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PubMedDate not supplied

Perspectives on physiological monitoring: junctional-type potentials in the food ventricle.

1. Many toads monitored throughout survival with no support other than protection against drying, pass terminally through a remarkable evolution which is described here in the full details of a single experiment lasting some 40 hours. 2. The essential features of this particular sequence is block of the Luciani-Wenckebach type affecting SA, AV, and intraventricular conduction. SA block was apparently the major cause of periods of arrest and of cycles of heart beats. Periodically PR delay based on progressive AV block was observed but it was not an outstanding feature. 3. Progressive, rate-determined intraventricular block during the cycles of ventricular beats was the first new feature of these observations. 4. As intraventricular block progressed, an initial ventricular deflection separated itself from the rest of QRS. 5. This initial deflection diminished in amplitude throughout each cycle of ventricular beats, its rate of rise diminished, and the interval separating it from the rest of the ventricular complex increased until the whole initial deflection was revealed. 6. Thereafter, with a small decrease in amplitude of the initial deflection, the remainder of the ventricular electrogram failed to follow and the complex stood alone. 7. Its polarity indicated its origin at the base of the ventricle, the interval separating it from the origin of P indicated that it was downstream from the AV conduction mechanism. 8. This deflection, now a local ventricular potential (LVP) then progressively declined in amplitude and disappeared. 9. The possibility has been discussed that the potential represents (a) a true action potential localized by block or (b) a local, nonpropagated potential akin to junctional potentials like: (1) end-plate potentials, (2) generator potentials, (3) excitatory postsynaptic potentials (EPSPs), or (c) a pacemaker potential. The experiments that have revealed the phenomenon have not provided other than suggestive but inconclusive information about its nature. 10. The observations are new or certainly not well known and further study should shed light on the problem of intracardial impulse formation and conduction.

Animals↗

PubMed1994

Synaptic potentiation and depression in slices of mediorostral neostriatum-hyperstriatum complex, an auditory imprinting-relevant area in chick forebrain.

Long-term potentiation, a tetanic stimulation-evoked, persistent increase in synaptic efficiency, is the most extensively studied form of synaptic plasticity. Intracellular correlates of long-term potentiation have been analysed in mammalian hippocampus and cortex, but not in bird cortical analogues. We present here studies on long-term potentiation in slices of the chick forebrain area mediorostral neostriatum-hyperstriatum complex which receives thalamic afferents and is relevant for auditory filial imprinting. Following afferent tetanic stimulation, population spike potentiation was extracellularly recorded in 25% of the tested neurons for longer than 40 min. Using intracellular recordings, the membrane potential, the amplitude of excitatory postsynaptic potentials, the latency between the test stimulus and the evoked action potentials, and the cellular excitability (excitatory postsynaptic potential-spike relationship) were found to change after the tetanus. A long-term depression following the tetanus was also seen in some units in this area. Furthermore, the mechanisms underlying long-term potentiation were investigated. A large depolarization of resting membrane potential (approx. 36 mV) was characteristic after the tetanic stimulation. N-methyl-D-aspartate receptor channels are necessary for induction of this depolarization, as well as for long-term potentiation, as demonstrated by the effect of DL-2-amino-5-phosphonovaleric acid. After intracellular recordings, the cells were injected with Lucifer Yellow. The combination of electrophysiological characterization and morphological identification suggested that the potentiation came chiefly from type I neurons, which have the largest soma among the neuron types in this area and up to eight dendrites. The results demonstrate that the recognized major phenomena of long-term potentiation are found in an auditory imprinting-relevant area of the chick forebrain, and that this potentiation is dependent on N-methyl-D-aspartate receptor channels. It is noteworthy that behavioural imprinting was previously shown to induce a reduction of up to 47% of the spine frequency of type I neurons and a growth of the remaining spine synapses, all resembling a synaptic selection process. Therefore, the intriguing possibility emerges that mechanisms underlying long-term potentiation are instrumental for this selection process, which involves regressive and proliferative morphological changes.

Acoustic Stimulation↗

PubMed1986

Amino acid receptor-mediated transmission at primary afferent synapses in rat spinal cord.

Intracellular recording techniques have been used to provide information on the identity of excitatory transmitters released at synapses formed between dorsal root ganglion (DRG) and spinal cord neurones in two in vitro preparations. Explants of embryonic rat DRG were added to dissociated cultures of embryonic dorsal horn neurones and synaptic potentials recorded intracellularly from dorsal horn neurones after DRG explant stimulation. More than 80% of dorsal horn neurones received at least one fast, DRG-evoked, monosynaptic input. In the presence of high divalent cation concentrations (5 mmol l-1 Ca2+, 3 mmol l-1 Mg2+) the acidic amino acid receptor agonists, L-glutamate, kainate (KA) and quisqualate (QUIS) excited all dorsal horn neurones which received a monosynaptic DRG neurone input, whereas L-aspartate and N-methyl-D-aspartate (NMDA) had little or no action. 2-Amino-5-phosphonovalerate (APV), a selective NMDA receptor antagonist, was relatively ineffective at antagonizing DRG-evoked synaptic potentials and L-glutamate-evoked responses. In contrast, kynurenate was found to be a potent antagonist of amino acid-evoked responses and of synaptic transmission at all DRG-dorsal horn synapses examined. The blockade of synaptic transmission by kynurenate appeared to result from a postsynaptic action on dorsal horn neurones. Intracellular recordings from motoneurones in new-born rat spinal cord were used to study the sensitivity of the Ia excitatory postsynaptic potential (EPSP) to antagonists of excitatory amino acids. Superfusion of the spinal cord with APV did not inhibit the Ia EPSP but did suppress later, polysynaptic components of the afferent-evoked response. Kynurenate was a potent and selective inhibitor of the Ia EPSP, acting via a postsynaptic mechanism. These findings indicate that L-glutamate, or a glutamate-like compound, but not L-aspartate, is likely to be the predominant excitatory transmitter that mediates fast excitatory postsynaptic potentials at primary afferent synapses with both dorsal horn neurones and motoneurones.

Afferent Pathways↗

PubMed1993

The impaired long-term potentiation in the CA1 field of the hippocampus of cognitive deficient microencephalic rats is restored by D-serine.

Rat embryos exposed on gestational day 15 to methyl-azoxymethanol acetate develop a microencephaly characterized primarily by a hypoplasia of the neocortex and CA fields of the hippocampus that in adulthood is associated with disturbances in learning. In brain slices prepared from microencephalic rats, we have examined the field excitatory postsynaptic potentials and population spike in the CA1 field of the hippocampus evoked by stimulation of the stratum radiatum. These parameters did not differ from those obtained in slices from control rats. High frequency stimulation of the stratum radiatum afferent fibres, which readily induced long-term potentiation of the field excitatory postsynaptic potentials and population spike in the CA1 field of the hippocampus of control rats, failed to induce long-term potentiation in that of microencephalic rats. High frequency stimulation of the perforant path readily elicited long-term potentiation in the dentate gyrus of both control and microencephalic rats. Picrotoxin had no apparent effect on field excitatory postsynaptic potentials and population spike in the CA1 field of the microencephalic rats, indicating that little GABAergic inhibition was present in slices from these rats. D-2-Amino-phosphonovalerate suppressed the field potentials in slices from microencephalic rats by more than 50%, suggesting that N-methyl-D-aspartate receptors contributed markedly to the synaptic responses evoked by single stimuli. D-Serine, but not picrotoxin, restored long-term potentiation in the CA1 field of the microencephalic rats. The D-serine effect was prevented by pretreating the slices with either 7-chloro-kynurenate or D-2-amino-phosphonovalerate. The failure to induce long-term potentiation, if also found in vivo, may be among the factors related to the learning deficits displayed by these rats.

2-Amino-5-phosphonovalerate↗

PubMed1975

Molecular model of postsynaptic potential.

A molecular model of the excitatory postsynaptic membrane is given in terms of two biochemical cycles intimately associated: an acetylcholine cycle and a calcium cycle. The acetylcholine controls the Na ionophores while calcium ions control the tk ionophore. The two ionophores are spatially separated but interact in such a way that the variation in K conductance precedes that in Na conductance. Digital simulation shows that our model accounts quantitatively for both the evolution of excitatory postsynaptic potential and current in a variety of experimental conditions.

Acetylcholine↗

PubMed1986

Associative induction of posttetanic and long-term potentiation in CA1 neurons of rat hippocampus.

Electrical stimulation of fibers in the stratum radiatum causes an excitatory postsynaptic potential in CA1 neurons of the hippocampus. Other excitatory inputs to or direct depolarization of these CA1 neurons during stimulation of the stratum radiatum caused a subsequent increase in the excitatory postsynaptic potential. This enhancement was characterized as a brief potentiation (2 to 3 minutes, similar to posttetanic potentiation) and a long-term potentiation (presumed to be involved in learning and memory). These potentiations are probably induced by an interaction of the postsynaptic cell or other presynaptic terminals with the test presynaptic terminals.

Action Potentials↗

PubMed1983

Mechanisms regulating the activity of facial nucleus motoneurones--2. Synaptic activation from the caudal trigeminal nucleus.

Field and postsynaptic potentials of facial motoneurones evoked by stimulation of the caudal trigeminal nucleus were studied in cats by means of extra- and intracellular recording. Mono- and polysynaptic input onto facial motoneurones from the caudal trigeminal nucleus were shown. Four types of responses were distinguished: excitatory postsynaptic potentials generating a single action potential; a gradual shift of depolarization inducing multiple discharges; a rhythmic discharge of action potentials appearing at a low level of depolarization; excitatory postsynaptic potentials or a sequence of excitatory and inhibitory postsynaptic potentials. Multiple discharge was shown to appear as a result of effective summation of high frequency excitatory influences from efferent neurones of the caudal trigeminal nucleus projecting into the facial nucleus. Factors facilitating the development of gradual depolarization are: dendritic localization of synaptic terminals, dendritic origin of after-depolarizing processes and the high input resistance of the facial motoneurone membrane. It is thought that specific features of facial motoneurones and properties of afferent inputs are supposed to provide high sensitivity of neuronal organization of the facial nucleus to afferent signals as well as wide diversity in controlling its activity.

Animals↗

PubMed1995

Increases in non-N-methyl-D-aspartate glutamatergic transmission, but no change in gamma-aminobutyric acidB transmission, in CA1 neurons during withdrawal from in vivo chronic ethanol treatment.

Evoked fast excitatory postsynaptic potentials and slow inhibitory postsynaptic potentials were measured in mouse CA1 neurons in hippocampal slices after chronic ethanol treatment in vivo. Intracellular recordings were made 2, 4 and 6 hr after ethanol withdrawal, i.e., after the beginning of slice preparation. The resting membrane potentials were standardized to -60 mV by using constant current injection. The fast excitatory postsynaptic potentials were isolated by adding DL-2-amino-5-phosphonopentanoic acid, bicuculline and nitrendipine to the bathing solution and injecting QX-314 into the recording cell; stimulation then evoked a monophasic depolarization with a maximum of 16.3 mV at about 30 msec after stimulation, which was inhibited by 6-cyano-7-nitroquinozaline-2,3-dione. At 4 and 6 hr after withdrawal, but not at 2 hr, the estimated fast excitatory postsynaptic potential conductance in slices from ethanol-treated mice was significantly larger than in those from control animals. There were no changes in stimulus/response relation or voltage-dependency of the depolarization. In the presence of these blocking agents, the thresholds for elicitation of field potentials was decreased at 6 hr from withdrawal. The slow inhibitory postsynaptic potentials were isolated by adding DL-2-amino-5-phosphonopentanoic acid, 6-cyano-7-nitroquinozaline- 2,3-dione and bicuculline to the bathing solution; stimulation of the Schaffer collateral fibers then evoked a monophasic hyperpolarization with a maximum of 5.7 mV at about 180 msec after stimulation, which was inhibited by the gamma-aminobutyric acidB antagonist saclofen. At the three time points, the stimulus/response relation, voltage dependency of the hyperpolarization and estimated slow inhibitory postsynaptic conductance in ethanol-treated mice did not differ from control animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

Somatic and dendritic actions of gamma-aminobutyric acid agonists and uptake blockers in the hippocampus in vivo.

In rats under urethane anaesthesia gamma-aminobutyric acid agonists and uptake blockers were microiontophoretically applied in the pyramidal layer of CA1 and in the apical dendrites using a twin set of multibarrelled micropipettes. Thus, the somatic and dendritic field potentials elicited by commissural stimulation were recorded simultaneously and the effects of iontophoretic applications at either site studied. Somatic applications of gamma-aminobutyric acid, isoguvacine or muscimol produced an inhibition of the somatic population spike; this showed rapid fade and was followed by an "off" response i.e. an enhancement of the population spike discharge and the occurrence of a second (and occasionally third) spike. The order of potency with regard to the "off" response was muscimol greater than isoguvacine much greater than gamma-aminobutyric acid. In contrast, the inhibition of the population spike produced by 4,5,6,7-tetrahydroisoxazolo(5,4-C) pyridin 3-OL showed little fade and no prominent "off" response. The fade and "off" response were not associated with significant changes in the dendritic field excitatory postsynaptic potential concommittantly recorded and were exclusively restricted to the immediate vicinity of the pyramidal layer. Ejection of gamma-aminobutyric acid and its agonists in the stratum radiatum produced a reduction of the field excitatory postsynaptic potential and the somatic spike, this effect however showed no fade (even during prolonged applications of high doses) and no "off" response. Somatic applications of the uptake blockers nipecotic acid or guvacine consistently produced: an increase in the effectiveness of the inhibition produced by gamma-aminobutyric acid and its analogues: a decrease in the latency to peak of the inhibition and an increase in the time to recovery; a full blockade of the fade and the "off" response. All of these effects were rapid and fully reversible without significant changes in either the field excitatory postsynaptic potential or the (control) somatic spikes. The more specific glial uptake blocker, 4,5,6,7-tetrahydroisoxazolo(4,5-C) pyridin 3-OL occasionally blocked the "off" response, however it was less potent and also tended to reduce the spike amplitude. Dendritic applications of the uptake blockers reduced the excitatory postsynaptic potential and the somatic spike but failed to produce prominent changes in the action of gamma-aminobutyric acid and its analogues.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗

PubMed1992

Alterations in the properties of hippocampal pyramidal neurons in the aged rat.

The electrophysiological and pharmacological properties of CA1 hippocampal pyramidal neurons were studied in slices from young (three to four months) and aged (25-32 months) Sprague-Dawley rats having previously performed two behavioral tasks. About 20% of the aged rats were impaired in either the spontaneous alternation task or the water maze task. Electrophysiological parameters were measured and compared in young and aged animals using intracellular recordings. No age-related differences were observed in membrane potential, input resistance, amplitude of action potentials or amplitude of calcium spikes. The amplitude and duration of individual afterhyperpolarizations following a single spike were unchanged. In contrast, the neuronal excitability was significantly decreased and the spike duration significantly enhanced in aged rats as compared to young rats. The comparison of afterhyperpolarizations (which follow a burst of spikes) between young and aged rats was more complex. An increase in the amplitude and duration of afterhyperpolarizations generally occurred in aged animals. However, this increase was not consistent among animals and was dependent on the holding potential of the neuron and on the number of action potentials used to trigger the afterhyperpolarization. The depolarizing effect of bath-applied carbachol, as well as the associated increase in membrane resistance were reduced in neurons from aged rats. In contrast, the effects of carbachol on the depression of synaptic events and the blockade of the afterhyperpolarizations were similar in young and aged animals. In addition, the amplitude of the slow cholinergic excitatory postsynaptic potential induced by stimulation of cholinergic afferents in the presence of physostigmine was also decreased in aged rats. Excitatory postsynaptic potentials and inhibitory postsynaptic potentials following electrical stimulation of stratum radiatum were compared. The amplitude and duration of excitatory postsynaptic potentials were increased in aged rats. The amplitude and duration of the fast inhibitory postsynaptic potential were not significantly affected in aged animals. In contrast, the duration of the slow inhibitory postsynaptic potential was decreased in aged rats. Since the mean baclofen-induced hyperpolarization was only slightly reduced in aged rats, the most likely explanation is a decrease in the release of GABA rather than an alteration in the postsynaptic response mediated by GABAB receptors. A statistically significant correlation was found between the degree of impairment in the spontaneous alternation task and the amplitude of the carbachol-induced depolarization.

Acetylcholine↗

PubMed1984

Mu opioid receptors participate in the excitatory effect of opiates in the hippocampal slice.

The effects of the opioid peptides morphiceptin and [N-MePhe3-D-Pro4]morphiceptin (PL017), both mu receptor agonists, were examined by electrophysiological techniques in the rat hippocampal slice and ligand binding techniques in hippocampal membrane preparations. The electrophysiological actions of the mu agonists were similar to those of the previously studied delta receptor agonist [D-Ala2, D-Leu5]enkephalin. Thus, for a given size field excitatory postsynaptic potential the amplitude of both population spike and intracellular excitatory postsynaptic potential was increased by morphiceptin. These effects were concentration dependent and reversed by naloxone. The EC50 for morphiceptin was 1.6 microM, which is consistent with the mu-selective binding properties of this peptide. Similar results were obtained with the more potent analog PL017. Morphiceptin and morphine had similar displacement profiles in competition experiments performed with hippocampal membranes and a variety of radioligands. In Tris buffer morphiceptin potently inhibited the binding of the mu receptor marker [125I]FK 33,824 but displayed the expected shallow displacement isotherm against binding of the delta receptor marker [125I][D-Ala2, D-Leu5]enkephalin. A significant interaction of either morphiceptin or morphine with kappa binding sites is improbable since neither agonist could fully displace binding of [3H]ethylketocyclazocine or [3H]diprenorphine. The potency of morphiceptin in displacing [3H]naloxone from mu binding sites was reduced by inclusion of 100 mM NaCl or 100 microM GTP in the assay. The dissociation constant of morphiceptin for mu binding sites in physiological saline was 0.78 microM, comparable to its EC50 determined in electrophysiological experiments. It appears, therefore, that the electrophysiological properties of opioid peptides in the hippocampal slice may be mediated by both mu and delta receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1991

Neuropharmacology of the muscarinic antagonist telenzepine in myenteric ganglia of the guinea-pig small intestine.

Intracellular recording methods were used to investigate the actions of the putative M1 muscarinic receptor antagonist telenzepine on the electrical and synaptic behavior of myenteric neurons. Telenzepine had no effect on resting membrane potential, input resistance, excitability and antidromic potentials in both AH/type 2 and S/type 1 neurons, when applied in concentrations of 0.1-2000 nM, although higher concentrations (10-100 microM) did have a significant non-specific effect on the postsynaptic membrane. Micromolar concentrations of telenpzepine (1-2 microM) had no effect on excitatory responses to substance P, vasoactive intestinal peptide, the nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium or the nicotinic action of acetylcholine. Nicotinic fast excitatory postsynaptic potentials were also unaffected by 2 microM telenzepine. In contrast, at submicromolar concentrations (100 nM), telenzepine abolished responses to either muscarine or the muscarinic component of the acetylcholine response. The excitatory effect of muscarine at postsynaptic M1 receptors was dose dependently inhibited by telenzepine (0.1-1000 nM) at concentrations which had no effect on the electrical properties of the cells. This effect was slowly reversible, usually requiring more than 60 min for significant recovery. The threshold dose of telenzepine as an antagonist of the muscarinic depolarization in AH/type 2 neurons was in the range of 0.1-1 nM. The IC50 concentration of telenzepine needed to abolish the response was 8.5 nM. A small proportion of stimulus-evoked slow excitatory postsynaptic potentials in both AH/type 2 and S/type 1 cells were abolished by 1 microM telenzepine, while the majority of them remained unaffected, indicating that some slow excitatory postsynaptic potentials are mediated by the muscarinic action of released acetylcholine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Presynaptic and postsynaptic effects of histamine and histamine agonists in the superior cervical ganglion of the rat.

Extracellular and intracellular recording techniques were used to study the effects of histamine and the histamine agonists [impromidine (IMP) and 2-thiazolylethylamine (2-TH)] on synaptic transmission in the superior cervical ganglion of the rat in vitro. At the concentrations employed (up to 10(-5) M) these compounds did not produce detectable effects on the electrical properties of the postsynaptic neurons. Histamine produced a dose-dependent reduction in the amplitude of the extracellularly-recorded presynaptic and postsynaptic compound action potential. The H2 receptor agonist impromidine reduced only the postganglionic compound action potential. Cimetidine, a specific H2 receptor antagonist, produced parallel shifts in the log dose-response curves for impromidine. Impromidine also reduced the average size of the evoked excitatory postsynaptic potential. The reduction of the mean amplitude of the excitatory postsynaptic potential was due to a decrease in the amount of acetylcholine (ACh) liberated by each preganglionic volley (mean quantal content, m) and a diminution in quantal size. The H1 receptor agonist, 2-TH produced a dose-dependent increase in the presynaptic and postsynaptic compound action potential and in m. The increase in m was not associated with changes in quantal size. The H1 antagonists, pyrilamine and promethazine, did not prevent facilitation of ganglionic transmission induced by 2-TH. It is concluded that histamine H1 and H2 receptors exist on preganglionic axons, or terminals in sympathetic ganglia of the rat. Activation of H1 receptors facilitates release of ACh whereas H2 receptor activation results in depressed release.

Action Potentials↗

PubMed1991

Persistent enhancement of transmitter release accompanying long-term potentiation in the guinea pig hippocampus.

In order to examine temporal changes in enhancement of transmitter release during long-term potentiation (LTP), we examined amplitude fluctuation of excitatory postsynaptic potentials (EPSPs) for longer periods than 2 h after tetanic stimulation (up to 4 h in the longest observation). The relative magnitude of excitatory postsynaptic potentiation (EPSP) fluctuation (coefficient of variation, CV) reduced throughout the observation periods in association with an increase in EPSP amplitude after tetanic stimulation. The reciprocals of squared CVs (= mean2/variance) were almost in proportion to the magnitude of LTP, and the ratio of 1/CV2 and the LTP magnitude did not change significantly for up to 4 h. These findings suggest that a prolonged enhancement of transmitter release from presynaptic terminals underlies LTP, and the relative contribution of this presynaptic enhancement does not change significantly for 2 h (maybe up to 4 h, or longer) after tetanic stimulation.

Animals↗

PubMed1987

Postsynaptic membrane shifts during frequency potentiation of the hippocampal EPSP.

1. In some classes of central neurons, repetitive synaptic stimulation induces substantial changes in the postsynaptic membrane, in conjunction with robust frequency potentiation of the excitatory postsynaptic potential (EPSP). However, the nature and time course of these postsynaptic membrane shifts, or their possible contributions to EPSP frequency potentiation (e.g., by altering driving force or current pathways), have not been examined extensively. We therefore studied the simultaneous patterns of change in composite EPSP amplitude, postsynaptic input resistance (Rin), and postsynaptic membrane potential during a 4-min train of 10-Hz monosynaptic stimulation in CA1 neurons of hippocampal slices. Slices were maintained in media containing either control (4 mM) or high (6.5 mM) concentrations of K+. 2. Potentiation of the EPSP, hyperpolarization of the membrane, and a decline of Rin, all developed rapidly during 10-Hz synaptic stimulation; these responses reached maximal levels by 5-15 s of the stimulation train. In most cells, a membrane depolarization phase occurred between 15 and 45 s of stimulation, followed by rehyperpolarization by 1 min of stimulation. During the depolarization phase, both EPSP potentiation and the decline in Rin remained near maximal. No significant differences were seen as a function of K+ concentrations. 3. These results show that hyperpolarization is not invariably associated temporally with EPSP frequency potentiation. Moreover, if driving force and membrane conductance changes are assumed to be approximately similar in large dendrites and soma, then the increase in driving force due to membrane hyperpolarization was not sufficient to account for the three- and fourfold increases in EPSP amplitude seen during frequency potentiation. Further, based on similar assumptions and on dendritic models of EPSP attenuation, the decline in Rin should reduce EPSP amplitude at the dendritic synaptic site and, to a proportionately greater extent, at the soma. 4. Studies in which the membrane was hyperpolarized with injected current to approximately the IPSP reversal potential, or in which bicuculline methiodide was applied to the slices, indicated that depression of the IPSP by repetitive stimulation did not account for frequency potentiation of EPSP amplitude. 5. These data are therefore consistent with the conclusion that the frequency potentiation of composite EPSPs in central neurons depends on presynaptic mechanisms, rather than on generalized postsynaptic changes. However, our findings do not rule out localized postsynaptic changes in receptors or spines as possible contributing factors.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1987

Tiletamine is a potent inhibitor of N-methyl-aspartate-induced depolarizations in rat hippocampus and striatum.

N-methyl-D,L-aspartate (NMA) antagonists are of potential value in the treatment of epilepsy and ischemia, but commonly utilized compounds are of low potency and poorly penetrate the brain. Tiletamine hydrochloride is a lipophilic and potent veterinary anesthetic. This study shows tiletamine to be similar to ketamine and to phencyclidine, agents known to interact with the NMA receptor. Effects of tiletamine on synaptic transmission and on direct excitatory responses to exogenous amino acids were examined in rat hippocampal and striatal slices. In striatal slices, tiletamine inhibited the NMA-mediated, but not the spontaneous, release of [3H]acetylcholine, with an IC50 of 70 nM. In hippocampal CA1 cells, 3 microM tiletamine in the perfusate reversibly blocked the intracellularly recorded responses to ionophoretically applied NMA, but not to glutamate, quisqualate and kainate. Tiletamine, 3 to 100 microM, had no effect on the orthodromically elicited excitatory postsynaptic potential, action potential amplitude or duration, resting membrane potential, or input resistance. In Mg++-free perfusate, the excitatory postsynaptic potential was greatly augmented to give a paroxysmal depolarization shift and was reversibly blocked by 10 microM tiletamine. Our results show that tiletamine is a potent and reversible antagonist of NMA-mediated responses without itself having major effects in low concentrations on normal membrane and synaptic pyramidal cell properties.

Acetylcholine↗

PubMed1993

Laryngeal afferent inputs to the nucleus of the solitary tract.

The following study was undertaken to examine the integration of laryngeal afferent inputs within the nucleus of the solitary tract (NTS), the primary site of termination of laryngeal afferent fibers. Intracellular recordings were obtained from 63 cells that responded to electrical stimulation of the superior laryngeal nerve (SLN) with an excitatory postsynaptic potential (EPSP; n = 49), an excitatory-inhibitory postsynaptic potential (EPSP-IPSP) sequence (n = 13), or an IPSP (n = 1). Mechanical stimulation of laryngeal mechanoreceptors revealed a variety of response patterns (e.g., slowly and rapidly adapting depolarizations or hyperpolarizations). Two types of response to increasing SLN stimulus frequency were observed. In 11 cells SLN-evoked EPSP amplitude at 10 Hz was only 47 +/- 4% of the amplitude at 1 Hz, while in 6 cells EPSP amplitude at 10 Hz was virtually identical (93 +/- 3%) to that at 1 Hz. Time-dependent inhibitory interactions occurred between SLN inputs to NTS neurons at intervals between 50 and 400 ms and in the absence of any change in membrane potential. NTS neuronal responses to brief activation of laryngeal mechanoreceptors correspond well to discharge patterns described for individual laryngeal mechanoreceptors. Frequency-dependent filtering and time-dependent inhibitory interactions might modify NTS neuronal responses during more intense stimulation of laryngeal afferents.

Afferent Pathways↗

PubMed1982

Effect of substance P on colonic mechanoreceptors, motility, and sympathetic neurons.

Intracellular recording techniques were used in vitro to analyze the effects of substance P (SP) on synaptic transmission and electrical properties of sympathetic neurons in the inferior mesenteric ganglion (IMG) of the guinea pig. Intraluminal pressure-recording techniques were used to study the effects of SP on colonic motility. Superfusion of the ganglia with SP (10(-7) to 10(-6) M) depolarized the cell soma (2--12 mV) and increased cell input resistance (8--11 M omega). These effects converted synchronous excitatory postsynaptic potentials, in response to electrical stimulation of preganglionic nerves, and asynchronous excitatory postsynaptic potentials, in response to activation of colonic mechanoreceptors, to action potentials. Administration of SP to only the colon increased basal intraluminal pressure and the frequency and amplitude of phasic changes in intraluminal pressure. These changes increased mechanoreceptor synaptic input to neurons in the IMG. We conclude that SP facilitates synaptic transmission along noradrenergic pathways and increases colonic motility.

Animals↗