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PubMed1989

Effects of cisapride on cholinergic neurotransmission and propulsive motility in the guinea pig ileum.

The actions of cisapride on electrical behavior of single myenteric neurons and on the propulsive activity of segments of ileum were studied in vitro. Cisapride (10-300 nM) did not affect the membrane potential, resting properties, or active properties of S neurons. The amplitude of fast nicotinic excitatory postsynaptic potentials recorded from S cells was increased by cisapride in the concentration range of 10 nM to 1 microM. Higher cisapride concentrations (3-10 microM) reduced the amplitude of fast excitatory postsynaptic potentials. Potentiation of fast excitatory postsynaptic potentials by cisapride was antagonized by ICS 205-930 (1 microM) but was unaffected by GR 38032F (1 microM), both compounds being 5-HT3-receptor antagonists. Cisapride did not modify the electrical behavior of AH neurons except at the highest concentrations (3-10 microM), which caused hyperpolarization of some neurons. The propulsive efficiency (i.e., number of peristalses and total amount of fluid ejected per unit of time) of isolated segments of ileum was enhanced by cisapride (100 nM to 3 microM). Higher cisapride concentrations (6 or 10 microM) had a depressant action on propulsive activity. The stimulatory effect of cisapride on propulsion was not antagonized by ICS 205-930 (300 nM or 1 microM). These data indicate that cisapride facilitates cholinergic transmission in the myenteric plexus of guinea pig ileum and that this effect may be at least partially responsible for the increased propulsive efficiency observed in ileal segments.

Acetylcholine↗

PubMed1989

Selective antagonism of muscarinic potentials on the superior cervical ganglion of the rat.

Selective antagonists have been used to classify the muscarinic receptors involved in the slow excitatory postsynaptic potential and slow inhibitory postsynaptic potential of the superior cervical ganglia of the rat, as recorded in 1 microM neostigmine, using a grease-gap method. Cardioselective M2 antagonists, e.g. AF-DX 116, depressed the slow inhibitory postsynaptic potential and enhanced the slow excitatory postsynaptic potential. The M1 selective antagonist pirenzepine depressed both potentials equally. The high potency of pirenzepine against the slow excitatory postsynaptic potential, however, indicates that it is mediated by M1 receptors. The slow excitatory and inhibitory postsynaptic potentials were found to be pharmacologically similar to the muscarinic agonist-induced depolarisation and hyperpolarisation of this preparation, respectively. The actions of two muscarinic agonists on the postsynaptic potentials were also studied. It is concluded that the slow excitatory postsynaptic potential is mediated by M1 receptors and the slow inhibitory postsynaptic potential by cardiac-like M2 receptors.

Animals↗

PubMed1992

Ca2+ entry via postsynaptic voltage-sensitive Ca2+ channels can transiently potentiate excitatory synaptic transmission in the hippocampus.

We have studied the role of Ca2+ entry via voltage-sensitive Ca2+ channels in long-term potentiation (LTP) in the CA1 region of the hippocampus. Repeated depolarizing pulses, in the presence of the NMDA receptor antagonist D-APV and without synaptic stimulation, resulted in a potentiation of excitatory postsynaptic potentials (EPSPs) or currents (EPSCs). This depolarization-induced potentiation was augmented in raised extracellular Ca2+ and was blocked by intracellular BAPTA, a Ca2+ chelator, or by nifedipine, a Ca2+ channel antagonist, indicating that the effect was mediated by Ca2+ entry via voltage-sensitive Ca2+ channels. Although the peak potentiation could be as large as 3-fold, the EPSP(C)s decayed back to baseline values within approximately 30 min. However, synaptic activation paired with depolarizing pulses in the presence of D-APV converted the transient potentiation into a sustained form. These results indicate that a rise in postsynaptic Ca2+ via voltage-sensitive Ca2+ channels can transiently potentiate synaptic transmission, but that another factor associated with synaptic transmission may be required for LTP.

2-Amino-5-phosphonovalerate↗

PubMed1988

Pharmacological studies in frog sympathetic ganglion: support for the cholinergic monosynaptic hypothesis for slow IPSP mediation.

The slow inhibitory postsynaptic potential (slow IPSP), the slow excitatory postsynaptic potential (slow EPSP), the late slow excitatory postsynaptic potential (late slow EPSP), and the fast excitatory postsynaptic potential/compound action potential (fast EPSP) were recorded from the 9th or 10th paravertebral sympathetic ganglia of bullfrogs (and some Rana pipiens frogs) by the sucrose-gap technique. The adrenergic antagonists phentolamine, dihydroergotamine and propranolol did not show any antagonistic effect on the slow IPSP when used at concentrations of up to 10, 100 and 10 microM, respectively. U-0521 (3',4'-dihydroxy-2-methylpropriophenone, 50 micrograms/ml), a specific inhibitor of catechol-O-methyltransferase, did not show any potentiating effect on the slow IPSP. The cholinesterase inhibitor neostigmine (0.5-1 microM) induced a large increase in the duration and amplitude of slow IPSP. When phentolamine and propranolol at concentrations greater than 10 microM were used the slow IPSP (and all other synaptic potentials) were non-specifically reduced in amplitude by these drugs. The results reported in this paper do not lend any support to the hypothesis that the slow IPSP in frog sympathetic ganglia is mediated by an adrenergic interneuron. The results are consistent with the proposal that the slow IPSP in this ganglion is mediated by a direct action of acetylcholine released from cholinergic preganglionic fibers.

Action Potentials↗

PubMed1987

Synaptic control of pyramidal cell activation in the hippocampal slice preparation in the rat.

Recordings were made from CA1 pyramidal neurons in a rat hippocampal slice preparation to compare the effectiveness of orthodromic stimuli when delivered at different distances from the cells under study. A stimulating electrode placed in stratum radiatum was less effective in driving nearby pyramidal cells (within 200 micron) than those farther away (greater than 800 micron). Thus for a given field excitatory postsynaptic potential both the intracellular excitatory postsynaptic potential and the evoked population spike were smaller when evoked from a local stimulating electrode than from one more distant. Laminar mapping experiments indicated that the spatial distribution of activated excitatory synapses over the pyramidal cell dendrites was similar for local and distant stimuli. The firing threshold, and the amplitude of hyperpolarizing inhibitory postsynaptic potentials, were also similar for the two stimuli. Responses evoked by the local stimulating electrode were more sensitive to morphine, penicillin and pentobarbital than responses elicited by the distant stimulus, suggesting that some form of GABAergic inhibition limited the efficacy of the local stimulus. The data suggest that in the CA1 region a vertically oriented synaptic inhibitory system exists that powerfully regulates the ability of an orthodromic stimulus to activate pyramidal cells. These results also illustrate the practical importance of controlling the distance between stimulating and recording electrodes, when performing quantitative pharmacological studies of synaptic transmission in the hippocampus.

Animals↗

PubMed1985

Significance of slow synaptic potentials for transmission of excitation in guinea-pig myenteric plexus.

Intracellular recordings were made from neurones in myenteric ganglia of the guinea-pig ileum in vitro. Synaptic potentials were evoked by electrically stimulating presynaptic fibres as they entered the ganglion, using a small focal electrode. Slow synaptic depolarizations (excitatory postsynaptic potentials) were evoked in most myenteric neurones of both types. A single stimulus was more likely to evoke a slow excitatory postsynaptic potential in cells with nicotinic synaptic input (S cells; 50%) than in cells with long-lasting after-hyperpolarizations following the soma action potential (AH cells; 20%). Two pulses often evoked a slow excitatory postsynaptic potential in AH cells when one pulse was ineffective. The optimally effective time between the pulses was about 100 ms. Ten pulses resulted in slow excitatory postsynaptic potentials even when delivered at frequencies as low as 0.5 Hz. For the same frequency of presynaptic stimulation, the duration of the slow excitatory postsynaptic potential was greater in AH cells than in S cells and the amplitude of the slow excitatory postsynaptic potential was slightly greater in S than AH cells. Spontaneous depolarizations were observed which had time-courses and amplitudes similar to the evoked slow excitatory postsynaptic potential. They were not blocked by tetrodotoxin or atropine. The calcium-dependent after-hyperpolarization which follows one or more action potentials in AH cells was reduced or even abolished during the slow excitatory postsynaptic potential. Presynaptic nerve stimulation at intensities lower than those required to cause a slow excitatory postsynaptic potential caused a reduction in the calcium dependent after-hyperpolarization. It is concluded that the slow excitatory postsynaptic potential is generated by an intracellular intermediate process which is sensitive to the intracellular calcium concentration. The results suggest that the postsynaptic action of the synaptic transmitter is to interfere with the intracellular process which couples the entry of calcium to the increase in potassium conductance.

Animals↗

PubMed1987

Observations on the actions of substance P and [D-Arg1,D-Pro2,D-Trp7,9,Leu11)substance P on single neurons of the guinea pig submucous plexus.

Intracellular recordings were made from neurons of the guinea pig submucosal plexus and the effects of substance P and the substance P analogue [D-Arg1,D-Pro2,D-Trp7,9,Leu11]substance P were examined. Substance P (20-200 nM) depolarized all submucosal neurons; these depolarizations were shown to be due to a decrease in the resting (or "leak") potassium conductance of the membrane. In approximately 50% of the 46 neurons tested, superfusion with [D-Arg1,D-Pro2,D-Trp7,9,Leu11]substance P (0.2-20 microM) produced a dose-dependent membrane hyperpolarization. This hyperpolarization was prevented by the alpha 2-adrenoceptor antagonist idazoxan (300 nM) or by concentrations of cobalt which abolished all spontaneous and evoked synaptic potentials, indicating that it resulted from release of noradrenaline from sympathetic nerve terminals. [D-Arg1,D-Pro2,D-Trp7,9,Leu11]substance P depressed the amplitude of the three synaptic potentials recorded from submucosal neurons; the concentrations that caused 50% of the maximal inhibition of the fast excitatory postsynaptic potential, the inhibitory postsynaptic potential, and slow excitatory postsynaptic potential were 40 microM, 600 nM and 20 microM, respectively. When idazoxan was present, the substance P analogue was less effective in depressing the amplitudes of the fast and slow excitatory synaptic potentials suggesting that much of its presynaptic inhibition also resulted from release of noradrenaline. These results provide evidence that [D-Arg1,D-Pro2,D-Trp7,9,Leu11]substance P releases noradrenaline from sympathetic nerves in the submucosal plexus. One effect of this is a membrane hyperpolarization; another is a presynaptic inhibition of transmitter release. These actions much limit the usefulness of this "substance P antagonist" in efforts to show that synaptic potentials, such as the slow excitatory synaptic potential, are mediated by substance P.

Animals↗

PubMed1987

Corticofugal inhibitory effects on lingually induced postsynaptic potentials in cat hypoglossal motoneurons.

The suppression of lingually or cortically induced postsynaptic potentials produced by conditioning stimulation of the cerebral cortex or the lingual nerve was studied in cat hypoglossal motoneurons. We have demonstrated that lingually or cortically induced inhibitory postsynaptic potentials were effectively suppressed by a conditioning stimulus of the cerebral cortex or the lingual nerve. In hypoglossal motoneurons after blocking inhibitory postsynaptic potentials by the administration of strychnine, lingually induced excitatory postsynaptic potentials and spikes were effectively suppressed by cortical stimulation. Whereas, a conditioning stimulus of the lingual nerve suppressed only a long-latency excitatory postsynaptic potential evoked by a test stimulus of the cerebral cortex, while a short-latency excitatory postsynaptic potential was unaffected. Picrotoxin and bicuculline appeared to act by reducing the suppression of lingually induced excitatory postsynaptic potentials produced by cortical conditioning stimulation.

Action Potentials↗

PubMed1988

Presynaptic K-channel blockade counteracts the depressant effect of adenosine in olfactory cortex.

Slices of isolated olfactory cortex from guinea-pig have been used to study the action of adenosine at synapses between axons of the lateral olfactory tract and neurons in the olfactory cortex. Adenosine depressed the excitatory postsynaptic potential, and, with paired or multiple stimuli, the reduced excitatory postsynaptic potentials in adenosine showed more synaptic facilitation. Very small excitatory postsynaptic potentials which were estimated not to be affected by postsynaptic membrane conductance changes were highly sensitive to adenosine. Both observations indicate a presynaptic action of adenosine. To test whether a conductance increase to potassium ions mediated adenosine action, the K-channel blockers, 3,4-diaminopyridine (1-100 mumol/l) or 4-aminopyridine (100-500 mumol/l) were applied or Cs partially substituted for K. These substances reduced or prevented adenosine from having its depressant effect on synaptic transmission. These particular K-channel blockers also prolonged the action potential propagating along the lateral olfactory tract. When the increased excitability was counteracted by high Mg or low concentrations of tetrodotoxin, 3,4-diaminopyridine still blocked adenosine action. UO2 ions prolonged the lateral olfactory tract action potential without blockade of K-conductance, but still supported an adenosine depression of the excitatory postsynaptic potential. Veratridine also supported the adenosine depression. These observations suggest that the action of 3,4-diaminopyridine on adenosine was not solely the result of increased tissue excitability. In contrast, tetraethylammonium (20 mmol/l), Ba (0.5-4 mmol/l) or Rb replacement for K had a negligible effect on the duration of the presynaptic action potential and had no effect on the depressant action of adenosine. These data are compatible with the idea that adenosine enhances an aminopyridine-sensitive potassium conductance in nerve terminals and changes in Ca influx are consequential to this.

4-Aminopyridine↗

PubMed1988

Intracellular recordings from cells in the myenteric plexus of the rat duodenum.

Intracellular recordings were made in vitro from neurons in the myenteric plexus of freshly dissected preparations of the duodenum of the rat. Nearly one-quarter of neurons (18 out of 77) had long after-hyperpolarizations following their action potentials. Over 60% of neurons (20 out of 32) which were tested exhaustively by focal stimulation at seven points around the recording site were seen to receive fast excitatory synaptic inputs. These were of very short duration (10-30 ms) and were reversibly blocked by the nicotinic antagonist hexamethonium. Only four out of 18 after-hyperpolarization cells (22%) had visible fast synaptic inputs. Seven out of 32 neurons tested received slow excitatory synaptic inputs lasting up to 60 s that were associated with a decrease in conductance and an increase in excitability. No evidence for muscarinic synaptic potentials was seen; only four cells out of 30 with fast excitatory postsynaptic potentials had slow excitatory synaptic potentials visible after a single-shot stimulus; in none of these were the slow excitatory postsynaptic potentials blocked by atropine (up to 1 x 10(-5) M). No inhibitory postsynaptic potentials were recorded in any of the 77 neurons recorded in this study. The effects of five neurotransmitter candidates (acetylcholine, GABA noradrenaline, 5-hydroxytryptamine and substance P) applied by pressure microejection were studied. It is concluded that most of the neurophysiological features reported in the extensively studied guinea-pig small bowel myenteric plexus are present in the rat duodenum. However, the apparent lack of muscarinic synaptic potentials and inhibitory synaptic potentials suggests that there may be some differences between the two species. Our recordings also differ slightly from recently reported studies of rat myenteric neurons grown in cell culture.

Acetylcholine↗

PubMed1985

Slow postsynaptic potentials in neurones of submucous plexus of guinea-pig caecum and their mimicry by noradrenaline and various peptides.

Intracellular recordings of membrane potential and membrane currents were made from neurones in the submucous plexus of the guinea-pig caecum in vitro. Fast and slow excitatory postsynaptic potentials and slow inhibitory postsynaptic potentials were recorded from the majority of neurones following focal stimulation of presynaptic fibres in the plexus. The slow inhibitory postsynaptic potential was associated with an increase in membrane conductance and reversed its polarity at -90 mV; it was reversibly blocked by yohimbine. The slow excitatory postsynaptic potential and its underlying current was associated with a decrease in membrane conductance. Two kinds of voltage-dependence both of the slow excitatory postsynaptic potential and current were observed; in 80% of cells, the excitatory postsynaptic potential and current became smaller with membrane hyperpolarization and reversed polarity at -90 mV (reversing type) but in 20% of cells both the excitatory postsynaptic potential and current simply disappeared when the membrane potential reached -70 mV (non-reversing type). The effects of acetylcholine, adenosine 5'-triphosphate, bombesin, 5-hydroxytryptamine, neurotensin, noradrenaline, substance P and vasoactive intestinal polypeptide were examined. The only substance which mimicked the slow inhibitory postsynaptic potential was noradrenaline; brief applications of noradrenaline caused hyperpolarizations which had the same time-course, reversal potential and sensitivity to yohimbine as the slow inhibitory postsynaptic potential. The non-reversing type of slow excitatory postsynaptic potential was mimicked only by adenosine 5'-triphosphate. The reversing type of slow excitatory postsynaptic potential was mimicked by bombesin, neurotensin, substance P and vasoactive intestinal polypeptide. 5-Hydroxytryptamine and vasoactive intestinal polypeptide (in some neurones) caused a depolarization with an increase in membrane conductance. All three synaptic potentials were reversibly depressed by superfusion of noradrenaline but noradrenaline did not affect the potential changes evoked by brief application of exogenous acetylcholine or substance P. It is concluded that, in guinea-pig submucous plexus neurones, the slow inhibitory postsynaptic potential is mediated by noradrenaline and results from a potassium conductance increase.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗

PubMed1990

Calcium-dependent potentials with different sensitivities to calcium agonists and antagonists in guinea-pig hippocampal neurons.

Effects of organic Ca channel blockers, Ca channel activators and omega-conotoxin on guinea-pig hippocampal CA1 neurons in vitro preparations were studied with intracellular recording methods. Most of the Ca channel blockers, such as prenylamine, D 600, flunarizine, nifedipine, cinnarizine and nicardipine (0.2-4 microM), raised the threshold for Na-dependent spike generation and decreased the amplitude of the spike afterhyperpolarization. Verapamil (5 microM) and diltiazem (5 microM) did not significantly alter the threshold and amplitude of the Na spike. Action potentials elicited in the presence of either tetrodotoxin (0.5 microM) and tetraethylammonium (20 mM) or tetrodotoxin (0.5 microM) and Ba (1.25 mM) consisted of an initial spike component followed by a long depolarization. Both responses were abolished by addition of Co (2 mM) or Cd (0.25-0.5 mM), or by superfusion with a low Ca (0.25 mM)-high Mg(15 mM) medium, indicating that the potentials resulted from Ca entry. The Ca-dependent slow depolarization was preferentially blocked by most of the organic Ca channel blockers at approximately one-third the concentrations (0.1-2 microM) which were required to shorten the Ca spike. When the cell in a solution containing tetrodotoxin (0.5 microM), Co (2 mM) and 4-aminopyridine (2 mM) was hyperpolarized and then depolarized by passing current pulses across the membrane, a transient depolarizing hump occurred on the decay phase of the electrotonic potential. This transient depolarization was abolished by Co (2 mM), Ni (2 mM) or most of the organic Ca channel blockers (0.2-5 microM). Diltiazem (5 microM) did not significantly change these Ca-dependent potentials. The evoked excitatory postsynaptic potential was very resistant to the Ca channel blockers. Approximately 2-10 times higher concentrations (0.5-3 microM) were necessary to decrease the excitatory postsynaptic potential amplitude than to shorten the Ca spike. On the other hand, the minimal concentrations and order of potencies of the Ca channel blockers for depressing the evoked inhibitory postsynaptic potential and for elevating the threshold for Na spike generation were almost the same. Dihydropyridine Ca channel activators, such as Bay K 8644, CGP 28 392 and YC 170 at low concentrations (0.1-1 microM), decreased the Ca spike, the Ca-dependent slow depolarization and the evoked synaptic potentials, while the substances augmented the Ca-dependent transient depolarization. On the other hand, omega-conotoxin (5 microM) reversibly depressed the Ca spike and slow depolarization to the same degree, without affecting the transient depolarization and the evoked excitatory or inhibitory postsynaptic potentials.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1988

Phenytoin reduces excitatory synaptic transmission and post-tetanic potentiation in the in vitro hippocampus.

Phenytoin (10-100 microM) was studied on excitatory synaptic transmission and post-tetanic potentiation (PTP) in the in vitro rat hippocampus. Synaptic potentials were studied using extracellular, intracellular and single-electrode voltage clamp techniques. Field excitatory postsynaptic potentials were recorded from the apical dendrites of CA1 pyramidal cells after Schaffer collateral stimulation. Intracellularly recorded excitatory postsynaptic potentials and excitatory postsynaptic currents were recorded in CA3 pyramidal cells after mossy fiber stimulation and in the presence of 10 microM picrotoxinin. In the CA1 region, phenytoin elicited a reversible depression of field excitatory postsynaptic potentials as well as reduced the time constant of decay of PTP from 79 sec to 47 sec with no change in the magnitude of potentiation. Higher concentrations of phenytoin (100 microM) had a general depressant effect on both the amplitude and time course of PTP. In CA3 cells, phenytoin (10 microM) reduced the mossy fiber synaptic conductance but did not change its reversal potential. Phenytoin (10 microM) also reduced the time constant of decay of PTP of the mossy fiber to CA3 synapse, while having no effect on the magnitude of potentiation. These results show that therapeutically relevant concentrations of phenytoin depress both low-frequency synaptic transmission and the time course of short-term potentiation. Both actions may be involved in the anticonvulsant properties of phenytoin.

Animals↗

PubMed1989

Maintenance of long-term potentiation in rat dentate gyrus requires protein synthesis but not messenger RNA synthesis immediately post-tetanization.

The involvement of new protein and messenger ribonucleic acid synthesis in long-term potentiation was studied in the anaesthetized rat dentate gyrus using several inhibitors of protein synthesis (anisomycin, emetine, cycloheximide and puromycin) and an inhibitor of messenger ribonucleic acid synthesis (actinomycin D). When injected for 1 h just prior to tetanization, the four inhibitors of protein synthesis produced a mild reduction of long-term potentiation of the excitatory postsynaptic potential measured 10 min after tetanization. Anisomycin produced a significantly faster decay of long-term potentiation, while the other inhibitors had more moderate effects. Actinomycin D failed to affect long-term potentiation. In a second experiment, the time-dependency of the anisomycin effect was examined. Anisomycin injected immediately after tetanization promoted decay of long-term potentiation, but when injected after a 15-min delay, the drug had no effect. Inhibition of protein synthesis for 4 h prior to tetanization did not have any more effect on long-term potentiation than inhibition for 1 h. In no experiment was long-term potentiation of the population spike affected by drug manipulation. These results suggest that for long-term potentiation of the excitatory postsynaptic potential to be maintained for at least 3 h proteins must be synthesized from already existing messenger ribonucleic acid, and that this synthesis is mostly completed within 15 min after tetanization.

Animals↗

PubMed1988

Presynaptic inhibition produced by histamine at nicotinic synapses in enteric ganglia.

Intracellular methods were used to record fast excitatory postsynaptic potentials in myenteric neurons of the guinea-pig small intestine in vitro. The excitatory postsynaptic potentials were suppressed by hexamethonium, mimicked by acetylcholine and assumed to be mediated by nicotinic cholinergic receptors. Application of histamine either by addition to the superfusion solution or by focal application from fine-tipped pipettes reversibly reduced the amplitude or abolished the excitatory postsynaptic potentials. Postsynaptic responses to focal application of acetylcholine by pressure ejection from micropipettes were either unaffected or were potentiated by histamine. Failure of histamine to affect antidromic action potentials excluded a local anesthetic action on the presynaptic fibers. Neither 2-methylhistamine nor dimaprit, which are selective H1 and H2 agonists respectively, suppressed the excitatory postsynaptic potentials when applied in concentrations nearly one hundred times greater than the ED50 for histamine. The selective H1 and H2 antagonists, pyrilamine and cimetidine did not suppress the inhibitory action of histamine when applied separately or in combination. Based on these results, the presynaptic receptors involved in this inhibitory mechanism appeared to be of a pharmacologically atypical histamine receptor subtype. The putative histamine agonist, N,alpha-methylhistamine, which has been reported to have high stereoselectivity and activity for a receptor subtype classified as H3, potently reduced or abolished the excitatory postsynaptic potentials. The ED50 for N,alpha-methylhistamine was 8.8 nM compared to an ED50 of 220 nM for histamine. Burimamide, a histamine antagonist with higher activity at putative H3 receptors than H2 receptors, effectively reversed the inhibitory action of histamine on the excitatory postsynaptic potentials.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed1989

Effect of minaprine on electrical activity of the rat hippocampus in vivo.

The effects of minaprine on evoked field potentials recorded extracellularly in the synaptic layer (population excitatory postsynaptic potentials) and the granule cell body layer (population spike) of the dentate gyrus of the hippocampus were examined in urethane anesthetized rats. Field potentials were evoked by stimulation of the medial entorhinal cortex. Minaprine (up to 10 mg/kg, i.v.) did not alter the amplitude of the population excitatory postsynaptic potentials but dose-dependently increased in the amplitude of the population spike at doses between 1 and 10 mg/kg. Brief tetanic stimulation (400 Hz, 100 ms) to the entorhinal cortex produced a long-term potentiation (LTP) of both the population excitatory postsynaptic potentials and the population spikes. Minaprine (1-10 mg/kg) did not affect LTP of the population excitatory postsynaptic potentials. Treatment with minaprine 1 mg/kg, which per se did not affect the amplitude of the population spike significantly, augmented the LTP measured 25 and 35 min after tetanic stimulation. Thus, the mode of action of minaprine on electrical activity in the rat hippocampus may, at least in part, be related to an increase of the responsiveness of the granule cell body.

Animals↗

PubMed1991

Effects of axotomy on synaptic transmission and structure in frog sympathetic ganglia.

Axotomy was carried out on frog sympathetic neurons of the two last lumbar chain ganglia. At different times thereafter, synaptic transmission was analysed electrophysiologically by intracellular microelectrodes and compared with synaptic density, measured by electron microscopy in the same ganglia. For this purpose, modifications in synaptic transmission were estimated first, by the numbers of B and C sympathetic neurons exhibiting subthreshold excitatory postsynaptic potentials in response to 10 Hz orthodromic stimulation of preganglionic fibres, and second, by the amplitude and number of excitatory postsynaptic potentials occurring over 5-10 s periods of 10 Hz stimulation. By distinguishing two types of morphological relationships between the pre- and postsynaptic elements, two contact indices were defined: a synaptic index (ratio of the number of synapses encountered to the number of perikarya explored) and a simple contact index corresponding to the same type of contacts, but without any membrane differentiation. Both the electrophysiological and morphological results showed that the first effects were detectable 4 days after axotomy, and that the main alterations in synaptic transmission and density occurred at 2 weeks. In addition, while in normal ganglia the excitatory postsynaptic potentials of B and C neurons reached the threshold for action potential generation in response to 10 Hz stimulation, about 29% of the axotomized neurons had subthreshold excitatory postsynaptic potentials 1 week after section. At 2 weeks, this proportion reached 65%, and the synaptic and simple contact indices, at 90% and 60% respectively, were significantly lower than the control ganglion indices. At longer times after axotomy, there was a discrepancy between the morphological and electrophysiological results: at 1 month, the synaptic index seemed to rise as the decline in the efficacy of synaptic transmission became more marked. The amplitude of the subthreshold excitatory postsynaptic potentials recorded in B neurons was 5.5 +/- 2.8 mV (mean +/- SD, n = 18); this value was significantly lower by about 50% than that measured 1 week after axotomy. In addition, the number of excitatory postsynaptic potentials in B neurons reached an average maximum of 83 +/- 29 for 100 stimuli applied at 10 Hz. Similar results were obtained for C neurons. Two months after axotomy, the physiological and morphological parameters of synaptic efficacy began to recover and return to normal values, but had not reached them by 4 months. These observations show that some synaptic transmission remains possible, even with a much reduced number of synaptic complexes. It is suggested that after axotomy, simple contacts also might be involved in synaptic transmission.

Animals↗

PubMed1992

Excitatory synaptic potentials in neurons of the deep nuclei in olivo-cerebellar slice cultures.

Excitatory postsynaptic potentials evoked in neurons of the deep cerebellar nuclei, either by electrical stimulation within the nuclei in cerebellar slice cultures or by electrical stimulation of olivary explants in olivo-cerebellar co-cultures, were investigated in the rat by means of intracellular recordings. In neurons of the deep cerebellar nuclei, stimulation of the nuclear tissue, as well as stimulation of the olivary tissue, induced a fast rising excitatory postsynaptic potential, followed by an inhibitory postsynaptic potential and a long-lasting excitation. The fast rising excitatory postsynaptic potential and the following inhibitory postsynaptic potential were blocked by 6-cyano-7-nitroquinoxaline-2,3-dione. The remaining depolarization was abolished by D-(-)-2-amino-5-phosphonovalerate, suggesting that this potential was mediated by N-methyl-D-aspartate receptors. With only D-(-)-2-amino-5-phosphonovalerate added to the bath, the slow excitation was depressed, whereas the fast excitatory and inhibitory postsynaptic potentials were not affected. In the presence of bicuculline, the 6-cyano-7-nitroquinoxaline-2,3-dione- and the D-(-)-2-amino-5-phosphonovalerate-sensitive excitatory postsynaptic potentials elicited by stimulation of the olivary tissue had the same latency, and were both graded with stimulation strength. The time-to-peak and the duration of the D-(-)-2-amino-5-phosphonovalerate-sensitive excitatory postsynaptic potentials were considerably longer than those of the 6-cyano-7-nitroquinoxaline-2,3-dione-sensitive excitatory postsynaptic potentials.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Amino-5-phosphonovalerate↗