PubMed Health⌕ Search

Biomedical subjects

N Mo

Publications and source records attributed to N Mo.

12 recordsLinked to original sources
PubMed1990

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

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)

2-Amino-5-phosphonovalerate↗
PubMed1989

Calcitonin gene-related peptide evokes distinct types of excitatory response in guinea pig coeliac ganglion cells.

Pressure application of calcitonin gene-related peptide (CGRP) evoked in a population of guinea pig coeliac neurons 3 types of response: a fast, a slow and a biphasic depolarization. The responses were not appreciably affected in low Ca/high Mg or tetrodotoxin-containing Krebs solution. The fast depolarization was associated with a fall in membrane resistance; it was made larger on hyperpolarization and the estimated reversal potential was -24 mV. The fast response was reversibly blocked in a Na-free medium as well as by relatively high concentrations of d-tubocurarine (50-100 microM) but not by hexamethonium. The slow, CGRP-induced depolarization resistant to nicotinic and muscarinic antagonists, was associated with either a small increase or decrease of input resistance. Membrane hyperpolarization increased the slow response in the majority of coeliac neurons, with an estimated reversal potential of -44 mV. The biphasic depolarization displayed electrophysiological and pharmacological characteristics resembling the fast and slow responses. These results raise the possibility that CGRP acting via two distinct types of receptor elicits, respectively, a fast, Na-dependent excitatory response and a slow response, the mechanism of which remains to be established.

Action Potentials↗
PubMed1989

Inhibitory postsynaptic potentials in neonatal rat sympathetic preganglionic neurones in vitro.

1. Intracellular recordings were made from antidromically identified sympathetic preganglionic neurones (SPNs) in transverse sections of thoraco-lumbar spinal cord from neonatal (12-22 day) rats. 2. Two types of hyperpolarizing (inhibitory) postsynaptic potentials (IPSPs) were recorded in the SPNs. The first type, which we have termed unitary IPSPs, were small, discrete IPSPs that occurred spontaneously and also following chemical or electrical stimulation applied to the spinal cord slices. The second type IPSP was a hyperpolarizing response evoked by either dorsal or ventral root stimulation. 3. Spontaneously occurring unitary IPSPs had an amplitude of 1 to 5 mV, and reversal potential of -60 to -75 mV; they were reversibly abolished by low Ca2+, tetrodotoxin (TTX) or strychnine but not by bicuculline and picrotoxin. 4. Pressure application of N-methyl-D-aspartate (NMDA), an excitatory amino SPNs; these were abolished by either strychnine or by the NMDA receptor antagonist D-2-amino-5-phosphonovalerate. Furthermore, electrical stimulation of dorsal rootlets elicited in several SPNs the discharge of strychnine-sensitive unitary IPSPs. 5. Electrical stimulation applied to dorsal or ventral rootlets elicited in nineteen and eight SPNs, respectively, an IPSP of larger amplitude (5 to 15 mV). The IPSP exhibited a reversal potential of -60 to 75 mV; it was changed to a depolarizing response in a low [Cl-]o solution, but was not significantly affected in a low [K+]o. Strychnine but not bicuculline or picrotoxin reversibly blocked the IPSPs in nearly all the SPNs. Additionally, hexamethonium and d-tubocurarine antagonized the IPSPs evoked by ventral but not by dorsal root stimulations. 6. Our results suggest that unitary and evoked IPSPs recorded in SPNs are due primarily to an increase of Cl- conductance by glycine or a glycine-like substance, released from interneurones, that can be activated by NMDA. Furthermore, IPSPs evoked by ventral root stimulation appear to represent a disynaptic event whereby nicotinic activation of a glycine-releasing interneurone results in a release of the inhibitory transmitter; this is then analogous to the Renshaw cell circuitry of the spinal motoneurones.

Animals↗
PubMed1988

Calcitonin gene-related peptide evokes fast and slow depolarizing responses in guinea pig coeliac neurons.

Pressure application of calcitonin gene-related peptide (CGRP) evoked in a population of coeliac neurons three types of response: a fast, a slow and a biphasic depolarization consisting of the first two responses in sequence. The fast and slow depolarization exhibited distinct electrophysiological and pharmacological characteristics, suggesting that these two responses may be mediated by separate CGRP receptors. Moreover, our results show that CGRP is one of the few peptides known to date that cause a fast, sodium-sensitive depolarization.

Action Potentials↗
PubMed1988

In vitro effects of substance P on neonatal rat sympathetic preganglionic neurones.

1. Intracellular recordings were made from antidromically identified sympathetic preganglionic neurones (SPNs) in thin transverse neonatal rat thoracolumbar spinal cord slices. 2. Applied either by pressure ejection or superfusion, substance P (SP) caused a slow, monophasic depolarization in 60% of sympathetic preganglionic neurones; a biphasic response consisting of an initial hyperpolarization followed by a depolarization was observed in a few neurones. In addition, SP induced the occurrence of repetitive inhibitory postsynaptic potentials (IPSPs) in about 20% SPNs. 3. Low-Ca2+ or tetrodotoxin (TTX)-containing Krebs solution abolished the hyperpolarizing phase of the biphasic response and the small IPSPs, thereby augmenting the depolarizing response of SP. 4. SP-induced depolarizations were often associated with a moderate increase in membrane resistance. Generally, the response was made smaller on hyperpolarization and reversed at the membrane potential between -90 and -100 mV. These findings suggest that a reduction of membrane K+ conductance may underlie the depolarizing action of SP. 5. Subthreshold fast, excitatory postsynaptic potentials (EPSPs) evoked by stimulation of dorsal rootlets were consistently augmented during SP-induced depolarization, leading to cell discharge. 6. Focal stimulations elicited, in addition to a fast EPSP, a slow EPSP in about 40% of SPNs. The slow EPSP was often associated with an increased membrane resistance and became smaller on hyperpolarization. 7. In 15% of SPNs that generated a slow EPSP, the latter was reversibly abolished during SP-induced depolarization; the blockade persisted when the membrane potential was restored to the resting level by hyperpolarizing current. 8. It is concluded that SP is excitatory to SPNs and that its synaptic release may initiate a slow EPSP which serves to augment impulse transmission through SPNs. Further, it appears that inhibitory interneurones may also be sensitive to SP and their activation may provide a negative feed-back mechanism which can limit excessive excitation of SPNs by the peptide.

Action Potentials↗
PubMed1987

Excitatory postsynaptic potentials in neonatal rat sympathetic preganglionic neurons: possible mediation by NMDA receptors.

Excitatory postsynaptic potentials (EPSPs) evoked in antidromically identified sympathetic preganglionic neurons (SPNs) and membrane depolarizations induced by N-methyl-D-aspartate (NMDA) applied by pressure ejection were increased by removing Mg ions from the perfusing media and blocked by D-2-amino-5-phosphonovalerate (APV), DL-APV and ketamine. Further, the amplitude of EPSPs and NMDA-induced depolarizations were decreased and increased by membrane hyperpolarization in Krebs solution with and without Mg2+, respectively. These findings indicate that the excitatory amino acid receptor mediating the EPSPs in SPNs may be of the NMDA subtype.

Animals↗
PubMed1987

Is glycine an inhibitory transmitter in rat lateral horn cells?

Spontaneous inhibitory postsynaptic potentials (IPSPs) and evoked IPSPs were recorded from a portion of lateral horn cells situated in thin transverse thoracolumbar spinal cord slices removed from neonatal rats. The IPSPs were reduced by hyperpolarization and inverted at membrane potentials between -65 and -75 mV. Strychnine but not bicuculline reversibly eliminated the IPSPs. The hyperpolarizations elicited by exogenously applied glycine exhibited electrophysiological and pharmacological characteristics similar to that of IPSPs. The results are consistent with the suggestion that glycine mediates an IPSP in a population of lateral horn cells.

Animals↗
PubMed1986

Cholecystokinin octapeptide depolarizes guinea pig inferior mesenteric ganglion cells and facilitates nicotinic transmission.

Cholecystokinin octapeptide (CCK-8) applied either by superfusion (0.1-10 microM) or by pressure ejection elicited a slow depolarization in a portion of inferior mesenteric ganglion cells studied in vitro. The depolarization which persisted in a low Ca2+/high Mg2+ solution, or solution containing cholinergic antagonists, was often associated with a small to moderate increase in neuronal input resistance, and the response was reduced by conditioning hyperpolarization. Nicotinic excitatory postsynaptic potentials were consistently augmented during the course of CCK-8-induced depolarization. Our results, together with findings of the presence of CCK-immunoreactive fibers in the prevertebral ganglia, suggest that the peptide may serve to facilitate nicotinic transmission.

Animals↗
PubMed1986

Tubocurarine suppresses slow calcium-dependent after-hyperpolarization in guinea-pig inferior mesenteric ganglion cells.

Intracellular recordings were made from neurones of the isolated guinea-pig inferior mesenteric ganglia. Single-spike potentials evoked by either depolarizing current pulses applied through the recording micro-electrode or stimulation of the hypogastric nerves were followed by an after-hyperpolarization (a.h.). The spike a.h. in 40% of the neurones, referred to herein as type I, had a relatively short duration (less than 50 ms) and exhibited a monophasic decay with a mean time constant (tau) of 11.4 ms. In the remaining cells (type II), the spike was followed by a long a.h. (greater than 100 ms) having a double-exponential decay; the fast and slow components of the a.h. are termed a.h.f and a.h.s, respectively, and they had mean tau values of 11.4 and 74 ms, respectively. A.h.f and a.h.s of type II neurones were reduced by membrane hyperpolarization and reversed their polarities between -80 and -90 mV. The reversal potentials shifted in a manner closely predicted by the Nernst equation as external K+ concentration was increased. Superfusion of low-Ca2+ high-Mg2+ solution to type II neurones reduced the a.h.f and a.h.s by 32 and 82%, respectively, indicating that a.h.s is largely Ca2+-dependent. Application of (+)-tubocurarine (10-100 microM) reversibly suppressed the a.h.s without affecting a.h.f in a concentration-dependent manner. Following a short train of action potentials evoked from type II neurones, the post-tetanic hyperpolarization (p.t.h.) was similarly depressed by (+)-tubocurarine in a dose-dependent manner. (+)-tubocurarine did not significantly change the amplitude of Ca2+-dependent spike potentials evoked in neurones bathed in Na+-free high-Ca2+ plus tetraethylammonium (5-10 mM) solution. The results indicate that (+)-tubocurarine selectively suppresses a.h.s, a slow Ca2+-dependent a.h., the consequence of which is a facilitation of repetitive discharges of the cells.

Action Potentials↗
PubMed1985

Prostaglandin E1 inhibits calcium-dependent potentials in mammalian sympathetic neurons.

Prostaglandin E1 (PGE1, 10-500 nM) reversibly depressed 3 types of calcium-dependent potentials associated with the spike potential of rabbit superior cervical ganglion cells, namely, the spike after-hyperpolarization, the post-tetanic hyperpolarization, and the Ca2+ spike evoked in a Na+-free/high Ca2+ solution. The results suggest that PGE1 reduces Ca conductance and that this action may underlie its inhibitory action on transmitter release at adrenergic and cholinergic nerve terminals.

Action Potentials↗
PubMed1985

Facilitation and inhibition of nicotinic transmission by eserine in the sympathetic ganglia of the rabbit.

The effects of eserine on neurons and on ganglionic transmission of the isolated superior cervical ganglia of the rabbit were investigated by means of intracellular recording techniques. At the concentration of 10 microM or less, eserine reversibly increased the amplitude and duration of the fast excitatory postsynaptic potential (f-epsp) induced by preganglionic nerve stimulation and of the membrane depolarization evoked by iontophoretically-applied acetylcholine (ACh), but not carbachol. At the concentration of 50 microM or more, eserine consistently and reversibly depressed the fast excitatory postsynaptic potential as well as the depolarization induced by iontophoretic application of either ACh or carbachol. Furthermore, depolarization by ACh evoked in a low Ca/high Mg solution, which blocked the liberation of transmitter was similarly reduced by eserine in greater concentrations. The passive membrane properties of the sympathetic neurons were not significantly altered by eserine in the majority of neurons studied. The results indicate that the facilitatory action of eserine on ganglionic transmission may be explained by its anticholinesterase activity, whereas eserine-induced block of transmission appears to be related to a direct interaction between the compound and the postsynaptic ACh receptor-channel complex.

Acetylcholine↗