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PubMed1982

The actions of pentobarbitone, procaine and tetrodotoxin on synaptic transmission in the olfactory cortex of the guinea-pig.

1 It has been suggested that the depression of excitatory synaptic potentials produced by general anaesthetics can be attributed to a partial blockade of impulse conduction in the terminal branches of axons. This hypothesis has been tested by comparing the actions of pentobarbitone, procaine and tetrodotoxin (TTX) on synaptic transmission in the guinea-pig olfactory cortex. 2 Pentobarbitone (0.1-0.3mM) depressed the evoked synaptic potentials without any significant depression of impulse conduction in the afferent fibres of the lateral olfactory tract (1.o.t). It had no effect on the electrical excitability of either the l.o.t axons or the postsynaptic neurones. 3 Tetrodotoxin (TTX; 1-5x10(-8 M) slowed conduction of impulses in the l.o.t. and decreased the amplitude of the l.o.t compound action potential in proportion to the concentration applied. All concentrations of TTX elevated the electrical threshold of the l.o.t. axons and there was evidence to suggest that the threshold of the postsynaptic neurones was also elevated. The synaptic potentials were depressed in direct proportion to the depression of the l.o.t. compound action potential. 4 Procaine (0.1-0.5 mM) exhibited a pattern of activity intermediate between pentobarbitone and TTX. The most marked effect, seen at all concentrations tested, was a slowing of impulse conduction and a decrease in the electrical excitability of the l.o.t. axons. 5 It is concluded that general anaesthetics (exemplified by pentobarbitone) depress synaptic transmission by interfering with the processes involved in chemical transmission and not by blocking impulse conduction in the terminal branches of afferent nerves.

Animals↗
PubMed1983

Development of sensory-motor synapses in the spinal cord of the frog.

The development and specificity of monosynaptic sensory-motor synapses were studied in the brachial spinal cord of bullfrog tadpoles. Intracellular and extracellular recordings were made from motoneurones innervating several different muscles of the forelimb. Excitatory synaptic potentials (e.p.s.p.s) were elicited by stimulation of various peripheral muscle nerves. Sensory and motor axons in the triceps brachii muscle nerves were electrically excitable at stage XIII, the earliest stage studied. Their conduction velocities were 0.2-0.4 m/s. These velocities increased during subsequent development so that by stage XXII they were approximately 5 m/s. Before stage XVII, synaptic potentials evoked in motoneurones by stimulation of the triceps sensory fibres had a long central latency and fatigued easily. These potentials were probably mediated polysynaptically. At stage XVII, the first short-latency triceps synaptic potentials appeared. They had central latencies of less than 3 ms and represented the direct, monosynaptic input from muscle sensory cells on to motoneurones. During subsequent development the percentage of triceps motoneurones innervated by triceps sensory fibres increased, while the number of long-latency polysynaptic inputs decreased. Both the electrical and chemical components, characteristic of these monosynaptic e.p.s.p.s in adult frogs, were prominent from the time the e.p.s.p.s first appeared. The pattern of innervation of brachial motoneurones by triceps sensory afferents was specific from the beginning. Triceps sensory fibres innervated most triceps motoneurones but very few subscapular or pectoralis motoneurones, just as in adult frogs. At no time were there appreciable numbers of 'aberrant' connexions. The developmental time course of several different classes of sensory-motor connexions was similar. Thus the synaptic specificity of this system cannot be explained by a differential timing of synaptogenesis.

Animals↗
PubMed1990

Characterization of the neurons of the mouse hypogastric ganglion: morphology and electrophysiology.

The somata of mouse hypogastric ganglion cells injected with Lucifer yellow were ovoid in shape, lacked dendritic processes but gave rise to a single axonal process. Antidromic activation demonstrated that some of the cells contained in this ganglion innervated the vas deferens. The passive and active membrane properties of the ganglion cells were determined in current clamp experiments. Cells fired tetrodotoxin-sensitive action potentials in response to intracellularly-applied depolarizing current. In voltage clamp evidence was obtained for both a persistent inward calcium current at potentials between -30 and -40 mV and a transient calcium current evoked by step depolarizations to around -20 mV. In current clamp, however, cells did not fire calcium action potentials in the presence of tetrodotoxin. Three potassium currents, IM (blocked by 1 mM barium and by 30 microM bethanechol), IA (blocked by 2 mM 4-aminopyridine) and IK(Ca) fast (blocked by 100 microM cadmium and by 5 mM tetraethylammonium) were characterized in these neurons. In addition, IK(Ca) slow was observed in a small proportion of cells. Fast, all-or-nothing, excitatory synaptic potentials were recorded in response to single stimuli applied to the afferent fibres running to the ganglion. In most cells the excitatory synaptic potentials were suprathreshold for action potential initiation and were markedly reduced or abolished by 100 microM mecamylamine, 1 mM hexamethonium and following desensitization to 100 microM nicotine. Excitatory synaptic potentials arose from stimulation of a single presynaptic nerve process and are typical of strong synaptic inputs.

Action Potentials↗
PubMedDate not supplied

[Effect of Argiope lobata venom and its components on L[3H)glutamate binding with locust muscle membranes].

The Argiope lobata venom is shown to block synaptic potential at locust neuromuscular junctions and inhibit the high-affinity sodium independent L[3H]glutamate binding site in locust muscle membranes. The data obtained due to fractionation of venom evidence that it contains components which block synaptic potential and inhibit the binding of L[3H]glutamate (5 kDa and more) as well as components which block synaptic potential but do not inhibit the binding of L[3H]glutamate less than 5 kDa. These observations indicate that spider venom contains at least two components with different mechanism of action.

Animals↗
PubMed1974

Different properties of synapses between a single sensory neurone and two different motor cells in the leech C.N.S.

In leech ganglia, an individual sensory cell that responds specifically to noxious mechanical stimulation of the skin (N cell) excites two different motoneurones. One raises the annuli of the skin into ridges (the AE cell), while the other innervates logitudinal muscles and thereby shortens the body segment (L cell). A comparison has been made of the way in which these two synapses behave when their common presynaptic cell is stimulated in various conditions.1. Using previously described criteria, N sensory cells have been shown to make monosynaptic chemical connexions with both the AE and L motoneurones (Nicholls & Purves, 1972). Following a single stimulus, the excitatory synaptic potential recorded in the AE motoneurone was only about one tenth the size of that in the L cell (approximately 0.5 mV compared to 5 mV). Trains of impulses in the same N sensory cell gave rise to synaptic potentials in the AE and the L motoneurones that underwent phases of facilitation and depression; the facilitation, however, was characteristically greater and longer lasting at synapses upon the AE motoneurone.2. The differences between the two synapses were accentuated in Ringer fluid containing increased concentrations of Ca and also in the cold. Under both of these conditions repetitive firing by the N sensory cell could give rise to synaptic potentials in the AE motoneurone which progressively increased in amplitude, while those in the L motoneurone became smaller.3. The results suggest that the differences in synaptic transmission can be accounted for by variations in the amount of transmitter released at the presynaptic N cell terminals, rather than by differences in the post-synaptic cells. The animal's behaviour corresponds to expectations from the physiology of the synapses.

Action Potentials↗
PubMed1995

Synaptic interactions involving acetylcholine, glutamate, and GABA in rat auditory cortex.

Using electrophysiological techniques in the in vitro rat auditory cortex, we have examined how spontaneous acetylcholine (ACh) release modifies synaptic potentials mediated by glutamate and gamma-aminobutyric acid (GABA). Single stimulus pulses to lower layer VI elicited in layer III a four-component (A-D) extracellular field response involving synaptic potentials mediated by glutamate and GABA. The cholinesterases inhibitor eserine (10-20 microM) or the cholinergic agonist carbachol (25-50 microM) depressed by 10-50% the glutamatergic components A and C, and the GABAergic components B and D. Atropine reversed the depressive effects of eserine and carbachol. A novel finding was that the degree of depression of component A varied inversely with stimulus intensity. However, during partial pharmacological antagonism of GABAA receptors, depression of A varied directly, not inversely, with stimulus intensity. Normally, then, depression of A is offset by reduced GABAergic inhibition of A. We also tested for differential depression of responses mediated by N-methyl-D-aspartate (NMDA) versus non-NMDA glutamate receptors. Following physiological and pharmacological isolation of the responses, eserine depressed the non-NMDA, but not the NMDA, receptor-mediated potential. Since the isolated NMDA potential still could be depressed by carbachol, the data suggested that activation of NMDA receptors may reduce spontaneous ACh release. In support of this, preincubation of slices in NMDA (10-20 microM) largely prevented eserine's, but not carbachol's, depression of components A and B. These results permit three conclusions of relevance to cortical information processing: (1) spontaneous ACh release tonically depresses synaptic potentials mediated by glutamate and GABA; (2) ACh depresses responses to weak inputs to a greater degree than responses to strong inputs: (3) activation of NMDA receptors may "feedback" to reduce ACh release, a mechanism that could place regulation of local ACh release under glutamatergic afferent control.

Acetylcholine↗
PubMed2004

Suprathreshold excitation of frog tectal neurons by short spike trains of single retinal ganglion cell.

It has been established that coincident inputs from multiple presynaptic axons are required to achieve a suprathreshold level of excitation for the most of central neurons. The present study, however, was designed to determine whether a train of spikes of an individual retinal ganglion cell (that is, input from a single presynaptic axon) targeting a frog tectum layer F could evoke suprathreshold excitation of tectal neurons. The lungs of immobilized frog were artificially ventilated during experiments. An individual ganglion cell was electrically stimulated in the retina through a multi-channel electrode. Responses evoked in the tectum by the stimulation were recorded extracellularly from a terminal arborization of the retinotectal fiber using the carbon-fiber microelectrode. Negative and negative-positive spikes (referred to as first type population responses) and polyphasic spikes followed by excitatory synaptic potentials (referred to as second type population responses) were observed in the recordings of retinotectal activity. Usually, the population responses have ensued after the frequency facilitated first and/or second testing individual retinotectal synaptic potential and disappeared in a threshold manner with a reduction of retinotectal transmission by an application of kynurenic acid. These observations have suggested that the population responses were a consequence of a suprathreshold excitation of tectal neurons and, therefore, could serve as the sign for such an excitation. Recordings have also demonstrated that sources of the first type population responses (likely, the hillocks of axons or somas of postsynaptic neurons) lie deeper than the optic fiber layer F of the tectum, whereas sources of the second type population responses (likely, axon terminal arborizations of these postsynaptic neurons) are scattered throughout the optic fiber layers. The findings have suggested: 1) a short train of action potentials of an individual retinal ganglion cell (likely darkness, also known as 5th, detector) can excite tectal neurons to suprathreshold level; 2) tectal and perhaps, nucleus isthmi neurons that make up recurrent connection circuits to the optic fiber layers of the tectum are also activated; 3) a suprathreshold level for an individual retinotectal input is achieved primarily due to the frequency facilitation of synaptic potentials; and 4) an artificial ventilation of the lungs of immobilized frog favors the eliciting of a suprathreshold excitation of tectal neurons, demonstrating that the ventilation certainly improves the physiological condition of a frog.

Action Potentials↗
PubMed1982

Electrophysiological properties of neocortical neurons in vitro.

1. Intracellular recordings were obtained from neurons of the guinea pig sensorimotor cortical slice maintained in vitro. Under control recording conditions input resistances, time constants, and spiking characteristics of slice neurons were well within the ranges reported by other investigators for neocortical neurons in situ. However, resting potentials (mean of -75 mV) and spike amplitudes (mean of 93.5 mV) were 10-25 mV greater than has been observed in intact preparations. 2. Current-voltage relationships obtained under current clamp revealed a spectrum of membrane-rectifying properties at potentials that were subthreshold for spike generation. Ionic and pharmacologic analyses suggest that subthreshold membrane behavior is dominated by voltage-sensitive, very slowly inactivating conductances to K+ and Na+. 3. Action potentials were predominantly Na+ dependent under normal conditions but when outward K+ currents were reduced pharmacologically, it was possible, in most cells, to evoke a non-Na+-dependent, tetrodotoxin-(TTX) insensitive spike, which was followed by a prominent depolarizing after-potential. Both of these events were blocked by the Ca2+ current antagonists, Co2+ and Mn2+. 4. A small population of neurons generated intrinsic, all-or-none burst potentials when depolarized with current pulses or by synaptic activation. These cells were located at a narrow range of depths comprising layer IV and the more superficial parts of layer V. 5. Spontaneous excitatory synaptic potentials appeared in all neurons. Spontaneous inhibitory events were visible in only about 10% of the cells, and in those cases apparently reversed polarity at a level slightly positive to resting potential. Stimulation of the surface of the slice at low intensities evoked robust and usually concurrent excitatory and inhibitory synaptic potentials. Unitary inhibitory postsynaptic potentials (IPSPs) reversed at levels positive to rest. Stronger stimulation produced a labile, long-duration, hyperpolarizing IPSP with a reversal potential 15-20 mV negative to the resting level. 6. Neocortical neurons in vitro retain the basic membrane and synaptic properties ascribed to them in situ. However, the array of passive and active membrane behavior observed in the slice suggests that cortical neurons may be differentiated by specific functional properties as well as by their extensive morphological diversity.

Action Potentials↗
PubMed1994

Long-lasting potentiation and depression by novel isoproterenol and cholecystokinin 8-S interactions in the dentate gyrus.

In the in vitro hippocampal slice, novel interactions of a beta-adrenergic agonist (l-isoproterenol) and neuropeptide (cholecystokinin 8-S) differentially produce long-lasting modifications in the dentate gyrus. When co-applied, a low concentration of l-isoproterenol (50-75 nM) and cholecystokinin 8-S (1.0 microM) produce long-lasting depression of evoked action potentials (i.e., population spikes). In contrast, the same concentration of l-isoproterenol followed by a 30-min wash with artificial cerebrospinal fluid and application of cholecystokinin 8-S produces long-lasting potentiation of evoked action potentials. In neither condition are there corresponding modifications of excitatory post-synaptic potentials. These results indicate that l-isoproterenol and cholecystokinin 8-S temporally interact to differentially produce depression or potentiation of granule cell-activation In contrast to long-lasting modifications produced by continuous application of 1.0 microM l-iso-proterenol, in which both evoked action potentials and excitatory post-synaptic potentials are affected, the present novel paradigm may modify an extra-synaptic locus.

Animals↗
PubMed1986

Sustained membrane potential change of uropod motor neurons during the fictive abdominal posture movement in crayfish.

The occurrence of the uropod steering response as one of the equilibrium reflexes to body rolling in crayfish is significantly facilitated if the stimulus is given while the animal is performing the abdominal posture movement. This facilitation of the descending statocyst pathway by the abdominal posture system takes place between the uropod motor neurons and the statocyst interneurons, which directly project from the brain to the terminal abdominal ganglion where the motor neurons originate. To elucidate the synaptic mechanisms underlying the postural facilitation of the steering response, we analyzed in this study the activity of an identified set of uropod motor neurons during the fictive abdominal extension movement in the whole-animal preparation. Intracellular recordings from the dendritic branches of uropod motor neurons revealed that they were continuously excited during the fictive abdominal extension. The large fast motor neurons usually showed a sustained depolarization of the subthreshold magnitude. The small slow ones showed a suprathreshold sustained depolarization with spikes superimposed. Putative inhibitory motor neurons, on the other hand, showed a sustained hyperpolarization with their spontaneous spike discharge suppressed. The discrete synaptic potentials could hardly be distinguished and, instead, small fluctuations of the membrane potential were observed during the sustained depolarization of both the fast and slow motor neurons. Occasionally, large discrete synaptic potentials could be observed to be superimposed on the sustained depolarization. The occurring frequency of these synaptic potentials showed, however, no significant increase associated with the sustained depolarization. It hence seemed unlikely that these potentials were responsible for producing the sustained depolarization. Their amplitude during the sustained depolarization was smaller than that observed during the quiescent state. The sustained membrane potential change during the fictive abdominal movement was also observed in many neurons other than motor neurons, including local nonspiking interneurons and mechanosensory spiking interneurons. Both motor neurons and interneurons showed a decrease in their membrane resistance during the sustained membrane potential change. We concluded that the sustained depolarization of uropod motor neurons during the fictive abdominal extension was produced by the summation of small chemically transmitted postsynaptic potentials.(ABSTRACT TRUNCATED AT 400 WORDS)

Abdomen↗
PubMed2006

Distribution of synaptic field potentials induced by TTX-resistant skin and muscle afferents in rat spinal segments L4 and L5.

Previous results from our group and others showed that skin and muscle afferents are equipped with tetrodotoxin-resistant (TTX-r) channels. The great majority of the TTX-r fibres are unmyelinated (C or group IV) and are assumed to have nociceptive functions. Therefore, a block of the TTX-sensitive (TTX-s) fibres offers the possibility to study reactions of central nervous neurones to a purely nociceptive input. The present study compared spinal synaptic field potentials (SFPs) evoked by electrical stimulation of TTX-r afferent fibres from skin and muscle at various depths of the spinal segments L4 and L5 in the rat. Cutaneous input was produced by stimulation of the sural nerve (SU), input from muscle by stimulation of the gastrocnemius-soleus nerves (GS). To block the (non-nociceptive) TTX-s afferents, a pool containing TTX (concentration 1microM) was built around the dorsal roots L3-L6. As a measure of synaptic activity, the area of averaged SFPs was determined. After TTX application, the SFPs of fast conducting myelinated afferent fibres vanished completely. Simultaneously, the size of the potentials evoked by electrical stimulation of slowly conducting TTX-r skin and muscle afferents increased significantly. The field potentials of TTX-r GS afferents had a maximum in laminae IV-VI of the dorsal horn, whereas the SFPs induced by SU stimulation were more evenly distributed over all laminae. The results are a further indication that nociceptive input from skin and muscle is differently processed at the spinal level.

Animals↗
PubMed1988

M1 and M2 receptors mediate different effects on synaptically evoked potentials of the rat superior cervical ganglion.

The application of muscarine, carbachol or methylfurmethide to the rat superior cervical ganglion in vitro resulted in a complex mixture of effects as recorded from the internal carotid nerve using a greased-gap technique. In addition to the previously described depolarizing and hyperpolarizing responses, increases and decreases in the amplitudes of the synaptically evoked compound action potential and its related afterhyperpolarization were observed. The depolarization and the enhancing effects of the agonists were selectively antagonized by pirenzepine (0.3 microM) whereas the hyperpolarization and depressant effects were antagonized by gallamine (10 microM). Methylfurmethide only induced the pirenzepine-sensitive effects. It is concluded that M1 and M2 (cardiac-like) receptors exert different effects on the synaptically evoked potentials of this preparation.

Animals↗
PubMed1995

Intracellular recordings from intramural neurons in the guinea pig urinary bladder.

1. Intracellular recordings were made from intramural neurons in the urinary bladder of guinea pigs. 2. The neurons were located in two types of ganglia: those where the cells were densely packed and those where the neurons were loosely packed. Staining of the cells by intracellular injections of markers showed that the cells had between one to three long processes and several short dendrites. 3. The resting potential measured in 230 neurons was -55.20 +/- 0.67 (SE) mV, and the input resistance was 58.37 +/- 1.78 M omega. 4. Injection of depolarizing currents from the recording electrode evoked two types of firing patterns. In 86.2% of the neurons, depolarizing currents evoked a prolonged firing of action potentials (tonic cells). In the rest of the neurons, a depolarization elicited one to three action potentials only (phasic cells). In all the cells tested, the action potentials were reversibly blocked by tetrodotoxin (TTX; 1 microM). In the presence of TTX. Ca2+ spikes were observed in 50% of the cases. 5. Single action potentials were followed by fast hyperpolarizations having mean duration of 92.7 +/- 6.0 ms and amplitude of 13.3 +/- 1.0 mV. In 62.5% of the cells repetitive firing of action potentials was followed by delayed, slow hyperpolarizations (duration 3.8 +/- 0.5 s), which were diminished by the K+ channel blocker 4-aminopyridine and in Ca+2-free high-Mg2+ medium. These results indicate that the prolonged after-spike hyperpolarizations were due to opening of Ca(2+)-induced K+ channels. 6. Electrical stimulation of nerve fiber tracts evoked fast excitatory synaptic potentials that were blocked by the nicotinic receptor antagonist hexamethonium (0.2 mM). Exogenous acetylcholine elicited depolarizations that were also blocked by hexamethonium. Nerve stimulation at frequencies of 0.1 Hz or higher caused strong facilitation of the synaptic potentials. Stimulation at 10-20 Hz did not evoke slow synaptic potentials.

Acetylcholine↗
PubMed1993

Opioid actions at mu and delta receptors in the rat dentate gyrus in vitro.

Both mu and delta opioid receptors are abundant in the dentate gyrus of the hippocampus and proenkephalin-derived peptides are present in the perforant path fibers. Intracellular recordings were made from dentate granule cells in rat hippocampal slices; neurons were identified as granule cells by biocytin injection and subsequent histological examination. Opioids selective for either mu receptors ([D-Ala2,MePhe4,Gly5]enkephalin-ol) or delta receptors ([D-Pen2,5]enkephalin) and [Met5]enkephalin hyperpolarized most granule cells. The hyperpolarization by [Met5]enkephalin was potentiated by the enkephalinase and aminopeptidase inhibitors thiorphan and bestatin and blocked by antagonists selective for either mu receptors ([Cys2,Tyr3,Orn5,Pen7]somatostatinamide) or delta receptors (N,N-bisallyl-Tyr-(aminoisobutyrate)2-Phe-Leu-OH). Synaptic potentials mediated by gamma-aminobutyric acid (GABA) acting at GABAA receptors (blocked by bicuculline) or GABAB receptors (blocked by 2-hydroxysaclofen) were reduced by [Met5]enkephalin, [D-Ala2,MePhe4,Gly5]enkephalin-ol and [D-Pen2,5]enkephalin. Synaptic potentials mediated by excitatory amino acids (blocked by 6-cyano-7-nitroquinoxaline-2,3-dione and 2-amino-5-phosphonovaleric acid) were evoked by stimulation of the perforant path in the subiculum; opioids slightly reduced the amplitude of the initial peak and sometimes caused the appearance of one or more later components. It was concluded that the opioids selective for mu and delta receptors directly hyperpolarize granule cells and also inhibit GABAA and GABAB synaptic potentials.

Animals↗
PubMed1987

An intracellular study of spinocervical tract cell responses to natural stimuli and single hair afferent fibres in cats.

1. Intracellular recordings were made from spinocervical tract (s.c.t.) neurones in cats anaesthetized with chloralose and paralysed with gallamine triethiodide. 2. In one series of experiments the cells' receptive fields were examined with the use of natural stimuli. Hair movement within the impulse firing zone of the cell evoked excitatory post-synaptic potentials (e.p.s.p.s) from which impulses were generated; in addition, in the majority of s.c.t. cells tested, areas were found within the impulse firing zone where hair movement elicited both e.p.s.p.s and inhibitory post-synaptic potentials (i.p.s.p.s). Outside the firing zones, both regions evoking e.p.s.p.s and regions evoking i.p.s.p.s were observed in all neurones examined in detail (ten cells). The responses of these neurones to a variety of natural stimuli showed the receptive fields of s.c.t. cells to be more complex than previously thought. 3. In a second series of experiments, intracellular recordings from s.c.t. cells were combined with intracellular recording and stimulation of single dorsal root ganglion cells belonging to group II hair follicle afferent fibres. When the afferent fibres innervated skin within the impulse firing zone of the s.c.t. cell, single afferent impulses evoked e.p.s.p. complexes consisting of both mono- and polysynaptic components; no i.p.s.p.s were observed in response to single hair follicle afferent impulses or to trains. Although the monosynaptic e.p.s.p. component was often large and had a fast rise time, s.c.t. cell impulses usually arose from the later components. Afferent fibres innervating the central region of the s.c.t. cell firing zones tended to evoke relatively large e.p.s.p.s with fast rise times. The rise times and amplitudes of the e.p.s.p.s evoked by afferent fibres from the periphery, however, varied between afferent fibres but included the slowest and smallest in the total sample of synaptically coupled pairs. Afferent fibres from outside the s.c.t. cell's firing zone were usually ineffective in setting up post-synaptic potentials, but one group III hair follicle afferent fibre, from an inhibitory receptive field component, gave rise to i.p.s.p.s. 4. The effects of pairs and trains of afferent impulses at intervals of 10, 25, 50, 100 and 200 ms were examined. At 25 ms the response to the second afferent impulse was profoundly less than that evoked by the first and was still substantially reduced at 200 ms interval. In all synaptically coupled pairs studied, the e.p.s.p. complex evoked by the second afferent impulse was smaller in amplitude than that evoked by the first.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1977

Synaptic excitation and inhibition resulting from direct action of acetylcholine on two types of chemoreceptors on individual amphibian parasympathetic neurones.

1. Synaptic transmission was studied in visually identified parasympathetic ganglion cells that modulate the heart beat of the mudpuppy Necturus maculosus).2. The brief pulse of acetylcholine (ACh) released from terminals of the vagus nerve after each impulse can produce two distinct post-synaptic responses in individual principal cells of the ganglion: (i) within a milli-second of release, ACh generates a rapid and strong excitatory post-synaptic potential (e.p.s.p.) that normally initiates a post-synaptic impulse; (ii) this excitation is usually followed by a slow hyperpolarizing inhibitory post-synaptic potential (i.p.s.p.) that lasts for several seconds. The magnitude and time course of the i.p.s.p. depends on the frequency and number of vagal stimuli. When the hydrolysis of ACh is inhibited by prostigmine, a train of nerve stimuli may be followed by an i.p.s.p. lasting half a minute or longer.3. The rapid e.p.s.p. and slow i.p.s.p. result from the direct action of ACh on two different types of chemoreceptors in the post-synaptic membrane of the principal cell. The e.p.s.p. can be preferentially blocked by the nicotinic antagonist dihydro-beta-erythroidine (5 x 10(-7)M), while the i.p.s.p. is selectively blocked by the muscarinic antagonist atropine (5 x 10(-9)M).4. Potentials resembling nerve-evoked e.p.s.p.s and i.p.s.p.s can be produced by iontophoretic release of ACh from micropipettes onto the post-synaptic membrane. Application of the muscarinic agonist bethanechol generates exclusively inhibitory responses.5. The reversal potential for the i.p.s.p. is about -105 mV, which is approximately the equilibrium potential for potassium (E(K)). When the external K(+) concentration is altered, the reversal potential for inhibition is shifted to the new value of E(K) as expected from the Nernst equation. Changes in the external Na(+) and Cl(-) concentrations have no appreciable effect on the reversal potential. Thus, the i.p.s.p. is the result of a conductance increase for K(+).6. The conductance change producing the i.p.s.p. is voltage sensitive. When the membrane potential is shifted from -40 to -60 mV, the i.p.s.p becomes larger and longer. Beyond -60 mV the inhibitory response decreases in proportion to the driving force on K(+) without any further change in time course.7. The inhibitory response produced by an iontophoretically applied pulse of bethanechol has a delayed onset of about 150 msec at 24 degrees C. The early portion of this response, including the delay, is proportional to t(3), where t is time. The proportionality factor (the apparent rate constant) decreases elevenfold when the temperature is lowered by 10 degrees C. This suggests that a multi-step process is involved in the activation of the conductance increase that leads to the inhibitory response. Inhibitory responses with similar kinetics were produced in heart muscles of the mudpuppy upon application of ACh.

Acetylcholine↗
PubMed1982

The effect of lesions in the neural crest on the formation of synaptic connexions in the embryonic chick spinal cord.

1. The pattern of synaptic activity in lateral gastrocnemius (l.g.) motoneurones in the lumbar spinal cord of chick embryos (Stage 44-45, 19-21 d of incubation) has been examined using intracellular recording. In the motoneurones of normal chick embryos, stimulation of different peripheral, sciatic nerve branches gave rise to characteristic synaptic responses. Stimulation of the lateral gastrocnemius nerve caused a monosynaptic e.p.s.p. which was graded by the intensity of nerve stimulation. Stimulation of synergistic muscle afferents also caused a brief latency e.p.s.p., followed by longer latency excitatory and inhibitory synaptic potentials. Stimulation of antagonistic muscle afferents or cutaneous afferents gave rise to longer latency inhibitory and excitatory synaptic potentials respectively.2. The synaptic activity of l.g. motoneurones was also recorded in embryos in which short segments of the lumbar neural crest had been destroyed by microcautery at 3 d of incubation (Stage 18). The embryos developed without sensory ganglia and dorsal roots in the corresponding region.3. At 19-21 d of incubation, the amplitude of the l.g. e.p.s.p. of l.g. motoneurones in deafferented segments was on the average only a half to a third of the amplitude seen in motoneurones of intact spinal segments. However, both the l.g. and synergist e.p.s.p.s were larger than those seen in acutely deafferented segments of normal embryos.4. In spite of the weak monosynaptic input from l.g. and synergistic afferents, the pattern of synaptic activity evoked by antagonistic muscle afferent or cutaneous afferent stimulation was not different from normal. This was even the case for gastrocnemius motoneurones in which no early e.p.s.p. could be evoked by stimulating the l.g. or synergistic muscle nerves.5. No muscle spindles could be seen in sections of l.g. muscles from embryos with extensive lesions of the lumbosacral neural crest. Incomplete lesions of l.g. segments reduced the number of spindles in the muscle.6. These results suggest that when motoneurones are deprived of part of their normal synaptic input before the formation of peripheral connexions, the identity of the motoneurones (in terms of the origin of their synaptic input) is preserved. Missing synaptic inputs are either replaced by appropriate afferent fibres, if they are available, or not at all. The chick sensory ganglion cells with monosynaptic connexions to motoneurones appear to be unable to compensate significantly for peripheral or central defects in the innervation of the hind limb. They behave as if their developmental possibilities were quite rigidly determined at an early embryonic stage.

Animals↗
PubMed2001

An endogenous adrenoceptor ligand potentiates excitatory synaptic transmission in cultured hippocampal neurons.

Noradrenergic inputs modulate hippocampal function via distinct receptors. In hippocampal neuronal cultures, mRNA expression of adrenoceptor subtypes is maintained from 1 day in vitro (DIV) to 22 DIV. Noradrenaline dose-dependently stimulates phosphoinositide (PI) breakdown in both immature and mature cultures through the activation of alpha1 receptors. At 22 DIV, basal PI breakdown depends on excitatory synaptic activity since it is decreased by tetrodotoxin or glutamate receptor antagonists. At 22 DIV, a similar decrease of basal PI breakdown is also observed with alpha1, alpha2 or beta adrenoceptor antagonists. These effects are not additive with that produced by tetrodotoxin. Adrenergic antagonists also strongly reduce spontaneous excitatory post-synaptic currents (sEPSC) as evidenced by whole cell recording. Therefore, in hippocampal cultures, excitatory transmission is modulated by a tonic activation of adrenoceptors probably produced by an endogenous ligand. Indeed, (i) the depletion of catecholamine pools by reserpine also decreases both basal PI metabolism and sEPSC; (ii) hippocampal neurons possess both tyrosine hydroxylase (TH) and dopamine-beta-hydroxylase mRNAs, encoding enzymes required for catecholamine synthesis; and (iii) some hippocampal neurons show TH-immunoreactivity. TH-positive cells are also detected in E18 hippocampal sections. Thus, cultured hippocampal neurons synthesize and release an adrenergic-like ligand, which tonically potentiates excitatory synaptic transmission in mature cultures.

Adrenergic Uptake Inhibitors↗