scholarly journals Muscarinic acetylcholine receptors enhance neonatal mouse hypoglossal motoneuron excitability in vitro

2012 ◽  
Vol 113 (7) ◽  
pp. 1024-1039 ◽  
Author(s):  
Matthew F. Ireland ◽  
Gregory D. Funk ◽  
Mark C. Bellingham
Keyword(s):  
Firing Rate ◽  
Brain Stem ◽  
Cellular Response ◽  
Muscarinic Acetylcholine Receptors ◽  
Repetitive Firing ◽  
Muscarinic Agonists ◽  
Single Action ◽  
High K ◽  
Brain Stem Slices ◽  
Stem Slices

In brain stem slices from neonatal ( postnatal days 0–4) CD-1 mice, muscarinic ACh receptors (MAChRs) increased rhythmic inspiratory-related and tonic hypoglossal nerve discharge and depolarized single hypoglossal motoneurons (HMs) via an inward current without changing input resistance. These responses were blocked by the MAChR antagonist 1,1-dimethyl-4-diphenylacetoxypiperidinium iodide (4-DAMP; 100 nM). MAChRs shifted voltage-dependent activation of the hyperpolarization-activated cation current to more positive levels. MAChRs increased the HM repetitive firing rate and decreased rheobase, with both effects being blocked by 4-DAMP. Muscarinic agonists reduced the afterhyperpolarization of single action potentials (APs), suggesting that small-conductance Ca2+-dependent K+ current inhibition increased the HM firing rate. Muscarinic agonists also reduced the AP amplitude and slowed its time course, suggesting that MAChRs inhibited voltage-gated Na+ channels. To compare muscarinic excitation of single HMs to muscarinic excitatory effects on motor output in thicker brain stem slices requiring higher extracellular K+ for rhythmic activity, we tested the effects of muscarinic agonists on single HM excitability in high-K+ artificial cerebrospinal fluid (aCSF). In high-K+ aCSF, muscarinic agonists still depolarized HMs and altered AP size and shape, as in standard aCSF, but did not increase the steady-state firing rate, decrease afterhyperpolarization, or alter threshold potential. These results indicate that the basic cellular response of HMs to muscarinic receptors is excitatory, via a number of distinct mechanisms, and that this excitatory response will be largely preserved in rhythmically active brain stem slices.

Two Types of Actions of Norepinephrine on Identified Auditory Efferent Neurons in Rat Brain Stem Slices

1997 ◽  
Vol 78 (4) ◽  
pp. 1800-1810 ◽  
Author(s):  
Xueyong Wang ◽  
Donald Robertson
Keyword(s):  
Brain Stem ◽  
Rat Brain ◽  
Inhibitory Response ◽  
Current Clamp ◽  
Inward Current ◽  
Current Clamp Mode ◽  
Efferent Neurons ◽  
Auditory Efferent ◽  
Brain Stem Slices ◽  
Stem Slices

Wang, Xueyong and Donald Robertson. Two types of actions of norepinephrine on identified auditory efferent neurons in rat brain stem slices. J. Neurophysiol. 78: 1800–1810, 1997. Whole cell voltage-clamp recordings were performed on auditory olivocochlear neurons in the ventral nucleus of the trapezoid body (VNTB) of brain stem slices from neonatal rats. Each neuron was identified by retrograde labeling with Fast Blue injected into the cochlea. Bath application of norepinephrine (NE; 1–10 μM) reversibly induced an inward current in 26 of 38 labeled neurons that were voltage clamped at −75 mV. This was responsible for the membrane depolarization to NE observed in current-clamp mode. The NE-induced inward current appeared to be more prominent at −55 mV than at −75 mV and reversed at around −100 mV. It was attenuated but not prevented by 20 mM tetraethylammonium, and it persisted when the perfusate contained 2 mM Cs+ or 100 μM Cd2+. However, the NE-induced inward current was attenuated to varying degrees in a zero-Ca2+ solution. Current-voltage plots revealed that NE caused a decrease in membrane K+ conductance. A suppression of voltage-gated Ca2+ currents by NE was also observed. The excitatory action of NE was blocked by the α-adrenoreceptor antagonist phentolamine. The α1-adrenoreceptor agonist phenylephrine had an effect similar to that of NE. In 6 of 38 labeled neurons, an inhibitory action of NE (1–10 μM) was observed that appeared to be due to an activation of an inwardly rectified K+ current, which caused hyperpolarization of resting membrane potentials in current-clamp mode. This inhibitory response was independent of external Ca2+ and was abolished by 2–5 mM Cs+ or 0.5 mM Ba2+ applied in the perfusate. The receptors involved in the inhibitory actions of NE are not clear. The effect was partially and reversibly blocked by propranolol (10 μM), a β-adrenoreceptor antagonist. However, isoprenaline (10 μM), a β-adrenoreceptor agonist, failed to induce any effect. On the other hand, the inhibitory effect was irreversibly blocked by pretreatment with phentolamine (5–10 μM). Phenylephrine (5–10 μM) had no effect.

Substance P-Induced Inward Current in Identified Auditory Efferent Neurons in Rat Brain Stem Slices

1998 ◽  
Vol 80 (1) ◽  
pp. 218-229 ◽  
Author(s):  
Xueyong Wang ◽  
Donald Robertson
Keyword(s):  
Substance P ◽  
Brain Stem ◽  
Rat Brain ◽  
Inward Rectifier ◽  
Equilibrium Potential ◽  
Inward Current ◽  
Efferent Neurons ◽  
Auditory Efferent ◽  
Brain Stem Slices ◽  
Stem Slices

Wang, Xueyong and Donald Robertson. Substance P-induced inward current in identified auditory efferent neurons in rat brain stem slices. J. Neurophysiol. 80: 218–229, 1998. The effects of substance P (SP) on whole cell currents were studied in neurons of the medial olivocochlear efferent system (MOCS) in the ventral nucleus of the trapezoid body (VNTB) of brain stem slices from neonatal rats. Each neuron was identified by retrograde labeling with Fast Blue injected into the cochlea. Bath application of SP (0.1–10 μM) reversibly induced an apparent inward current in 49 of 63 labeled neurons when voltage clamped at near resting voltages. This apparent inward current was consistent with the SP-induced membrane depolarization observed in current-clamp mode. The SP-induced change in current was dose dependent with a half-maximal response dose of 200 nM. It was mimicked by [Cys3,6, Tyr8, Pro9]-SP, a neurokinin (NK1) receptor selective agonist, whereas [Succinyl-Asp6, MePhe8]-SP 6–11 (Senktide), a NK3 receptor agonist, had no detectable effect. The SP effect was not blocked by 10-6 M tetrodotoxin (TTX) and persisted when the perfusate contained 30 mM tetraethylammonium (TEA) or 100 μM Cd2+ or was in a 0-Ca solution. In a TTX-containing solution, SP caused a voltage-dependent decrease of membrane conductance, and the SP-evoked current reversed at a potential at around −105 mV. The predicted K+ equilibrium potential was −93.8 mV under the experimental conditions. The SP-induced inward current was attenuated by 66% when the perfusate contained 3 mM Cs+. We conclude that the apparent inward current is partly caused by SP decreasing an outward current normally maintained by the inward rectifier K+ channels in these cells. In the presence of Cs solution in the recording pipette and with a perfusate containing 3 mM Cs+, 0.1 mM Cd2+ and 10-6 M TTX, a residual SP-induced inward current was observed at test voltages ranging from −120 to 40 mV. This subcomponent reversed its polarity at ∼20 mV. This inward current was reduced substantially (but not abolished) when all NaCl in the external solution was replaced by TEA-Cl. The results indicate that SP also opens an unknown cation channel, which the available data suggests may be relatively nonselective. The results suggest that MOCS neurons are subject to modulation by SP, which depolarizes the cell membrane by decreasing the activity of inward rectifier K+ channels as well as concurrently activating a separate cation conductance. It also was found that in MOCS neurons responsive to both SP and norepinephrine, the norepinephrine effect was abolished by TTX, suggesting that an interneuronal population excited by norepinephrine converges selectively onto SP-sensitive MOCS neurons in the VNTB.

Optical illustration of glutamate-induced cell swelling coupled with membrane depolarization in embryonic brain stem slices

Neuroreport ◽  
1997 ◽  
Vol 8 (16) ◽  
pp. 3559-3563 ◽  
Author(s):  
Katsushige Sato ◽  
Yoko Momose-Sato ◽  
Yoshiyasu Arai ◽  
Akihiko Hirota ◽  
Kohtaro Kamino
Keyword(s):  
Brain Stem ◽  
Membrane Depolarization ◽  
Cell Swelling ◽  
Embryonic Brain ◽  
Brain Stem Slices ◽  
Stem Slices

Nucleus raphé obscurus modulates hypoglossal output of neonatal rat in vitro transverse brain stem slices

2001 ◽  
Vol 90 (1) ◽  
pp. 269-279 ◽  
Author(s):  
John H. Peever ◽  
Aleksandar Necakov ◽  
James Duffin
Keyword(s):  
Brain Stem ◽  
Control Region ◽  
Motor Output ◽  
Discharge Frequency ◽  
Burst Discharge ◽  
Burst Amplitude ◽  
Chemical Ablation ◽  
Brain Stem Slices ◽  
Stem Slices

Nucleus raphéobscurus (NRo) modulates hypoglossal (XII) nerve motor output in the in vitro transverse brain stem slice of neonatal rats (1–5 days old); chemical ablation of NRo and its focal CO2 acidification modulated the bursting rhythm of XII nerves. We microinjected a 4.5 mM solution of kainic acid into the NRo to disrupt cellular activity and observed that XII nerve activity was temporarily abolished ( n = 10). We also microinjected CO2-acidified (pH = 6.00 ± 0.01) artificial cerebrospinal fluid (aCSF) into the NRo ( n = 6), the pre-Bötzinger complex (PBC) ( n = 6), as well as a control region in the lateral tegmental field equidistant to NRo, PBC, and the XII motor nuclei ( n = 12). CO2acidification of the control region had no effect on XII motor output. CO2 acidification of the NRo significantly ( P < 0.05) increased the burst discharge frequency of XII nerves by 77%; integrated burst amplitude and burst duration increased by 64% and 52%, respectively. CO2 acidification of the PBC significantly ( P < 0.05) increased the burst discharge frequency of XII nerves by 65%, but neither integrated burst amplitude nor burst duration changed. These results demonstrate that chemical ablation of the NRo can abolish XII nerve bursting rhythm and that stimulation of the NRo with CO2-acidified aCSF can excite XII nerve bursting activity. From these observations, we conclude that, in transverse brain stem slices, the NRo contains pH/CO2-sensitive cells that modulate XII motor output.

Hypophysectomy, ACTH1–10 andin vitro protein synthesis in rat brain stem slices

1974 ◽  
Vol 81 (3) ◽  
pp. 571-575 ◽  
Author(s):  
M.E.A. Reith ◽  
P. Schotman ◽  
W.H. Gispen
Keyword(s):  
Protein Synthesis ◽  
Brain Stem ◽  
Rat Brain ◽  
Brain Stem Slices ◽  
Stem Slices ◽  
Vitro Protein
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