Neonatal Rat Brainstem-spinal Cord Research Articles

Dorsal column nuclei neurons recorded in a brain stem-spinal cord preparation: characteristics and their responses to dorsal root stimulation.

Recordings were obtained from dorsal column nucleus (DCN) neurons in a neonatal rat brain stem-spinal cord preparation to study their basic electrophysiological properties and responses to stimulation of a dorsal root. Whole-cell patch-clamp recordings were made from 21 neurons that responded to dorsal root stimulation with a fast excitatory postsynaptic potential (EPSP). These neurons were located lateral to, but at the level of, the area postrema at depths of 100-268 microm below the dorsal surface of the brain. The neurons could be divided into groups according to the shape of their action potentials or voltage responses to hyperpolarizing current steps; however, the response profiles of the groups of neurons to dorsal root stimulation were not significantly different and all neurons were considered together. Dorsal root stimulation elicited excitatory postsynaptic potentials (EPSPs) in all neurons with a very low variability in onset latency and an ability to follow 100-Hz stimulation, indicating that they were mediated by activation of a monosynaptic pathway. The peak amplitude of the EPSP increased with membrane hyperpolarization, and applications of the non-NMDA receptor antagonists 6-nitro-7-sulfamoylbenzo[f]quinoxaline-2, 3-dione (NBQX) and 6,7-dinitroquinoxaline-2,3-dione (DNQX) decreased the amplitude of the EPSP to 14.2% of the control response (n = 6). The descending phase of the EPSP decreased with membrane hyperpolarization and was reduced by the N-methyl-D-aspartate (NMDA) receptor antagonist AP-5 (n = 2). The EPSPs were also reduced in amplitude by applications of the gamma-aminobutyric acid-B (GABA(B)) receptor agonist baclofen, which had no effect on membrane potential or input resistance. These results show that fast EPSPs in DCN neurons elicited by dorsal root stimulation are mediated by an excitatory amino acid acting at both non-NMDA and, to a lesser extent, NMDA receptors. In addition, GABA acting at presynaptic GABA(B) receptors can inhibit these responses.

Alpha1-adrenergic receptor-induced slow rhythmicity in nonrespiratory cervical motoneurons of neonatal rat spinal cord.

Previous studies have reported that the alpha1-adrenergic system can activate spinal rhythm generators belonging to the central respiratory network. In order to analyse alpha1-adrenergic effects on both cranial and spinal motoneuronal activity, phenylephrine (1-800 microM) was applied to in vitro preparations of neonatal rat brainstem-spinal cord. High concentration of phenylephrine superfusion exerted multiple effects on spinal cervical outputs (C2-C6), consisting of a lengthening of respiratory period and an increase in inspiratory burst duration. Furthermore, in 55% of cases a slow motor rhythm recorded from the same spinal outputs was superimposed on the inspiratory activity. However, this phenylephrine-induced slow motor rhythm generated at the spinal level was observed neither in inspiratory cranial nerves (glossopharyngeal, vagal and hypoglossal outputs) nor in phrenic nerves. Whole-cell patch-clamp recordings were carried out on cervical motoneurons (C4-C5), to determine first which motoneurons were involved in this slow rhythm, and secondly the cellular events underlying direct phenylephrine effects on motoneurons. In all types of motoneurons (inspiratory and nonrespiratory) phenylephrine induced a prolonged depolarization with an increase in neuronal excitability. However, only nonrespiratory motoneurons showed additional rhythmic membrane depolarizations (with spiking) occurring in phase with the slow motor rhythm recorded from the ventral root. Furthermore the tonic depolarization produced in all motoneurons results from an inward current [which persists in the presence of tetrodotoxin (TTX)] associated with a decrease in neuron input conductance, with a reversal potential varying as a Nernstian function of extracellular K+ concentration. Our results indicate that the alpha1-adrenoceptor activation: (i) affects both the central respiratory command (i.e. respiratory period and inspiratory burst duration) and spinal inspiratory outputs; (ii) induces slow spinal motor rhythmicity, which is unlikely to be related to the respiratory system; and (iii), increases motoneuronal excitability, probably through a decrease in postsynaptic leak K+ conductance.

Potential role for imidazole in the rhythmic respiratory activity of the in vitro neonatal rat brainstem

We used the imidazole-binding agent, diethylpyrocarbonate (DEPC), to test the hypothesis that rhythmic respiratory activity of the in vitro neonatal rat brainstem-spinal cord preparation was functionally dependent on imidazole. Neural activity was recorded from spinal nerves (C1-C4) during superfusion with 95%O 2/5%CO 2 buffer at pH 7.3 and T=26°C. Superfusate containing DEPC (40 mM) caused cessation of rhythmic activity within minutes. In eight of 33 preparations, microinjection of DEPC (32 nmol) onto the ventral medullary surface (VMS) reduced burst amplitude by at least 50% within 10 min, and in 12 of 33 preparations, microinjection of DEPC produced neural apnea. Therefore, we conclude that proteins containing imidazole near the VMS are critically important for the maintenance of rhythmic respiratory activity in vitro. Furthermore, alphastat regulation of respiration may be an essential trait of this preparation.

Serotonergic inhibition of phrenic motoneuron activity: an in vitro study in neonatal rat

In vitro experiments were conducted on neonatal rat brainstem-spinal cord preparations to test the hypothesis of an inhibitory modulation of phrenic activity by serotonin (5-HT) via non-5-HT 2A receptors [Lindsay, A.D. and Feldman, J.L., Modulation of respiratory activity of neonatal rat phrenic motoneurones by serotonin, J. Physiol., 461 (1993) 213–233]. The changes induced by 5-HT and related agents on phrenic root discharges and membrane currents in identified phrenic motoneurons were analysed after blockade of spinal 5-HT 2A receptors. Spinal application of 5-HT 1B (but not 5-HT 1A) receptor agonists depressed the phrenic activity and the effect was prevented by pretreatment with 5-HT 1B (but not 5-HT 1A, 5-HT 2A and 5-HT 3) receptor antagonists. Results from phrenic motoneuron whole cell recordings do not reject a presynaptic location of the 5-HT receptors responsible for this depression.

Stimulation within the rostral ventrolateral medulla can evoke monosynaptic GABAergic IPSPs in sympathetic preganglionic neurons in vitro.

The inhibitory responses of identified sympathetic preganglionic neurons (SPNs) to stimulation within the rostral ventrolateral medulla (RVLM) were studied to determine their nature and pharmacology. Whole cell patch-clamp recordings were made from 36 SPNs in the upper thoracic segments of the spinal cord in a neonatal rat brain stem-spinal cord preparation. Neurons were identified as SPNs on the basis of their antidromic activation after stimulation of the ipsilateral segmental ventral root and their morphology and location in the intermediolateral cell column and intercalated nucleus. In all SPNs, electrical stimulation of the RVLM evoked fast excitatory postsynaptic potentials (EPSPs) that were mediated by non-N-methyl-D-aspartate (NMDA) and NMDA receptors. These excitatory responses were the most prominent response in control artificial cerebrospinal fluid and have been studied previously. In 22 of the SPNs, RVLM stimulation also elicited fast inhibitory postsynaptic potentials (IPSPs), which increased in amplitude as the membrane was depolarized. Five of these neurons were not studied further as they responded occasionally with IPSPs that had highly variable onset latencies indicating the involvement of a polysynaptic pathway. In the remaining SPNs (n = 17), the evoked IPSPs persisted in the presence of the excitatory amino acid antagonists 6-cyano-7-nitroquinoxaline-2,3,-dione and D,L-2-amino-5-phosphonopentanoic acid. In eight of these SPNs, it was necessary to block the EPSPs to reveal the IPSPs. In the 7 SPNs tested, the onset latencies of the IPSPs were not significantly different from the onset latencies of the fast EPSPs. The low sweep-to-sweep fluctuations in onset latency of individual IPSPs (absolute average deviation: 0.4 ms) indicated that the IPSPs were elicited by activation of a monosynaptic pathway. The amplitudes of the IPSPs decreased in amplitude as the membrane was hyperpolarized and reversed in polarity at -70.3 +/- 1.7 mV (mean +/- SD), which was close to the equilibrium potential for chloride ions. In addition, in seven SPNs, bath applications of 5 microM bicuculline, a gamma-aminobuturic acid-A (GABAA) antagonist, abolished or reduced the evoked IPSPs. Five SPNs also were studied that displayed ongoing IPSPs. The amplitudes of these IPSPs increased with membrane depolarization and were blocked by bath applications of 5 microM bicuculline, suggesting that they also were mediated by activation of GABAA receptors. These results demonstrate the existence of a bulbospinal GABAergic pathway impinging directly onto SPNs. This pathway may be tonically active in the neonatal rat brain stem-spinal cord preparation.

Effects of ethanol on respiratory activity in the neonatal rat brainstem-spinal cord preparation

Ethanol (1–12 mM) added to the superfusion medium of the isolated brainstem-spinal cords of newborn rats did not affect phrenic activity but significantly reduced hypoglossal activity by 54%, 67% and 55% at 3, 6 and 12 mM, respectively. Although the reasons for the suppression of hypoglossal activity remain unknown, this preparation may be a useful model for determining why cranial motoneurons are more vulnerable than phrenic motoneurons to various agents and, more generally, how ethanol impairs neural function.

Medullary‐evoked EPSPs in neonatal rat sympathetic preganglionic neurones in vitro.

1. Whole-cell patch clamp recordings were made from twenty-three sympathetic preganglionic neurones (SPNs) in the upper thoracic segments of a neonatal rat brainstem-spinal cord preparation to study their synaptic responses to stimulation of the rostral ventrolateral medulla (RVLM) and the receptors involved. 2. SPNs were identified by their antidromic activation following stimulation of a ventral root, their morphology and their location in the spinal cord. 3. Electrical stimulation within the RVLM elicited EPSPs in all SPNs tested (n = 23). These EPSPs consisted of one or more components that had different time courses, voltage relationships and pharmacological sensitivities. 4. All SPNs responded to RVLM stimulation with a constant-latency fast EPSP that increased in size as the membrane was hyperpolarized. This EPSP was reduced in amplitude by the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (10-20 microM). 5. In thirteen SPNs the response to RVLM stimulation was a complex EPSP consisting of a fast EPSP and a slow EPSP that either followed or summed with the fast EPSP. The amplitude of the slow EPSP was (i) either reduced in size or not affected as the membrane was hyperpolarized, and (ii) reduced by the NMDA receptor antagonist, D, L-2-amino-5-phosphonovaleric acid (50 microM). 6. Selective activation of neuronal cell bodies in the RVLM by chemical stimulation elicited slow depolarizations and increases in synaptic activity in SPNs. 7. These results provide evidence that an excitatory amino acid is involved in transmitting sympathoexcitatory drive from the RVLM, partly via a monosynaptic pathway. Both non-NMDA and NMDA receptors play a role in mediating this drive.

Opioid depression of respiration in neonatal rats.

1. The effects of opioid receptor agonists and antagonists on the breathing pattern of neonatal rats were studied. Three experimental approaches were taken. In the first approach, the effects of opioid agonists and antagonists on the spontaneous respiratory neural activity generated by brainstem-spinal cords isolated from neonatal rats aged 0-4 days postnatal (P0-4) maintained in vitro were studied. Secondly, similar studies were performed utilizing medullary slice preparations consisting of respiratory rhythm-generating regions (pre-Bötzinger complex). Thirdly, whole-body plethysmographic recordings were obtained from unanaesthetized neonatal (P0-18) rats before and after I.P. administration of opioid-receptor agonists and antagonists. 2. The mu-receptor agonists morphiceptin and DAGO (Tyr-D-Ala-Gly-[NMePhe]-Gly-ol), when added either to the solutions bathing the brainstems of neonatal rat brainstem-spinal cord preparations or bathing the medullary slice preparations, resulted in a naloxone-reversible, dose-dependent decrease in the frequency of respiratory rhythmic discharge. 3. The respiratory burst frequency and amplitude in vitro were unaffected by the addition of the delta-opioid receptor agonist DPDPE ([D-pen2,5]-enkephalin) and the kappa-opioid receptor agonist U50488 (trans-[+]-3,4-dichloro-N-methyl-N-(2-[1- pyrrolidinyl]cyclohexyl) benzene-acetamide) or the opioid receptor antagonist naloxone. 4. Intraperitoneal administration of the mu-opioid receptor agonist fentanyl resulted in a naloxone-reversible, dose-dependent decrease in the frequency and amplitude of breathing of unanaesthetized neonatal rats (P0-P10). I.P. administration of the delta-opioid receptor agonist DPDPE did not affect breathing of neonatal rats until the second week postnatally. 5. We conclude that opioids suppress the frequency of neonatal rat respiration by acting via mu-opioid receptors located within regions of the ventral medulla containing respiratory rhythm-generating centres (the pre-Bötzinger complex). delta-Opioid receptor activation does not affect breathing in neonatal rats until approximately the second week postnatally.

A study of sympathetic preganglionic neuronal activity in a neonatal rat brainstem-spinal cord preparation

Extracellular recordings were made from 46 sympathetic preganglionic neurones (SPNs) in a neonatal rat brainstem-spinal cord preparation. Neurones were identified as SPNs as they were: ( i) activated at constant latencies (2–10 ms) following stimulation of the ventral root, which indicated antidromic activation and ( ii) recorded at sites located either in the intermediolateral cell column or the intercalated nucleus of the thoracic spinal cord. Over one-third of the neurones ( n = 17) recorded displayed ongoing activity with firing frequencies of 0.3–5 Hz. Of the neurones analyzed only one showed a very obvious phasic firing pattern. Dorsal root stimulation evoked firing in 16 of 26 SPNs recorded from the same spinal segment (6 of 10 with ongoing activity). The types of responses observed varied between neurones. The excitation of all neurones was characterised by a response occurring at a latency of 6–50 ms. In addition, SPNs in ‘spinalised’ preparations ( n = 2) responded with latencies of 10–40 ms, similar to those observed in the intact preparation. The latencies of responses in SPNs were longer and more variable than those observed in ventral horn motor neurones. This indicates that a spinal polysynaptic pathway was involved in mediating these responses. In 7 SPNs dorsal root stimulation also elicited longer latency responses which were observed up to 1000 ms after stimulation. These responses may involve activation of bulbospinal and/or propriospinal pathways. These results show that the neonatal rat brainstem-spinal cord preparation is viable for studying SPNs and that dorsal root-SPN reflexes are intact.

Compared effects of serotonin on the inspiratory activity of glossopharyngeal, vagal, hypoglossal and cervical motoneurons in neonatal rat brain stem-spinal cord preparations

Experiments were performed on isolated brain stem-spinal cord preparations from neonatal rats, with a view to comparing the effects of serotonin (5-HT) on the rhythmic inspiratory activity recorded in the glossopharyngeal (IX), vagal (X), hypoglossal (XII) and cervical motor roots. Under normal medium, the inspiratory bursts recorded on the different roots presented slight changes in amplitude from one cycle to the other which were significantly correlated only between IX and X nerves. When the normal medium was replaced by a medium containing 5-HT (30 microM), the frequency of occurrence of the inspiratory bursts increased. After 6 min 5-HT superfusion, the inspiratory bursts observed in the IX, X and cervical recordings decreased slightly but significantly, whereas the XII inspiratory discharges decreased drastically. Upon returning to the control conditions, a total recovery was observed in all the recordings apart from the XII discharge, which remained depressed. Although 5-HT qualitatively depressed all the inspiratory motor outputs, the quantitatively drastic and long-lasting depression of the XII inspiratory activity was particularly noteworthy. 5-HT therefore seems to have specific effects on XII inspiratory activity which may be responsible for obstructive apnea in cases involving abnormal 5-HT biosynthesis mechanisms.

Quantal synaptic transmission in phrenic motor nucleus.

1. The quantal nature of excitatory synaptic transmission was studied in respiratory interneurons and phrenic motoneurons of intact neonatal rat brain stem-spinal cord preparations in vitro. Synaptic currents were recorded with whole-cell patch-clamp recording techniques. 2. Because the most important factor for quantal detection is the ratio of quantal size to quantal standard deviation, factors that influence this ratio were evaluated so that experimental techniques that enhance this ratio could be defined. 3. Under favorable conditions, we directly observed quantal amplitude fluctuations in spontaneous excitatory postsynaptic currents (EPSCs) in spinal cord respiratory neurons. The quantal conductance size was 55-100 pS. With fast decay of these EPSCs, the charge reaching the soma for a single quantum is only approximately 15 fC (Vh = -80 mV). 4. We also studied miniature EPSC amplitude distributions. These were skewed, as previously reported; however, distinct quantal intervals were observed. Furthermore, in three cells tested, the quantal size in the miniature EPSC amplitude distribution was similar to the quantal size in the spontaneous EPSC amplitude distribution. 5. We conclude that excitatory synaptic transmission in the mammalian spinal cord is quantal and that the apparent skewness of miniature EPSC distributions results from summation of events with multiple quantal peak amplitudes.

Whole-cell patch-clamp recordings from respiratory neurons in neonatal rat brainstem in vitro

Whole-cell recordings were obtained from respiratory neurons by applying patch-clamp techniques in the en bloc medulla of in vitro neonatal rat brainstem-spinal cord preparations. Stable voltage-clamp recordings of excitatory or inhibitory synaptic drive currents and current-clamp recordings of spike discharge of inspiratory and expiratory neurons could be maintained for periods of 1–2 h. Parameters of whole-cell recording, including membrane seal resistances and series resistances, obtained in the en bloc medulla were similar to those obtained in corresponding regions of thin slices where neurons were directly visualized to optimize conditions for whole-cell patch clamp.

Role of excitatory amino acids in the generation and transmission of respiratory drive in neonatal rat.

1. The involvement of excitatory amino acids in the generation and transmission of rhythmic respiratory drive was studied in an in vitro neonatal rat brain stem-spinal cord preparation. The subclasses of excitatory amino acid receptors studied included: (i) N-methyl-D-aspartate (NMDA) receptors, (ii) (R, S)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid hydrobromide (AMPA) and kainate (non-NMDA) receptors and (iii) 2-amino-4-phosphonobutyric acid (AP-4)-sensitive receptors. Respiratory motoneurone population discharge was recorded from glossopharyngeal (IX), vagus (X), and hypoglossal (XII) cranial nerves, as well as cervical (C1-C5) and thoracic (T2-T5) spinal ventral roots. This activity is generated in the motoneurone pools that transmit respiratory drive to upper airway, accessory, diaphragm and intercostal muscles. Perturbations of motor nerve discharge were analysed after excitatory amino acid receptor antagonists or agonists were added to bathing solutions surrounding either the spinal cord or brain stem. The excitatory amino acid receptor antagonists included: (i) NMDA receptor antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d] cyclohepten-5,10-imin-H-maleate (MK-801) and (ii) non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). The agonists included: (i) NMDA, (ii) non-NMDA receptor agonists AMPA and kainic acid. The effects of perturbations of AP-4-sensitive receptors with AP-4, and of inhibiting excitatory amino acid uptake with dihydrokainic acid (DHK) were also studied. 2. Block of non-NMDA receptors in the medulla by CNQX resulted in an antagonist concentration-dependent decrease in the respiratory motoneuronal burst frequency. Non-NMDA receptor activation with kainic acid or AMPA caused a concentration-dependent increase in burst frequency, with competitive interactions with CNQX. 3. Inhibition of excitatory amino acid uptake in the medulla with DHK resulted in a reversible, dose-dependent increase in respiratory frequency. A similar increase in respiratory frequency was induced by DHK when medullary NMDA receptors were blocked with MK-801, confirming that endogenously released excitatory amino acids act at non-NMDA receptors to modulate rhythm. 4. Non-NMDA receptor block reduced and ultimately abolished the amplitude of integrated cranial and spinal respiratory motoneuronal discharge when added to the solution bathing the medulla and spinal cord, respectively. 5. NMDA receptor block in the medulla with MK-801 did not perturb the spontaneous respiratory burst frequency, although bath application of NMDA produced a dose-dependent increase in frequency, with non-competitive interactions with MK-801. MK-801 also did not perturb the amplitude of cranial or bulbospinal premotoneurone discharge.(ABSTRACT TRUNCATED AT 400 WORDS)

Locomotion Induced by Spinal Cord Stimulation in the Neonate Rat In Vitro

The present studies employed the neonate rat brain stem-spinal cord preparation to determine whether electrical stimulation of the lumbosacral enlargement (LE) of the spinal cord itself can be used to elicit locomotion, and whether or not such stimulation persists in inducing locomotion following midthoracic spinal cord transection or hindlimb deafferentation. Results suggest that (1) stimulation of the dorsal columns or ventral funiculus of the LE is effective in inducing airstepping in the neonatal rat brain stem-spinal cord limb-attached preparation; (2) central disconnection by midthoracic spinal cord transection does not alter LE-stimulation-induced airstepping and may lead to an increase in stepping frequency if suprathreshold stimulation is used; and (3) dorsal root section also leads to an increase in the frequency of suprathreshold LE-stimulation-induced locomotion, but there is not further increase in frequency if a spinal cord transection is performed in addition to dorsal rhizotomy.

Neural mechanisms generating respiratory pattern in mammalian brain stem-spinal cord in vitro. I. Spatiotemporal patterns of motor and medullary neuron activity

1. An analysis of the spatial and temporal patterns of activity of neurons of the respiratory motor-pattern generation system in an in vitro neonatal rat brain stem-spinal cord preparation is presented. Impulse discharge patterns of spinal and cranial moto-neurons as well as respiratory neurons in the medulla were analyzed. Patterns of motoneuronal discharge were characterized at the population level from recordings of motor-nerve discharge and at the single-cell level from intracellular recordings. These patterns were compared to patterns generated in the neonatal rat and adult mammal in vivo to establish the correspondence between in vitro and in vivo states. 2. The in vitro system generated a complex spatiotemporal pattern of spinal and cranial motoneuron activity during inspiratory (I) and expiratory (E) phases of the respiratory cycle. The respiratory cycle consisted of three distinct phases of neuronal activity (I, early E, and late E phase) similar to the temporal organization of the cycle in the intact mammal. The spike discharge pattern of motoneurons during the I phase consisted of a rapidly peaking-slowly decrementing discharge envelope with a high degree of synchronization on a time scale of 25-50 ms (approximately 20-40 Hz). A similar pattern was generated in the neonate in vivo under conditions comparable with the in vitro state (i.e., nervous system isolated from mechanosensory afferent inputs). However, the I-phase-motoneuron discharge pattern and cycle-phase durations differed from those characteristic of the intact neonatal or adult systems in vivo. This difference could be accounted for primarily by removal of vagal mechanosensory afferent inputs. 3. The synaptic drive potentials of spinal motoneurons during the I phase in vitro consisted of a rapidly peaking-slowly decrementing potential envelope similar in shape to the spike-frequency histogram of single motoneurons and the envelope of the motoneuron-population discharge. The drive potentials had prominent high-frequency amplitude fluctuations superimposed on the slower drive-potential envelope that were temporally correlated with the generation of motoneuron action potentials. The dominant frequency components of these fast-membrane-potential oscillations (20-35 Hz) were similar to the frequency components of the amplitude fluctuations in the motoneuron-population discharge. One class of medullary neurons with I-phase discharge also exhibited a rapidly peaking-slowly decrementing pattern of impulse discharge and synaptic drive potential with similar high-frequency components.(ABSTRACT TRUNCATED AT 400 WORDS)

Intracellular recording from phrenic motoneurons receiving respiratory drive in vitro.

Stable, long-term (2-4 h) intracellular recordings were obtained from phrenic motoneurons receiving respiratory drive in an in vitro neonatal rat brainstem-spinal cord preparation. Several passive and active phrenic motoneuron properties in vitro, including resting membrane potential, inspiratory drive potentials, and threshold depolarization levels, are similar to those in the adult mammal in vivo. Manipulations of the extracellular fluid environment by the addition or washout of chemicals affecting motoneuronal activity and spinal synaptic transmission of respiratory drive did not affect the quality of the intracellular recordings. These results establish the feasibility of long-term intracellular recording from the in vitro brainstem-spinal cord preparation for studies of cellular and synaptic mechanisms underlying control of respiratory movements.

Analysis of background firing of single sympathetic preganglionic neurons of cat cervical nerve.

Analysis of background firing of single sympathetic preganglionic neurons of cat cervical nerve.A Mannard, and C PolosaA Mannard, and C PolosaPublished Online:01 May 1973https://doi.org/10.1152/jn.1973.36.3.398MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByFractal Activity Generated Independently by Medullary Sympathetic Premotor and Preganglionic Sympathetic NeuronsHakan S. Orer, Mahasweta Das, Susan M. Barman, and Gerard L. Gebber1 July 2003 | Journal of Neurophysiology, Vol. 90, No. 1Fractal Properties of Sympathetic Nerve DischargeMahasweta Das, Gerard L. Gebber, Susan M. Barman, and Craig D. Lewis1 February 2003 | Journal of Neurophysiology, Vol. 89, No. 2Rhythmic sympathetic nerve discharges in an in vitro neonatal rat brain stem-spinal cord preparationChun-Kuei Su1 September 1999 | Journal of Applied Physiology, Vol. 87, No. 3The role of tonic preganglionic neuron firing in the turnover of the large dense-cored vesicle store in sympathetic preganglionic nerve terminalsNeuroscience, Vol. 62, No. 2Interaction between medullary and cervical regulation of renal sympathetic activityBrain Research, Vol. 599, No. 2Naloxone-sensitive inhibition of nicotinic transmission in the superior cervical ganglion of the catBrain Research, Vol. 548, No. 1-2Sympathetic preganglionic neurones in neonatal rat spinal cord in vitro: electrophysiological characteristics and the effects of selective excitatory amino acid receptor agonistsBrain Research, Vol. 525, No. 2Organization of the tonically active pathways through the superior cervical ganglion of the rabbitJournal of the Autonomic Nervous System, Vol. 30Characteristics of the sympathetic preganglionic neuron and its synaptic inputProgress in Neurobiology, Vol. 31, No. 1Noradrenaline induces rhythmic bursting in sympathetic preganglionic neuronsBrain Research, Vol. 420, No. 1Discharge characteristics of sympathetic efferents to the knee joint of the catJournal of the Autonomic Nervous System, Vol. 19, No. 2Splenic, renal, and cardiac nerves have unequal dependence upon tonic supraspinal inputsBrain Research, Vol. 338, No. 1An intracellular study of the synaptic input to sympathetic preganglionic neurones of the third thoracic segment of the catJournal of the Autonomic Nervous System, Vol. 13, No. 3Mechanisms mediating the sympathetic silent period: Studies in the isolated spinal cord of the neonatal ratBrain Research, Vol. 329, No. 1-2Cardiovascular Instability Following Acute Cervical Spinal Cord TraumaCentral Nervous System Trauma, Vol. 2, No. 3Effects of 4-aminopyridine on sympathetic preganglionic neuron activityJournal of the Autonomic Nervous System, Vol. 11, No. 2Serotonergic excitation of sympathetic preganglionic neurons: a microiontophoretic studyBrain Research, Vol. 289, No. 1-2Sympathetic preganglionic neurons in the isolated spinal cord of the neonatal ratBrain Research, Vol. 269, No. 2What is the ongoing activity of sympathetic neurons?Journal of the Autonomic Nervous System, Vol. 7, No. 3-4Inhibition of the activity of sympathetic preganglionic neurones and neurones activated by visceral afferents, by alpha-methylnoradrenaline and endogenous catecholaminesNeuropharmacology, Vol. 22, No. 1Single-unit and multiunit analyses of renorenal reflexes elicited by stimulation of renal chemoreceptors in the ratJournal of the Autonomic Nervous System, Vol. 6, No. 2Parasympathetic preganglionic neurons in the sacral spinal cordJournal of the Autonomic Nervous System, Vol. 5, No. 1Temporal patterns of antidromic invasion latencies of sympathetic preganglionic neurons related to central inspiratory activity and pulmonary stretch receptor reflexBrain Research, Vol. 135, No. 1Effect of post-impulse depression on background firing of sympathetic preganglionic neuronsBrain Research, Vol. 126, No. 2The relation between end-tidal CO2 and discharge patterns of sympathetic preganglionic neuronsBrain Research, Vol. 122, No. 2The effect of the pattern of cardiac sympathetic activity on myocardial contractile force and norepinephrine overflow in the dog heart.Circulation Research, Vol. 39, No. 3Neuronal activity with relation to cardiac rhythm in the lower brain stem of the dogBrain Research, Vol. 106, No. 2The probabilistic behavior of central ‘vasomotor’ neuronsBrain Research, Vol. 96, No. 1Patterning of sympathetic preganglionic neuron firing by the central respiratory driveBrain Research, Vol. 87, No. 2-3A search for medullary neurons with activity patterns similar to those in sympathetic nervesBrain Research, Vol. 87, No. 2-3Central neural regulation of heart and blood vessels in mammalsProgress in Neurobiology, Vol. 5Reflex sympathetic firing in response to electrical stimulation of the carotid sinus nerve in the catBrain Research, Vol. 80, No. 1 More from this issue > Volume 36Issue 3May 1973Pages 398-408 https://doi.org/10.1152/jn.1973.36.3.398PubMed4349058History Published online 1 May 1973 Published in print 1 May 1973 Metrics

Periodicities in efferent discharge of splanchnic nerve of the cat.

Periodicities in efferent discharge of splanchnic nerve of the cat.