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Biomedical subjects

N Mo

Publications and source records attributed to N Mo.

18 recordsLinked to original sources
PubMed1998

Laser speckle photography to measure surface displacements on cortical bone--verification of an automated analysis system.

A non-contact strain measurement method that could be used in a physiological environment was adapted to determine accurately the mechanical properties of bone. The technique of laser speckle photography was applied to record in-plane surface displacements. An automated image analysis system, based on a Fast Fourier Transform algorithm, was developed for data acquisition and its accuracy and precision verified. It was established that the technique could be used at magnifications of up to 60x , providing an ultimate resolution of approximately 1 microm. Displacement measurements on cortical bone submerged in water were demonstrated, which is of great value in determining the true physiological properties of bone.

Biomechanical Phenomena↗
PubMed1997

Adrenoceptor agonists inhibit calcium-dependent potentials in rat stellate ganglion neurons.

AIM: To study the effects of adrenoceptor agonists on the stellate ganglion neurons. METHODS: Intracellular recordings were made from neurons of the isolated rat stellate ganglia. RESULTS: Noradrenaline and clonidine (10-30 mumol.L-1) reversibly depressed 3 types of calcium-dependent potentials, namely, the action potential shoulder; the spike after-hyperpolarization; the Ca2+ spike evoked in Krebs' solution containing TTX and TEA and fast excitatory postsynaptic potential (f-EPSP). CONCLUSION: The adrenoceptor agonists inhibitied the 3 calcium-dependent potentials; f-EPSP was inhibited by reducing Ca2+ influx at presynaptic site in population of neurons.

Action Potentials↗
PubMed1996

Cardiac neurones of autonomic ganglia.

The properties of the postganglionic sympathetic neurones supplying the heart and arising in the stellate and adjacent paravertebral ganglia of various species are discussed with respect to their location, morphology, synaptic input and membrane characteristics. Results from our laboratory on the morphology of rat stellate neurones projecting to the heart were obtained either by intracellular injection of hexammine cobaltic (III) chloride or by retrograde labelling of cells using cobalt-lysine complex. Intracellular recordings were made from cells using electrodes filled either with potassium chloride plus hexammine cobaltic chloride or potassium acetate. Neurones which projected axons into cardiac nerve branches arising from the stellate ganglion were termed putative cardiac neurones, because of the possibility that some supply pulmonary targets. Putative cardiac neurones had unbranched axons and were ovoid or polygonal in shape, but showed considerable variation in soma size and in the complexity of dendritic trees. The mean two-dimensional surface area was 463 microns2 and the mean number of primary dendrites was seven. Other studies have found that the morphology of rat stellate ganglion neurones is similar to that of superior cervical ganglion cells. However, in strains of rat displaying spontaneous hypertension, dendritic length may be increased. Histochemical studies do not, as yet, seem to have demonstrated a distinctive neurochemical profile for stellate cardiac neurones, but various types of peptide-containing intraganglionic nerve fibres have been identified in the guinea pig. In our electrophysiological studies, putative cardiac neurones were found to receive a complex presynaptic input arising from the caudal sympathetic trunk and from T1 and T2 thoracic rami. In addition, 16% of cardiac neurones received a synaptic input from the cardiac nerve. The properties of postganglionic parasympathetic neurones distributed in the cardiac plexus and termed intrinsic cardiac neurones are discussed, including the results of studies on cultures of these neurones.

Animals↗
PubMed1994

Properties of putative cardiac and non-cardiac neurones in the rat stellate ganglion.

Intracellular recordings were made from isolated left or right stellate ganglia of Wistar rats and the morphology of neurones studied after intracellular injection of hexammine cobaltic chloride or back-filling from the post-ganglionic nerve with cobalt lysine complex. The experiments attempted to identify the location, electrophysiological properties, morphology and chemosensitivity of putative cardiac neurones in the ganglion. These were identified by antidromic activation of the axon in a cardiac nerve and compared with neurones projecting towards the brachial plexus (non-cardiac neurones). Putative cardiac neurones were localized in the ganglion around the postganglionic nerve entry zone and showed considerable morphological diversity. They had complex dendritic trees with, on average, seven dendrites. They included both phasic and tonic neurones and were depolarized by muscarinic agonists, angiotensin and substance P; they invariably had a synaptic input from the sympathetic trunk and from a T1 or T2 ramus and, in 16% of cells, from a cardiac nerve. Non-cardiac neurones were more widely scattered through the stellate ganglion but were not clearly different in morphology, resting membrane potential or the proportion of phasic and tonic cells from putative cardiac neurones. They also showed depolarizing responses to muscarinic agonists, angiotensin and substance P. Angiotensin responses of stellate ganglion cells were blocked by the peptide antagonist, saralasin (1 microM).

Action Potentials↗
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↗
PubMed1984

Vasoactive intestinal polypeptide facilitates muscarinic transmission in mammalian sympathetic ganglia.

Vasoactive intestinal polypeptide (VIP) in the concentration of 1 microM or less markedly and selectively increased the amplitude and duration of the muscarinic slow excitatory postsynaptic potential (EPSP) without appreciably affecting the nicotinic fast EPSP or the non-cholinergic EPSP of guinea pig inferior mesenteric ganglion cells. The membrane depolarization evoked by the muscarinic agonist, acetyl-beta-methylcholine in these neurons was similarly enhanced by VIP. Our results suggest that the peptide may be a neuromodulator effective in enhancing the sensitivity of postsynaptic muscarinic receptors to acetylcholine in the vertebrate sympathetic ganglia.

Acetylcholine↗
PubMed1984

Long-term facilitation of peptidergic transmission by catecholamines in guinea-pig inferior mesenteric ganglia.

Intracellular recordings were obtained from neurones of isolated guinea-pig inferior mesenteric ganglia. Repetitive stimulation (10-20 Hz for 1-2 s) of the hypogastric nerves evoked, in addition to the fast excitatory post-synaptic potential (e.p.s.p.), a non-cholinergic e.p.s.p. the mediator of which has previously been suggested to be substance P or a related peptide. When applied to the ganglia in the concentrations of 1-100 microM for 3-5 min, adrenaline, isoprenaline and noradrenaline produced an initial, short-lasting depression which was followed by a marked augmentation of the non-cholinergic e.p.s.p. lasting from minutes to over hours. Employed in comparable concentrations dopamine caused a slight depression that was not followed by a detectable increase of the non-cholinergic e.p.s.p. The catecholamine-induced depression and subsequent enhancement of the non-cholinergic e.p.s.p. was prevented by alpha-adrenergic antagonists (dihydroergotamine and phenoxybenzamine, 1-10 microM) and beta-adrenergic antagonists (propranolol and dichlorisoprenaline, 5-10 microM), respectively. The membrane depolarization induced by the putative transmitter substance P (1 microM) was augmented by isoprenaline; the enhancement which could be blocked by beta-antagonists was not preceded by a depression. Application of dibutyryl cyclic AMP (10 microM-1 mM) by either superfusion or intracellular ionophoresis mimicked the enhancing effect of catecholamines. It is concluded that catecholamines, with the noticeable exception of dopamine, exerted a biphasic effect on the non-cholinergic e.p.s.p. of the inferior mesenteric ganglion cells: an initial depression that was mediated by alpha-adrenergic receptors and probably reflected a presynaptic inhibitory effect of catecholamines and, on the other hand, an enduring facilitation mediated by beta-adrenergic receptors which appeared to be linked to activation of post-ganglionic cyclic AMP.

Action Potentials↗