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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↗
PubMed2000

Participation of low-threshold calcium spikes in excitatory synaptic transmission in guinea pig medial frontal cortex.

We studied the activation of low-threshold calcium spikes (LTS) by excitatory postsynaptic potentials in pyramidal neurons from guinea pig medial frontal cortex with intracellular recording. We used extracellular bicuculline and phaclofen and intracellular QX-314 to block inhibitory synaptic potentials and sodium currents. Postsynaptic potentials were evoked by stimulation of layer I. We found that large (> 10-15 mV) excitatory synaptic potentials evoked from membrane potentials more negative than -75 mV were able to trigger LTS. The activation of LTS resulted in an increase of the rising slope or amplitude of the synaptic potentials depending on the size of the excitatory postsynaptic potential (EPSP). We used 100 microM NiCl2 to confirm the presence of LTS as part of the EPSPs. The N-methyl-D-aspartate (NMDA) and non-NMDA components of the excitatory synaptic potentials were isolated using (+/-)2-amino-5-phosphonovaleric acid (APV; 50 microM) or 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 20 microM); both components could, independently, trigger an LTS. With recordings made with K+ acetate-filled electrodes, we show that the activation of LTS was critical to allow excitatory synaptic potentials to reach the threshold of action potential firing; also, this amplification of synaptic responses produced the firing of more than a single action potential by the postsynaptic cell. These results demonstrate that in cortical pyramidal neurons the activation of low-threshold calcium spikes results in the amplification of synaptic responses.

2-Amino-5-phosphonovalerate↗
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↗
PubMed1996

Histamine H3 receptor-mediated depression of synaptic transmission in the dentate gyrus of the rat in vitro.

1. The effects of histamine on excitatory synaptic transmission in the dentate gyrus region of rat hippocampal slices were examined using extracellular and whole-cell patch-clamp recording techniques. The GABAA receptor antagonist picrotoxin (50 microM) was present in the bath in all experiments. 2. Histamine (0.7-70 microM) reversibly depressed field excitatory postsynaptic potentials (fEPSPs) or excitatory postsynaptic currents (EPSCs) recorded intracellularly by up to 30%. The presynaptic fibre volley and EPSC reversal potential were unaffected by histamine, as were responses following pressure ejection of the glutamate receptor agonist S-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (S-AMPA) into the slice. 3. Histamine (7 microM) depressed equally the AMPA and N-methyl-D-aspartate (NMDA) components of the dual-component EPSC, recorded at -40 mV. 4. In addition to depressing synaptic transmission, histamine also reduced the magnitude of paired-pulse depression (PPD; 40 ms interpulse interval) of the medial perforant path EPSC. 5. Histamine depressed medial perforant path EPSCs more strongly than lateral perforant path EPSCs. Paired-pulse facilitation (PPF; 40 ms interpulse interval) in the lateral perforant path was enhanced by histamine. 6. The effects of histamine on synaptic transmission and PPD were mimicked by the selective H3 receptor agonist R-alpha-methylhistamine (0.1-10 microM) but not by the selective H2 receptor agonist dimaprit (10 microM). Similarly, the H3 receptor antagonist thioperamide (10 microM) blocked the effect of histamine whereas the H1 antagonist mepyramine (1 microM) and the H2 receptor antagonist cimetidine (50 microM) were ineffective. 7. Histamine actions on synaptic transmission and PPD were not occluded by application of the metabotropic glutamate agonist L-2-amino-4-phosphonobutyrate (AP4). 8. The results indicate that histamine depresses synaptic transmission in the dentate gyrus by binding to histamine H3 receptors located on perforant path terminals. The mechanism by which histamine depresses transmission is independent of that used by class III metabotropic glutamate receptors.

Animals↗
PubMed1996

Differential responsiveness of neocortical areas in the parieto-occipital region to low-intensity stimulation in vitro.

1. Extracellular recording techniques were used to map the responses to low-intensity stimuli across rat neocortical slices prepared from the parieto-occipital region. Intracellular recordings were obtained in regions of particular interest. After electrophysiological recording, slices were fixed in paraformaldehyde (4%) and Nissl-stained to allow identification of cytoarchitectonically discrete areas. 2. In most neocortical areas of the parieto-occipital region (Par1, HL, Fr1, Fr2), low-intensity stimuli applied to layer V evoked only short monophasic field excitatory postsynaptic potentials (fEPSPs) in layer II/III. In Oc2 (secondary visual cortex, rostral part), however, a long-lasting potential (up to 450 ms) consistently followed the short monophasic response seen in the other areas. 3. The late response observed in Oc2 was characterized by its inter-stimulus variability, polyphasic appearance and N-methyl-D-aspartate (NMDA)-receptor dependence. Intracellular recordings obtained from layer II/III pyramidal neurons located in Oc2 revealed short-latency, monophasic early excitatory postsynaptic potentials (eEPSPs) followed by long-lasting excitatory postsynaptic potentials (eEPSPs) followed by long-lasting excitatory postsynaptic potentials (EPSPs), which often triggered several action potentials 4. Recordings with two extracellular electrodes, one positioned directly above the stimulation electrode and the other at a variable distance (but also in layer II/III), suggested that the corresponding excitation spreads across the slice, but does not cross the cytoarchitectonic borders of Oc2. 5. Our data indicate that the electrophysiological responses to low-intensity stimuli differ within the parieto-occipital region of the rat neocortex. The type of response elicited depends on the cytoarchitectonic area in which the stimulus is applied. The results raise the question of whether further differences between neocortical subregions, with respect to basic electrophysiological properties, exist.

Animals↗
PubMed1998

Long-term cellular dysfunction after focal cerebral ischemia: in vitro analyses.

The long-term (< or = six months) functional consequences of permanent middle cerebral artery occlusion were studied with in vitro extra- and intracellular recording techniques in adult mouse neocortical slices. After survival times of one to three days, 28 days and six months, intracellular recordings from layers II/III pyramidal cells in the vicinity of the infarct did not reveal any statistically significant changes in the intrinsic membrane properties when compared to age-matched control animals. However, a pronounced hyperexcitability could be observed upon orthodromic synaptic stimulation in neocortical slices obtained from mice 28 days after induction of ischemia. Low-intensity electrical stimulation of the afferents elicited particularly in this group epileptiform extracellular field potential responses and intracellular excitatory postsynaptic potentials, that were longer in duration as compared to the controls. When the N-methyl-D-aspartate receptor-mediated excitatory postsynaptic potential was pharmacologically isolated in a bathing solution containing 0.1 mM Mg2+ and 10 microM 6-cyano-7-nitroquinoxaline-2,3-dione, the synaptic responses were longer and larger in the ischemic cortex as compared to the controls. Higher stimulus intensities evoked in normal medium a biphasic inhibitory postsynaptic potential, that contained in the 28 days post-ischemia group a prominent amino-phosphonovaleric acid-sensitive component, indicating a strong concurrent activation of a N-methyl-D-aspartate receptor-mediated excitatory postsynaptic potential. This pronounced co-activation could only be observed in the 28 days ischemic group, and neither after one to three days or six months post-ischemia nor in the controls. The quantitative analysis of the efficiency of stimulus- evoked inhibitory postsynaptic potentials recorded in amino-phosphono-valeric acid revealed a reduction of GABA-mediated inhibition in ischemic cortex. Although this reduction in intracortical inhibition may already contribute to an augmentation of N-methyl-D-aspartate receptor-mediated excitation, our results do also indicate that the function of N-methyl-D-aspartate receptors is transiently enhanced in the ischemic cortex. This transient hyperexcitability does not only cause cellular dysfunction in the vicinity of the infarct, but may also contribute to neuronal damage due to excitotoxicity.

Animals↗
PubMed1997

Synaptic excitation in the dorsal nucleus of the lateral lemniscus: whole-cell patch-clamp recordings from rat brain slice.

The synaptic events underlying the excitation of neurons in the rat's dorsal nucleus of the lateral lemniscus were studied by whole-cell patch-clamp recordings in a brain slice preparation of the auditory midbrain. Both current-clamp and voltage-clamp data were obtained with the brain slice submerged in artificial cerebrospinal fluid. The rats were between 21 and 35 days of age at the time the recordings were made. Synaptic responses were evoked by a bipolar stimulating electrode placed on the lateral lemniscus just ventral to the dorsal nucleus. To eliminate glycinergic inhibitory responses, all physiological data were gathered with 0.5 microM strychnine added to the saline bath. Under current-clamp conditions, excitatory postsynaptic potentials could be subdivided into early and late components. The early component produced a single, highly reliable, short-latency spike and the later component produced a more variable, long-latency spike or train of spikes. The non-N-methyl-D-aspartate antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione, completely blocked the early excitatory postsynaptic potential and its associated action potential. The N-methyl-D-aspartate antagonist, D,L-2-amino-5-phosphonovaleric acid, blocked the later excitatory postsynaptic potential and its action potentials. Typically, both early and late excitatory postsynaptic potentials could be recorded from the same cell, but the early excitatory postsynaptic potential was evoked at lower stimulus levels and had a larger amplitude than the later excitatory postsynaptic potential. Under voltage-clamp conditions, dorsal nucleus of the lateral lemniscus neurons responded to stimulation of the lateral lemniscus with excitatory postsynaptic currents. Outward excitatory postsynaptic currents were recorded with holding potentials that depolarized the cell membrane and inward currents were seen when the cell was hyperpolarized. The current-voltage (I-V) relation of the early peak portion of the excitatory postsynaptic current was nearly linear, whereas the I-V relation of the later excitatory postsynaptic current (12 ms after the peak) was non-linear over the range between -50 and - 100 mV. The outward excitatory postsynaptic current consisted of an early current that was selectively blocked by 6-cyano-7-nitroquinoxaline-2,3-dione and a later current that was blocked by D,L-2-amino-5-phosphonovaleric acid. In artificial cerebrospinal fluid with normal concentrations of Mg2+, the inward excitatory postsynaptic current was blocked by 6-cyano-7-nitroquinoxaline-2,3-dione, but was not affected by D,L-2-amino-5-phosphonovaleric acid. In Mg2+-free artificial cerebrospinal fluid. however, the early component of the inward excitatory postsynaptic current was selectively blocked by 6-cyano-7-nitroquinoxaline-2,3-dione and a later component was blocked by D,L-2-amino-5-phosphonovaleric acid. The results indicate that both N-methyl-D-aspartate and non-N-methyl-D-aspartate receptor-mediated synaptic responses are present in dorsal nucleus of the lateral lemniscus neurons of rats at 21-35 days of age. The N-methyl-D-aspartate component had a longer time-course and a higher threshold than the non-N-methyl-D-aspartate component, and was subject to a voltage-dependent Mg2+ block when the cell's membrane was hyperpolarized. The long-duration N-methyl-D-aspartate component is probably responsible for the prolonged inhibitory effect of dorsal nucleus of the lateral lemniscus neurons on physiological responses in the rat's inferior colliculus.

Action Potentials↗
PubMed1998

Adenosine A2 receptors modulate hippocampal synaptic transmission via a cyclic-AMP-dependent pathway.

Blockade of adenosine A2 receptors has been shown to significantly reduce the level of tetanus-induced long-term potentiation in area CA1 of rat hippocampus [Kessey K. et al. (1997) Brain Res. 756, 184-190; Sekino Y. et al. (1991) Biochem. biophys. Res. Commun. 181, 1010-1014]. In the present study, the effects of A2 receptor activation and blockade on the modulation of normal synaptic transmission and tetanus-induced long-term potentiation were examined at the Schaffer-CA1 synapse in rat hippocampal slices. A2 receptor activation reversibly enhanced synaptic transmission evoked by low-frequency test pulses as measured by the dendritic field excitatory postsynaptic potential. In the presence of A1 receptor blockade, A2 activation further enhanced the excitatory postsynaptic potential, while A2 receptor blockade resulted in a reversible decrease of the excitatory postsynaptic potential. The A2a receptor agonist, CGS21680, had no effect on the excitatory postsynaptic potential, suggesting that tonic activation of A2b receptors contributes to synaptic transmission under normal physiological conditions. Furthermore, we investigated the contribution of A2 receptors to the level of tetanus-induced long-term potentiation. Under control conditions, a single tetanus potentiated the excitatory postsynaptic potential by 63.5% relative to baseline 30 min post-tetanus. In contrast, tetanus-induced long-term potentiation during A2 blockade was 21.3%. A2 receptor activation increased the level of tetanus-induced long-term potentiation to 90.2%. Because A2 receptors are known to stimulate cyclic-AMP accumulation, the possible involvement of cyclic-AMP was examined. Forskolin, a direct adenylate cyclase activator, and 8-bromo-cyclic-AMP, a membrane-permeable analog of cyclic-AMP, were able to reconstitute tetanus-induced long-term potentiation during A2 receptor blockade; however, the inactive analog 1,9-dideoxyforskolin had no effect, indicating that the effects of A2 activation on synaptic transmission were mediated largely through the regulation of intracellular cyclic-AMP. Because A1 receptors exert an opposing effect on synaptic transmission relative to A2 receptors, these results suggest that the stoichiometry of A1 versus A2 receptor activation appears to play an important role in the modulation of normal synaptic transmission and long-term potentiation in the CA1 region of the hippocampus.

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↗
PubMed1997

On the role of muscarinic and peptidergic receptors in ganglionic transmission in bullfrogs in vivo.

Synaptic activity of individual B and C cells in the paravertebral sympathetic ganglia of urethan-anesthetized bullfrogs was monitored with intracellular electrodes. Postganglionic activity from the B and C fiber populations was monitored with suction electrodes. Intravenous infusion of muscarine (0.1 ml of 8 microM) excited individual B cells and increased the amplitude and rate of spontaneous, postganglionic B fiber population discharges. Muscarine also increased the number of action potentials (APs) within each burst of synaptic activity in individual C cells. Because atropine (0.1 ml of 0.1 microM) had little or no effect on postganglionic population B or C fiber activity, the muscarinic slow inhibitory postsynaptic potentials and slow excitatory postsynaptic potentials (EPSPs) are unlikely to be involved in the transmission, modulation, or integration of postganglionic outflow in vivo. Atropine did, however, decrease the number of APs per burst in individual C cells, an effect that could be explained if excitatory presynaptic muscarinic receptors exist on C fiber terminals. Stimulation of preganglionic C fibers at "physiological" frequencies evoked a lasting afterdischarge in postganglionic B fibers that was blocked by a combination of atropine and [D-pyro-Glu1,D-Phe2,D-Trp3,6]-luteinizing hormone-releasing hormone (LHRH). Release of LHRH from C fiber terminals and activation of the peptidergic, late-slow EPSP mechanism in B cells may therefore play a role in ganglionic transmission in vivo.

Action Potentials↗
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↗
PubMed1998

Increasing age reduces expression of long-term depression and dynamic range of transmission plasticity in CA1 field of the rat hippocampus.

Long-term depression, depotentiation and long-term potentiation of field excitatory postsynaptic potentials in the CA1 field of the hippocampus were studied in slices from two-, 12-, 24- and 36-week-old rats. Long-term potentiation was induced by stimulating afferent fibres for 1 s at 100 Hz. Long-term depression was induced either by stimulating the afferent pathways twice for 15 min at 1 Hz (protocol 1), giving in total 1800 pulses, or by stimulating the fibres at 5 min intervals twice at 1 Hz for 5 min followed by 5 min stimulation at 5 Hz (protocol 2), giving in total 2100 pulses. We found significant long-term depression in slices of all groups stimulated with protocol 1; however, the magnitude of long-term depression in slices from 24- and 36-week-old rats was significantly lower than that in slices from two- and 12-week old rats, although there was no such difference in the magnitude of long-term potentiation between slices. Stimulation protocol 2 induced long-term depression only in slices from two- and 12-week-old rats. Comparison of the dynamic range of transmission plasticity in slices from two- and 36-week-old rats, calculated as the difference between the nearly saturated long-term potentiation and nearly saturated depotentiation, revealed a significantly smaller dynamic range in slices from 36-week-old rats in comparison with slices from two-week-old animals. The decrease in the dynamic range in slices from 36-week-old rats was due to a diminished capacity to depotentiate the nearly saturated long-term potentiation and not due to a decreased long-term potentiation expression in these slices. In contrast to long-term depression, in which the slope of the field excitatory postsynaptic potentials consistently and significantly decreased below the baseline level, the nearly saturated depotentiation did not decrease below the original, pre-long potentiation baseline level. The results demonstrate that increasing age reduces expression of long-term depression and the dynamic range of transmission plasticity.

Aging↗
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↗
PubMed1998

Synaptic interactions between crista hair cells in the statocyst of the squid Alloteuthis subulata.

Intracellular injections of the fluorescent dye Lucifer yellow into the various cell types within the anterior transverse crista segment of the statocyst of squid revealed that the primary sensory hair cells and both large and small first-order afferent neurons have relatively simple morphologies, each cell having a single, unbranched axon that passes directly into the small crista nerve that innervates the anterior transverse crista. However, the small first-order neurons have short dendritic processes occurring in the region of the sensory hair cells. The secondary sensory hair cells have no centripetal axons, but some have long processes extending from their bases along the segment. Simultaneous intracellular recordings from pairs of the different cell types in the anterior transverse crista segment demonstrated that electrical coupling is widespread; secondary sensory hair cells are coupled electrically along a hair cell row, as are groups of primary sensory hair cells. Secondary sensory hair cell also are coupled to neighboring small first-order afferent neurons. However, this coupling is rectifying in that it only occurs from secondary sensory hair cells to first-order afferent neurons. Direct electrical stimulation of the small crista nerve to excite the efferent axons revealed efferent connections to both the primary sensory hair cells and the small first-order afferent neurons. These efferent responses were of three types: excitatory or inhibitory postsynaptic potentials and excitatory postsynaptic potentials followed by inhibitory postsynaptic potentials. The functional significance of the cell interactions within the crista epithelium of the statocyst of squid is discussed and comparisons drawn with the balance organs of other animals.

Action Potentials↗
PubMed2000

Noradrenergic regulation of parvocellular neurons in the rat hypothalamic paraventricular nucleus.

Noradrenergic projections to the hypothalamic paraventricular nucleus have been implicated in the secretory regulation of several anterior pituitary hormones, including adrenocorticotropin, thyroid-stimulating hormone, growth hormone and prolactin. In an attempt to elucidate the effects of norepinephrine on the central control of pituitary hormone secretion, we looked at the actions of norepinephrine on the electrical properties of putative parvocellular neurons of the paraventricular nucleus using whole-cell current-clamp recordings in hypothalamic slices. About half (51%) of the putative parvocellular neurons recorded responded to norepinephrine with either a synaptic excitation or a direct inhibition. Norepinephrine (30-300microM) caused a marked increase in the frequency of excitatory postsynaptic potentials in about 36% of the parvocellular neurons recorded. The increase in excitatory postsynaptic potentials was blocked by prazosin (10microM), but not by propranolol (10microM) or timolol (20microM), indicating that it was mediated by alpha(1)-adrenoreceptor activation. It was also blocked by ionotropic glutamate receptor antagonists, suggesting that the excitatory postsynaptic potentials were caused by glutamate release. The increase in excitatory postsynaptic potentials was completely abolished by tetrodotoxin, indicating the spike dependence of the norepinephrine-induced glutamate release. In a separate group comprising 14% of the parvocellular neurons recorded, norepinephrine elicited a hyperpolarization (6.2+/-0.69mV) that was blocked by the beta-adrenoreceptor antagonists, propranolol (10microM) and timolol (20microM), but not by the alpha(1)-receptor antagonist, prazosin (10microM). This response was not blocked by tetrodotoxin (1.5-3microM), suggesting that it was caused by a direct postsynaptic action of norepinephrine. The topographic distribution within the paraventricular nucleus of the norepinephrine-responsive and non-responsive parvocellular neurons was mapped based on intracellular biocytin labeling and neurophysin immunohistochemistry. These data indicate that one parvocellular subpopulation, consisting of about 36% of the paraventricular parvocellular neurons, receives an excitatory input from norepinephrine-sensitive local glutamatergic interneurons, while a second, separate subpopulation, representing about 14% of the parvocellular neurons in the paraventricular nucleus, responds directly to norepinephrine with a beta-adrenoreceptor-mediated inhibition. This suggests that excitatory inputs to parvocellular neurons of the paraventricular nucleus are mediated mainly by an intrahypothalamic glutamatergic relay, and that only a relatively small subset of paraventricular parvocellular neurons receives direct noradrenergic inputs, which are primarily inhibitory.

Adrenergic alpha-Agonists↗