Nucleus tractus solitarius and excitatory amino acids in afferent-evoked inspiratory termination

1994 ◽  
Vol 76 (3) ◽  
pp. 1293-1301 ◽  
Author(s):  
D. R. Karius ◽  
L. Ling ◽  
D. F. Speck
Keyword(s):  
Nmda Receptors ◽  
Nucleus Tractus Solitarius ◽  
Excitatory Amino Acid ◽  
Superior Laryngeal Nerve ◽  
Nmda Antagonist ◽  
Intercostal Nerve ◽  
Laryngeal Nerve ◽  
Receptor Antagonists ◽  
Adult Cats ◽  
Stimulation Of

This study tested the hypothesis that excitatory amino acid (EAA) neurotransmission at non-N-methyl-D-aspartate (non-NMDA), but not NMDA, receptors within medial regions of the nucleus tractus solitarius (NTS) is required in the inspiratory termination elicited by vagal or intercostal nerve (ICN) stimulation. Adult cats were anesthetized, decerebrated, vagotomized, and ventilated. After control responses to stimulation of the superior laryngeal nerve (SLN), vagus, and ICN were obtained, EAA receptor antagonists were injected into the medial aspects of the NTS. Injections of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) or 6,7-dinitro-quinoxaline-2,3-dione (DNQX), EAA receptor antagonists; (+/-)-2-amino-5-phosphonopentanoic acid (AP5), an NMDA antagonist; or 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline (NBQX), a non-NMDA antagonist, ipsilateral to the vagus abolished the termination response. The SLN-elicited response persisted after AP5 injection but was abolished by NBQX injections. The ICN-elicited response persisted after bilateral injections of CNQX/DNQX or procaine. We conclude that the inspiratory termination elicited by ICN stimulation is independent of the regions medial to the NTS. Inspiratory termination elicited by vagal or SLN stimulation requires non-NMDA-mediated EAA neurotransmission within medial aspects of the NTS, but the vagally elicited response also requires NMDA receptors.

Excitatory amino acid neurotransmission in superior laryngeal nerve-evoked inspiratory termination

1993 ◽  
Vol 74 (4) ◽  
pp. 1840-1847 ◽  
Author(s):  
D. R. Karius ◽  
L. Ling ◽  
D. F. Speck
Keyword(s):  
Amino Acid ◽  
Nucleus Tractus Solitarius ◽  
Excitatory Amino Acid ◽  
Superior Laryngeal Nerve ◽  
Laryngeal Nerve ◽  
Neural Pathways ◽  
Medial Nucleus ◽  
Inspiratory Motor ◽  
Adult Cats ◽  
Stimulation Of

Superior laryngeal nerve (SLN) stimulation elicits a transient inhibition of inspiration (single shocks) or inspiratory termination (stimulus trains). The neural pathways mediating these responses are unknown, but the medial nucleus tractus solitarius (mNTS) has been implicated in the termination reflex. This study tested the hypothesis that SLN-evoked inspiratory termination requires excitatory amino acid (EAA) neurotransmission in medial aspects of the NTS. Experiments were conducted in decerebrate, vagotomized, and paralyzed adult cats. Inspiratory motor output was recorded from the phrenic nerve. After control responses to SLN stimulation were recorded, a unilateral injection of the EAA antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX, 10 mM) was made into the mNTS. The transient inhibitions were not altered by DNQX. Inspiratory termination elicited by stimulation of the SLN contralateral to the injection persisted after DNQX (n = 4). Stimulation of the ipsilateral SLN no longer elicited termination (5 of 9 animals) or did so only at greatly elevated thresholds (4 of 9). We conclude that EAA neurotransmission in the mNTS is not required in the transient reflex but is necessary for the production of the SLN-evoked inspiratory termination.

scholarly journals Rostral ventrolateral medullary but not medullary lateral tegmental field neurons mediate sympatho-sympathetic reflexes in cats

2010 ◽  
Vol 299 (5) ◽  
pp. R1269-R1278 ◽  
Author(s):  
Susan M. Barman ◽  
Hakan S. Orer
Keyword(s):  
Nmda Receptors ◽  
Nucleus Tractus Solitarius ◽  
Excitatory Amino Acid ◽  
Critical Role ◽  
Area Under The Curve ◽  
Splanchnic Nerve ◽  
Ventrolateral Medulla ◽  
Afferent Fibers ◽  
The Right ◽  
Stimulation Of

This study was designed to build on past work from this laboratory by testing the hypothesis that medullary lateral tegmental field (LTF) neurons play a critical role in mediating sympathoexcitatory responses to activation of sympathetic afferent fibers. We studied the effects of microinjection of N-methyl-d-aspartate (NMDA) or non-NMDA receptor antagonists or muscimol bilaterally into the LTF on the area under the curve of the computer-averaged sympathoexcitatory potential in the right inferior cardiac nerve elicited by short trains of stimuli applied to afferent fibers in the left inferior cardiac or left splanchnic nerve (CN, SN) of baroreceptor-denervated and vagotomized cats anesthetized with a mixture of diallylbarbiturate and urethane. In contrast to our hypothesis, sympathoexcitatory responses to stimulation of CN ( n = 5–7) or SN ( n = 4–7) afferent fibers were not significantly affected by these procedures. We then determined whether the rostral and caudal ventrolateral medulla (RVLM, CVLM) and nucleus tractus solitarius (NTS) were involved in mediating these reflexes. Blockade of non-NMDA, but not NMDA, receptors in the RVLM significantly reduced the area under the curve of the sympathoexcitatory responses to electrical stimulation of either CN ( P = 0.0110; n = 6) or SN ( P = 0.0131; n = 5) afferent fibers. Neither blockade of excitatory amino acid receptors nor chemical inactivation of CVLM or NTS significantly affected the responses. These data show that activation of non-NMDA receptors in the RVLM is a critical step in mediating the sympatho-sympathetic reflex.

Induction of long-term potentiation without participation of N-methyl-D-aspartate receptors in kitten visual cortex

1991 ◽  
Vol 65 (1) ◽  
pp. 20-32 ◽  
Author(s):  
Y. Komatsu ◽  
S. Nakajima ◽  
K. Toyama
Keyword(s):  
Nmda Receptors ◽  
Stimulus Frequency ◽  
Low Frequency ◽  
Nmda Antagonist ◽  
Long Term Potentiation ◽  
Conditioning Stimulation ◽  
Postsynaptic Potential ◽  
Term Potentiation ◽  
Stimulation Of

1. Intracellular recording was made from layer II-III cells in slice preparations of kitten (30-40 days old) visual cortex. Low-frequency (0.1 Hz) stimulation of white matter (WM) usually evoked an excitatory postsynaptic potential (EPSP) followed by an inhibitory postsynaptic potential (IPSP). The postsynaptic potentials (PSPs) showed strong dependence on stimulus frequency. Early component of EPSP and IPSP evoked by weak stimulation both decreased monotonically at frequencies greater than 0.5-1 Hz. Strong stimulation similarly depressed the early EPSP at higher frequencies (greater than 2 Hz) and replaced the IPSP with a late EPSP, which had a maximum amplitude in the stimulus frequency range of 2-5 Hz. 2. Very weak WM stimulation sometimes evoked EPSPs in isolation from IPSPs. The falling phase of the EPSP revealed voltage dependence characteristic to the responses mediated by N-methyl-D-aspartate (NMDA) receptors and was depressed by application of an NMDA antagonist DL-2-amino-5-phosphonovalerate (APV), whereas the rising phase of the EPSP was insensitive to APV. 3. The early EPSPs followed by IPSPs were insensitive to APV but were replaced with a slow depolarizing potential by application of a non-NMDA antagonist 6,7-dinitro-quinoxaline-2,3-dione (DNQX), indicating that the early EPSP is mediated by non-NMDA receptors. The slow depolarization was mediated by NMDA receptors because it was depressed by membrane hyperpolarization or addition of APV. 4. The late EPSP evoked by higher-frequency stimulation was abolished by APV, indicating that it is mediated by NMDA receptors, which are located either on the recorded cell or on presynaptic cells to the recorded cells. 5. Long-term potentiation (LTP) of EPSPs was examined in cells perfused with solutions containing 1 microM bicuculline methiodide (BIM), a gamma-aminobutyric acid (GABA) antagonist. WM was stimulated at 2 Hz for 15 min as a conditioning stimulus to induce LTP, and the resultant changes were tested by low-frequency (0.1 Hz) stimulation of WM. 6. LTP of early EPSPs occurred in more than one-half of the cells (8/13) after strong conditioning stimulation. The rising slope of the EPSP was increased 1.6 times on average. 7. To test involvement of NMDA receptors in the induction of LTP in the early EPSP, the effect of conditioning stimulation was studied in a solution containing 100 microM APV, which was sufficient to block completely synaptic transmission mediated by NMDA receptors. LTP occurred in the same frequency and magnitude as in control solution.

Cross-Innervation of the Thyroarytenoid Muscle by a Branch from the External Division of the Superior Laryngeal Nerve

1997 ◽  
Vol 106 (7) ◽  
pp. 594-598 ◽  
Author(s):  
Sina Nasri ◽  
Joel A. Sercarz ◽  
Pouneh Beizai ◽  
Young-Mo Kim ◽  
Ming Ye ◽  
...  
Keyword(s):  
Vocal Fold ◽  
Superior Laryngeal Nerve ◽  
Laryngeal Nerve ◽  
Spasmodic Dysphonia ◽  
Clinical Implications ◽  
Motor Innervation ◽  
Vocal Fold Vibration ◽  
Adductor Spasmodic Dysphonia ◽  
Thyroarytenoid Muscle ◽  
Stimulation Of

The neuroanatomy of the larynx was explored in seven dogs to assess whether there is motor innervation to the thyroarytenoid (TA) muscle from the external division of the superior laryngeal nerve (ExSLN). In 3 animals, such innervation was identified. Electrical stimulation of microelectrodes applied to the ExSLN resulted in contraction of the TA muscle, indicating that this nerve is motor in function. This was confirmed by electromyographic recordings from the TA muscle. Videolaryngostroboscopy revealed improvement in vocal fold vibration following stimulation of the ExSLN compared to without it. Previously, the TA muscle was thought to be innervated solely by the recurrent laryngeal nerve. This additional pathway from the ExSLN to the TA muscle may have important clinical implications in the treatment of neurologic laryngeal disorders such as adductor spasmodic dysphonia.

Influences from laryngeal afferents on expiratory bulbospinal neurons and motoneurons

1988 ◽  
Vol 64 (4) ◽  
pp. 1337-1345 ◽  
Author(s):  
J. S. Jodkowski ◽  
A. J. Berger
Keyword(s):  
Electrical Stimulation ◽  
Cold Water ◽  
Superior Laryngeal Nerve ◽  
Intercostal Nerve ◽  
Firing Frequency ◽  
Neuronal Responses ◽  
Water Infusion ◽  
Afferent Activation ◽  
Expiratory Neurons ◽  
Stimulation Of

The purpose of this study is to analyze the reflex effects of laryngeal afferent activation on respiratory patterns in anesthetized, vagotomized, paralyzed, ventilated cats. We recorded simultaneously from the phrenic nerve, T10 internal intercostal nerve, and single bulbospinal expiratory neurons of the caudal ventral respiratory group (VRG). Laryngeal afferents were activated by electrical stimulation of the superior laryngeal nerve (SLN) or by cold-water infusion into the larynx. Both types of stimuli caused inhibition of phrenic activity and facilitation of internal intercostal nerve activity, indicating expiratory effort. The activity of 46 bulbospinal expiratory cells was depressed during SLN electrical stimulation, and 13 of them were completely inhibited. In 44 of 56 neurons tested, mean firing frequency (FFmean) was decreased in response to cold-water infusion and 8 others responded with increased FFmean; in the remaining 4 neurons, FFmean was unchanged. Possible reasons for different neuronal responses to SLN electrical stimulation and water infusion are discussed. We conclude that bulbospinal expiratory neurons of VRG were not the source of the reflex motoneuronal expiratory-like activity produced by SLN stimulation. Other, not yet identified inputs to spinal expiratory motoneurons are activated during this experimental condition.

Influences of superior laryngeal afferent stimulation on expiratory activity in cats

1988 ◽  
Vol 65 (1) ◽  
pp. 385-392 ◽  
Author(s):  
F. Bongianni ◽  
M. Corda ◽  
G. Fontana ◽  
T. Pantaleo
Keyword(s):  
Superior Laryngeal Nerve ◽  
Laryngeal Nerve ◽  
Tetanic Stimulation ◽  
Bötzinger Complex ◽  
Dependent Activity ◽  
Inspiratory Activity ◽  
Polysynaptic Reflex ◽  
Expiratory Muscles ◽  
Excitatory Responses ◽  
Stimulation Of

The effects of superior laryngeal nerve (SLN) stimulation on the activity of the expiratory muscles and medullary expiration-related (ER) neurons were investigated in 24 pentobarbital-anesthetized cats. In some experiments the animals were also paralyzed and artificially ventilated. Sustained tetanic stimulation of SLN consistently caused an apneic response associated with the appearance of tonic CO2-dependent activity in the expiratory muscles and in ER neurons located in the caudal ventral respiratory group (VRG) and the Botzinger complex. Single shocks or brief tetani at the same stimulation intensities failed to evoke excitatory responses in the expiratory muscles and in the vast majority of ER neurons tested. At higher stimulation strengths, single shocks or short tetani elicited excitatory responses in the expiratory muscles (20- to 35-ms latency) and in the majority of ER neurons of the caudal VRG (7.5- to 15.5-ms latency). These responses were obtained only during the expiratory phase and proved to be CO2 independent. On the contrary, only inhibitory responses were evoked in the activity of Botzinger complex neurons. The observed tonic expiratory activity most likely represents a disinhibition phenomenon due to the suppression of inspiratory activity; activation of expiratory muscles at higher stimulation intensities appears to be a polysynaptic reflex mediated by ER neurons of the caudal VRG but not by Botzinger complex neurons.

scholarly journals Chronic Electrical Stimulation of the Superior Laryngeal Nerve in the Rat: A Potential Therapeutic Approach for Postmenopausal Osteoporosis

Biomedicines ◽  
2020 ◽  
Vol 8 (9) ◽  
pp. 369
Author(s):  
Kaori Iimura ◽  
Nobuhiro Watanabe ◽  
Philip Milliken ◽  
Yee-Hsee Hsieh ◽  
Stephen J. Lewis ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Thyroid Gland ◽  
Venous Blood ◽  
Disease Model ◽  
Superior Laryngeal Nerve ◽  
Laryngeal Nerve ◽  
Mineral Density ◽  
Ovx Rats ◽  
Chronic Electrical Stimulation ◽  
Stimulation Of

Electrical stimulation of myelinated afferent fibers of the superior laryngeal nerve (SLN) facilitates calcitonin secretion from the thyroid gland in anesthetized rats. In this study, we aimed to quantify the electrical SLN stimulation-induced systemic calcitonin release in conscious rats and to then clarify effects of chronic SLN stimulation on bone mineral density (BMD) in a rat ovariectomized disease model of osteoporosis. Cuff electrodes were implanted bilaterally on SLNs and after two weeks recovery were stimulated (0.5 ms, 90 microampere) repetitively at 40 Hz for 8 min. Immunoreactive calcitonin release was initially measured and quantified in systemic venous blood plasma samples from conscious healthy rats. For chronic SLN stimulation, stimuli were applied intermittently for 3–4 weeks, starting at five weeks after ovariectomy (OVX). After the end of the stimulation period, BMD of the femur and tibia was measured. SLN stimulation increased plasma immunoreactive calcitonin concentration by 13.3 ± 17.3 pg/mL (mean ± SD). BMD in proximal metaphysis of tibia (p = 0.0324) and in distal metaphysis of femur (p = 0.0510) in chronically SLN-stimulated rats was 4–5% higher than that in sham rats. Our findings demonstrate chronic electrical stimulation of the SLNs produced enhanced calcitonin release from the thyroid gland and partially improved bone loss in OVX rats.

Excitatory amino acid receptor-mediated transmission in geniculocortical and intracortical pathways within visual cortex

1991 ◽  
Vol 66 (1) ◽  
pp. 293-306 ◽  
Author(s):  
L. J. Larson-Prior ◽  
P. S. Ulinski ◽  
N. T. Slater
Keyword(s):  
Visual Cortex ◽  
Amino Acid ◽  
Cortical Neurons ◽  
Excitatory Amino Acid ◽  
Nmda Antagonist ◽  
Receptor Subtypes ◽  
Excitatory Amino Acid Receptor ◽  
Visual Cortical ◽  
Stimulation Of

1. A preparation of turtle (Chrysemys picta and Pseudemys scripta) brain in which the integrity of the intracortical and geniculocortical pathways in visual cortex are maintained in vitro has been used to differentiate the excitatory amino acid (EAA) receptor subtypes involved in geniculocortical and intracortical synapses. 2. Stimulation of the geniculocortical fibers at subcortical loci produces monosynaptic excitatory postsynaptic potentials (EPSPs) in visual cortical neurons. These EPSPs are blocked by the broad-spectrum EAA receptor antagonist kynurenate (1-2 mM) and the non-N-methyl-D-aspartate (NMDA) antagonist 6, 7-dinitroquinoxaline-2,3-dione (DNQX, 10 microM), but not by the NMDA antagonist D,L-2-amino-5-phosphonovalerate (D,L-AP-5, 100 microM). These results indicate that the geniculocortical EPSP is mediated by EAAs that access principally, if not exclusively, EAA receptors of the non-NMDA subtypes. 3. Stimulation of intracortical fibers evokes compound EPSPs that could be resolved into three components differing in latency to peak. The component with the shortest latency was not affected by any of the EAA-receptor antagonists tested. The second component, of intermediate latency, was blocked by kyurenate and DNQX but not by D,L-AP-5. The component of longest latency was blocked by kynurenate and D,L-AP-5, but not by DNQX. These results indicate that the compound intracortical EPSP is comprised of three pharmacologically distinct components that are mediated by an unknown receptor, by quisqualate/kainate, and by NMDA receptors, respectively. 4. Repetitive stimulation of intracortical pathways at 0.33 Hz produces a dramatic potentiation of the late, D,L-AP-5-sensitive component of the intracortical EPSP. 5. These experiments lead to a hypothesis about the subtypes of EAA receptors that are accessed by the geniculocortical and intracortical pathways within visual cortex.

Sympatholytic response to stimulation of superior laryngeal nerve in rats

1991 ◽  
Vol 260 (2) ◽  
pp. R290-R297 ◽  
Author(s):  
D. H. Huangfu ◽  
P. G. Guyenet
Keyword(s):  
Receptor Antagonist ◽  
Superior Laryngeal Nerve ◽  
Single Pulse ◽  
Laryngeal Nerve ◽  
Ventrolateral Medulla ◽  
Gamma Aminobutyric Acid ◽  
Onset Latency ◽  
Medullary Reticular Formation ◽  
Pulse Stimulation ◽  
Stimulation Of

The central pathway mediating a sympatholytic response to stimulation of the superior laryngeal nerve (SLN) was studied in halothane-anesthetized, paralyzed rats. Single-pulse stimulation of SLN inhibited lumbar sympathetic nerve discharge (LSND) with onset latency of 113 +/- 1.7 ms. LSND inhibition was markedly attenuated by bilateral microinjection of kynurenic acid (Kyn, glutamate receptor antagonist, 4.5 nmol/side) into the caudal ventrolateral medulla (CVL) or by bilateral administration of bicuculline methiodide (Bic; gamma-aminobutyric acid-receptor antagonist, 225 pmol/side) into the rostral ventrolateral medulla (RVL). In 13 of 14 cases, the baroreceptor reflex was also severely reduced. Injections of Bic or Kyn elsewhere in the medullary reticular formation were ineffective. Single-pulse stimulation of SLN inhibited 19 of 26 RVL reticulospinal barosensitive cells (onset latency 46 +/- 1.4 ms). This inhibition was attenuated (from 92 +/- 6 to 14 +/- 12%) by iontophoretic application of Bic (n = 7), which also reduced the cells' inhibitory response to aortic coarctation. The remaining seven barosensitive neurons were unaffected by SLN stimulation. In conclusion, the sympathetic baroreflex and the sympathoinhibitory response to SLN stimulation appear to be mediated by similar medullary pathways.

Effects of respiratory afferent stimulation on phrenic neurogram during hypoxic gasping in the cat

1993 ◽  
Vol 75 (5) ◽  
pp. 2091-2098 ◽  
Author(s):  
J. E. Melton ◽  
L. O. Chae ◽  
N. H. Edelman
Keyword(s):  
Pattern Formation ◽  
Carotid Sinus ◽  
Superior Laryngeal Nerve ◽  
Laryngeal Nerve ◽  
Carotid Sinus Nerve ◽  
Burst Frequency ◽  
Burst Pattern ◽  
Progressive Hypoxia ◽  
Stimulation Period ◽  
Stimulation Of

Previous studies suggested that phrenic motor output is largely refractory to afferent stimuli during gasping. We tested this concept by electrically stimulating the carotid sinus nerve (CSN) or the superior laryngeal nerve (SLN) of anesthetized peripherally chemodenervated vagotomized ventilated cats during eupnea or gasping induced by hypoxia. During eupnea, phrenic neurogram amplitude (PNA) increased by 110% during 30 s of supramaximal CSN stimulation, but burst frequency did not change. Progressive hypoxia caused gasping after arterial O2 content was reduced by 75%. During gasping, CSN stimulation caused premature onset of gasp in 12 of 13 trials, shortened intergasp interval [6.3 +/- 0.9 vs. 14.8 +/- 2.5 (SE) s], and resulted in a small (20%) but significant increase in PNA. Intensity of SLN stimulation was adjusted to abolish phrenic activity during the 30-s eupneic stimulation period. During gasping, SLN stimulation of the same intensity tended to delay onset of the next gasp, increased intergasp interval (16.9 +/- 1.9 vs. 13.3 +/- 1.2 s), and reduced PNA by 32%. Thus the respiratory burst pattern formation circuitry responds to afferent stimuli during gasping, albeit in a manner different from the eupneic response. These observations suggest that gasping is the output of a modified eupneic burst pattern formation circuit.

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