Electrophysiological properties of sympathetic preganglionic neurons in the cat spinal cord in vitro

1986 ◽  
Vol 406 (2) ◽  
pp. 91-98 ◽  
Author(s):  
M. Yoshimura ◽  
C. Polosa ◽  
S. Nishi
Keyword(s):  
Spinal Cord ◽  
Sympathetic Preganglionic Neurons ◽  
Electrophysiological Properties ◽  
Preganglionic Neurons

Stimulation Within the Rostral Ventrolateral Medulla Can Evoke Monosynaptic GABAergic IPSPs in Sympathetic Preganglionic Neurons In Vitro

1997 ◽  
Vol 77 (1) ◽  
pp. 229-235 ◽  
Author(s):  
Susan A. Deuchars ◽  
K. Michael Spyer ◽  
Michael P. Gilbey
Keyword(s):  
Spinal Cord ◽  
Brain Stem ◽  
Rostral Ventrolateral Medulla ◽  
Neonatal Rat ◽  
Ventrolateral Medulla ◽  
Sympathetic Preganglionic Neurons ◽  
Preganglionic Neurons ◽  
Neonatal Rat Brain ◽  
Stimulation Of

Deuchars, Susan A., K. Michael Spyer, and Michael P. Gilbey. Stimulation within the rostral ventrolateral medulla can evoke monosynaptic GABAergic IPSPs in sympathetic preganglionic neurons in vitro. J. Neurophysiol. 77: 229–235, 1997. 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 μM bicuculline, a γ-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 μM 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.

Orexins/hypocretins excite rat sympathetic preganglionic neurons in vivo and in vitro

2001 ◽  
Vol 281 (6) ◽  
pp. R1801-R1807 ◽  
Author(s):  
Vagner R. Antunes ◽  
G. Cristina Brailoiu ◽  
Ernest H. Kwok ◽  
Phouangmala Scruggs ◽  
Nae J. Dun
Keyword(s):  
Spinal Cord ◽  
Receptor Antagonist ◽  
Adrenergic Receptor ◽  
Intrathecal Injection ◽  
Sympathetic Outflow ◽  
Orexin A ◽  
Sympathetic Preganglionic Neurons ◽  
Preganglionic Neurons

The two recently isolated hypothalamic peptides orexin A and orexin B, also known as hypocretin 1 and 2, are reported to be important signaling molecules in feeding and sleep/wakefulness. Orexin-containing neurons in the lateral hypothalamus project to numerous areas of the rat brain and spinal cord including the intermediolateral cell column (IML) of the thoracolumbar spinal cord. An in vivo and in vitro study was undertaken to evaluate the hypothesis that orexins, acting on sympathetic preganglionic neurons (SPNs) in the rat spinal cord, increase sympathetic outflow. First, orexin A (0.3, 1, and 10 nmol) by intrathecal injection increased mean arterial pressure (MAP) and heart rate (HR) by an average of 5, 18, and 30 mmHg and 10, 42, and 85 beats/min in urethane-anesthetized rats. Intrathecal injection of saline had no significant effects. Orexin B (3 nmol) by intrathecal administration increased MAP and HR by an average of 11 mmHg and 40 beats/min. The pressor effects of orexin A were attenuated by prior intrathecal injection of orexin A antibodies (1:500 dilution) but not by normal serum albumin. Intravenous administration of the α1-adrenergic receptor antagonist prazosin (0.5 mg/kg) or the β-adrenergic receptor antagonist propranolol (0.5 mg/kg) markedly diminished, respectively, the orexin A-induced increase of MAP and HR. Second, whole cell patch recordings were made from antidromically identified SPNs of spinal cord slices from 12- to 16-day-old rats. Superfusion of orexin A or orexin B (100 or 300 nM) excited 12 of 17 SPNs, as evidenced by a membrane depolarization and/or increase of neuronal discharges. Orexin A- or B-induced depolarizations persisted in TTX (0.5 μM)-containing Krebs solution, indicating that the peptide acted directly on SPNs. Results from our in vivo and in vitro studies together with the previous observation of the presence of orexin A-immunoreactive fibers in the IML suggest that orexins, when released within the IML, augment sympathetic outflow by acting directly on SPNs.

APV-sensitive dorsal root afferent transmission to neonate rat sympathetic preganglionic neurons in vitro

1990 ◽  
Vol 64 (3) ◽  
pp. 991-999 ◽  
Author(s):  
E. Shen ◽  
N. Mo ◽  
N. J. Dun
Keyword(s):  
Receptor Antagonist ◽  
Dorsal Root ◽  
Resting Membrane Potential ◽  
Excitatory Postsynaptic Potential ◽  
Krebs Solution ◽  
Membrane Hyperpolarization ◽  
Sympathetic Preganglionic Neurons ◽  
Preganglionic Neurons ◽  
Stimulation Of

1. Intracellular recordings were made from antidromically identified sympathetic preganglionic neurons (SPNs) in transverse thoracolumbar spinal cord slices from neonate (12- to 22-day-old) rats. 2. Electrical stimulation of dorsal roots or dorsal root entry zone elicited in SPNs an excitatory postsynaptic potential (EPSP) or multiple EPSPs of varying latencies. The EPSP could be graded by varying the stimulus intensity and, on reaching the threshold, discharged an action potential. 3. The dorsal root-evoked EPSPs had a mean synaptic latency of 2.6 ms (range: 1.2-11 ms), suggesting a polysynaptic pathway. The EPSPs were characteristically slow in onset with a mean rise time and half-decay time of 8.3 and 23 ms, respectively. 4. At the resting membrane potential of -50 to -60 mV, the amplitude of EPSPs recorded in normal (1.3 mM Mg2+) Krebs solution was reduced by membrane hyperpolarization or depolarization. In Mg2(+)-free solution, EPSPs were potentiated and reached threshold for spike discharge. 5. The EPSPs were suppressed by the nonselective glutamate receptor antagonist kynurenic acid (0.1-0.5 mM) and by the N-methyl-D-aspartate (NMDA) receptor antagonists D-2-amino-5-phosphonovaleric acid (APV; 1-10 microM) and ketamine (5-10 microM), but not by the quisqualate (QA)/kainate (KA) receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX, 1-10 microM). The latter depressed the EPSPs elicited by stimulation of lateral funiculus in the same SPNs. 6. NMDA applied by pressure elicited a depolarization in the SPNs. In normal Krebs solution the response was voltage dependent with the peak amplitude occurring around -60 mV; conditioning depolarization or hyperpolarization diminished the response.(ABSTRACT TRUNCATED AT 250 WORDS)

Intracellular recording from sympathetic preganglionic neurons in cat lumbar spinal cord

1994 ◽  
Vol 656 (2) ◽  
pp. 319-328 ◽  
Author(s):  
Paul Pilowsky ◽  
Ida J. Llewellyn-Smith ◽  
Leonard Arnolda ◽  
Jane Minson ◽  
John Chalmers
Keyword(s):  
Spinal Cord ◽  
Intracellular Recording ◽  
Lumbar Spinal Cord ◽  
Sympathetic Preganglionic Neurons ◽  
Preganglionic Neurons ◽  
Lumbar Spinal

Noradrenaline-induced afterdepolarization in cat sympathetic preganglionic neurons in vitro

1987 ◽  
Vol 57 (5) ◽  
pp. 1314-1324 ◽  
Author(s):  
M. Yoshimura ◽  
C. Polosa ◽  
S. Nishi
Keyword(s):  
Action Potential ◽  
Slow Component ◽  
Membrane Conductance ◽  
Repetitive Firing ◽  
Ca Channel ◽  
Membrane Hyperpolarization ◽  
Sympathetic Preganglionic Neurons ◽  
Preganglionic Neurons ◽  
Repolarization Phase

Sympathetic preganglionic neurons of the intermediolateral nucleus were identified by antidromic stimulation in the slice of the T2 or T3 segment of the cat spinal cord. In normal Krebs solution, the action potential of these neurons had a shoulder on the repolarization phase and was followed by a long-lasting afterhyperpolarization (AHP). The AHP had a fast and a slow component. Superfusion of the slice with noradrenaline (NA), 10-50 microM, resulted in depression of the shoulder on the repolarization phase of the action potential, in the appearance of an afterdepolarization (ADP), which was absent in control conditions, and in depression of the slow component of the AHP. These effects were present whether the membrane potential of the sympathetic preganglionic neurons was decreased, increased, or not changed by NA. A typical ADP had time to peak of 50 ms and decay time of 200-500 ms; the amplitude was variable and large ADPs could be suprathreshold, causing repetitive firing. The amplitude and duration of the ADP increased with NA concentration. The appearance of the ADP seemed to be independent of the depressant effect of NA on the slow AHP. The ADP was associated with a decrease in neuron input resistance and was voltage dependent, being depressed in nonlinear fashion by membrane hyperpolarization. The ADP decreased in amplitude or disappeared within a range of membrane potentials from -70 to -90 mV. The ADP was reversibly suppressed by the Ca-channel blocker cobalt (2 mM), by low Ca Krebs (0.25 mM), and by iontophoretic injection of ethyleneglycol-bis(B-aminoethyl-ether)-N,N'-tetraacetic acid into the cell. Increasing Ca concentration from 2.5 to 10.0 mM had no effect. The ADP was unaffected by tetrodotoxin, at a concentration blocking the Na spike, but was suppressed in Na-free medium, even when the Ca spike was prolonged by tetraethylammonium 20 mM. Changes in external K concentration from 3.6 to 2.5 or 10.0 mM did not change the ADP. Increasing intracellular Cl concentration or decreasing extracellular Cl concentration had no effect on the ADP. It is concluded that the ADP, evoked by NA, is due to an increase in membrane conductance involving Na and Ca ions, possibly a Ca-activated Na conductance. The ADP provides a mechanism with which NA may modulate sympathetic preganglionic neuron responsiveness to excitatory synaptic inputs.

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