganglia exhibited dramatic neurite extension secondary to adenovirus-mediated expression of TC10. It can be concluded that although TC10 expression is lower in developing and mature motor neurons compared with other Rho family members, TC10 expression is induced by nerve injury to play a crucial role in nerve regeneration, particularly neurite elongation, in cooperation with other family members. (+info)
Trajectory of the hypoglossal nerve in the hypoglossal canal: significance for the transcondylar approach.
(20/392)
A microanatomical study of the hypoglossal canal and its surrounding area was carried out using dry skulls and cadaveric heads to determine the course of the hypoglossal nerve in the hypoglossal canal, especially the significance for the transcondylar approach. The hypoglossal nerve enters the superomedial part of the hypoglossal canal as two bundles, which then change course abruptly to an anterosuperior direction, and unite as one trunk before exiting the canal. The hypoglossal nerve has an oblique course in the canal rather than being located in the center, and exits through the inferolateral part of the canal. A venous plexus surrounds the entire length of the nerve bundles in the canal. The present results suggest that during drilling the occipital condyle toward the hypoglossal canal from behind, the surgeon does not need to be overly concerned even if some bleeding occurs from the posterolateral edge of the hypoglossal canal. (+info)
Role of inspiratory pacemaker neurons in mediating the hypoxic response of the respiratory network in vitro.
(21/392)
In severe hypoxia the breathing frequency is modulated in a biphasic manner: an initial increase (augmentation) is followed by a depression and cessation of breathing (apnea). Using a mouse slice preparation that contains the functional respiratory network, we aimed at identifying the neurons responsible for this frequency modulation. Whole-cell patch recordings revealed that expiratory neurons become tonically active during anoxia, indicating that these neurons cannot be responsible for the respiratory frequency modulation. Inspiratory neurons tended to depolarize (by 6.9 mV; n = 9), and the frequency of rhythmic activity was significantly increased during anoxia (from 0.16 to 0.4 Hz; n = 9). After the blockade of network activity with 6-cyano-7-nitroquinoxaline-2, 3-dione, most inspiratory neurons became tonically active (72%; n = 25, non-pacemaker). In anoxia, the membrane potential of these non-pacemaker neurons did not change (-0.26 mV; n = 6), and their tonic activity ceased. Only a subpopulation of inspiratory neurons remained rhythmically active in the absence of network activity (pacemaker neurons, 28%, 7 of 25 inspiratory neurons). In anoxia two subgroups of pacemaker neurons were differentiated; one group showed a transient increase in the bursting activity, followed by a decrease and cessation of rhythmic activity. These neurons tended to depolarize (by 10.3 mV) during anoxia. The second group remained rhythmic during the entire anoxic exposure and exhibited no depolarization. The time course of the frequency modulation in all pacemaker neurons resembled that of the intact network. We conclude that pacemaker neurons are primarily responsible for the frequency modulation in anoxia and that in the respiratory network there is a strict separation between rhythm- and pattern-generating mechanisms. (+info)
Localization and contractile properties of intrinsic longitudinal motor units of the rat tongue.
(22/392)
Tongue dysfunction is a hallmark of many human clinical disorders, yet we lack even a rudimentary understanding of tongue neural control. Here, the location and contractile properties of intrinsic longitudinal motor units (MUs) of the rat tongue body are described to provide a foundation for developing and testing theories of tongue motor control. One hundred and sixty-five MUs were studied by microelectrode penetration and stimulation of individual motor axons coursing in the terminal portion of the lateral (retrusor) branch of the hypoglossal nerve in the rat. Uniaxial MU force was recorded by a transducer attached to the protruded tongue tip, and MU location was estimated by electromyographic (EMG) electrodes implanted into the anterior, middle, and posterior portions of the tongue body. All MUs produced retrusive force. MU twitch force ranged from 2-129 mg (mean = 35 mg) and tetanic force ranged from 9-394 mg (mean = 95 mg). MUs reached maximal twitch force in 8-33 ms (mean = 15 ms) and were resistant to fatigue; following 2 min of stimulation, MUs (n = 11) produced 78-131% of initial force. EMG data were collected for 105 MUs. For 65 of these MUs, the EMG response was confined to a single electrode location: for 26 MUs to the anterior, 21 MUs to the middle, and 18 MUs to the posterior portion of the tongue. Of the remaining MUs, EMG responses were observed in two (38/40) or all three (2/40) tongue regions. These data provide the first contractile measures of identified intrinsic tongue body MUs and the first evidence that intrinsic longitudinal MUs are restricted to a portion of tongue length. Localization of MU territory suggests a role for intrinsic MU in the regional control of the mammalian tongue observed during feeding and speech. (+info)
The TASK-1 two-pore domain K+ channel is a molecular substrate for neuronal effects of inhalation anesthetics.
(23/392)
Despite widespread use of volatile general anesthetics for well over a century, the mechanisms by which they alter specific CNS functions remain unclear. Here, we present evidence implicating the two-pore domain, pH-sensitive TASK-1 channel as a target for specific, clinically important anesthetic effects in mammalian neurons. In rat somatic motoneurons and locus coeruleus cells, two populations of neurons that express TASK-1 mRNA, inhalation anesthetics activated a neuronal K(+) conductance, causing membrane hyperpolarization and suppressing action potential discharge. These membrane effects occurred at clinically relevant anesthetic levels, with precisely the steep concentration dependence expected for anesthetic effects of these compounds. The native neuronal K(+) current displayed voltage- and time-dependent properties that were identical to those mediated by the open-rectifier TASK-1 channel. Moreover, the neuronal K(+) channel and heterologously expressed TASK-1 were similarly modulated by extracellular pH. The decreased cellular excitability associated with TASK-1 activation in these cell groups probably accounts for specific CNS effects of anesthetics: in motoneurons, it likely contributes to anesthetic-induced immobilization, whereas in the locus coeruleus, it may support analgesic and hypnotic actions attributed to inhibition of those neurons. (+info)
Main trajectories of nerves that traverse and surround the tympanic cavity in the rat.
(24/392)
To guide surgery of nerves that traverse and surround the tympanic cavity in the rat, anatomical illustrations are required that are topographically correct. In this study, maps of this area are presented, extending from the superior cervical ganglion to the otic ganglion. They were derived from observations that were made during dissections using a ventral approach. Major blood vessels, bones, transected muscles of the tongue and neck and supra and infrahyoid muscles serve as landmarks in the illustrations. The course of the mandibular, facial, glossopharyngeal, vagus, accessory and hypoglossal nerves with their branches, and components of the sympathetic system, are shown and discussed with reference to data available in the literature. Discrepancies in this literature can be clarified and new data are presented on the trajectories of several nerves. The course of the tympanic nerve was established. This nerve originates from the glossopharyngeal nerve, enters the tympanic cavity, crosses the promontory, passes the tensor tympani muscle dorsally, and continues its route intracranially to the otic ganglion as the lesser petrosal nerve after intersecting with the greater petrosal nerve. Auricular branches of the glossopharyngeal and of the vagus nerve were noted. We also observed a pterygopalatine branch of the internal carotid nerve, that penetrates the tympanic cavity and courses across the promontory. (+info)