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PubMed2006

Nerve growth factor acutely potentiates synaptic transmission in vitro and induces dendritic growth in vivo on adult neurons in airway parasympathetic ganglia.

Elevated levels of nerve growth factor (NGF) and NGF-mediated neural plasticity may have a role in airway diseases such as asthma and chronic obstructive pulmonary disease (COPD). Although NGF is known to affect sensory and sympathetic nerves, especially during development, little is known regarding its effect on parasympathetic nerves, especially on adult neurons. The purpose of this study was to analyze the acute and chronic effects of NGF on the electrophysiological and anatomical properties of neurons in airway parasympathetic ganglia from adult guinea pigs. Using single cell recording, direct application of NGF caused a lasting decrease in the cumulative action potential afterhyperpolarization (AHP) and increased the amplitude of vagus nerve-stimulated nicotinic fast excitatory postsynaptic potentials. Neuronal responsiveness to nicotinic receptor stimulation was increased by NGF, which was blocked by the tyrosine kinase inhibitor, K-252a, implicating neurotrophin-specific (Trk) receptors. Neurotrophin-3 and brain-derived neurotrophic factor had no effect on the synaptic potentials, AHP, or nicotinic response; inhibition of cyclooxygenase with indomethacin inhibited the effect of NGF on the cumulative AHP. Forty-eight hours after in vivo application of NGF to the trachealis muscle caused an increase in dendritic length on innervating neurons. These results are the first to demonstrate that NGF increases the excitability of lower airway parasympathetic neurons, primarily through enhanced synaptic efficacy and changes to intrinsic neuron properties. NGF also had dramatic effects on the growth of dendrites in vivo. Such effects may indicate a new role for NGF in the regulation of parasympathetic tone in the diseased or inflamed lower airways.

Action Potentials↗
PubMed2006

Characterization of myenteric sensory neurons in the mouse small intestine.

We recorded from myenteric AH/Dogiel type II cells, demonstrated mechanosensitive responses, and characterized their basic properties. Recordings were obtained using the mouse longitudinal muscle myenteric plexus preparation with patch-clamp and sharp intracellular electrodes. The neurons had an action potential hump and a slow afterhyperpolarization (AHP) current. The slow AHP was carried by intermediate conductance Ca2+ -dependent K+ -channel currents sensitive to charybdotoxin and clotrimazole. All possessed a hyperpolarization-activated current that was blocked by extracellular cesium. They also expressed a TTX-resistant Na+ current with an onset near the resting potential. Pressing on the ganglion containing the patched neuron evoked depolarizing potentials in 17/18 cells. The potentials persisted after synaptic transmission was blocked. Volleys of presynaptic electrical stimuli evoked slow excitatory postsynaptic potentials (EPSPs) in 9/11 sensory neurons, but 0/29 cells received fast EPSP input. The slow EPSP was generated by removal of a voltage-insensitive K+ current. Patch-clamp recording with a KMeSO4-containing, but not a conventional KCl-rich, intracellular solution reproduced the single-spike slow AHPs and low input resistances seen with sharp intracellular recording. Cell-attached recording of intermediate conductance potassium channels supported the conclusion that the single-spike slow AHP is an intrinsic property of intestinal AH/sensory neurons. Unitary current recordings also suggested that the slow AHP current probably does not contribute significantly to the high resting background conductance seen in these cells. The characterization of mouse myenteric sensory neurons opens the way for the study of their roles in normal and pathological physiology.

Animals↗
PubMed1985

Properties of persistent sodium conductance and calcium conductance of layer V neurons from cat sensorimotor cortex in vitro.

Properties of the persistent sodium conductance and the calcium conductance of layer V neurons from cat sensorimotor cortex were examined in an in vitro slice preparation by use of a single microelectrode, somatic voltage clamp, current clamp, intra- and extracellular application of blocking agents, and extracellular ion substitution. The persistent sodium current (INaP) attained its steady level within 2-4 ms of a step change in voltage at every potential where it could be examined directly [to about 40 mV positive to resting potential (RP)]. Because of its fast onset INaP can be activated during a single excitatory postsynaptic potential (EPSP) and can influence the subsequent voltage time course and cell excitability. Application of a depolarizing holding potential greater than or equal to 20 mV positive to RP could inactivate spikes, thus allowing examination of INaP at voltages positive to spike threshold. At every potential where INaP was visible, it was mixed with a slow outward current. After depressing potassium currents with blocking agents, INaP could be observed during depolarizations to about 40 mV positive to RP where it is normally hidden by the larger outward currents. Indirect evidence suggests that INaP is present and large during prolonged depolarizations greater than 50 mV positive to RP. INaP was blocked by intracellular injection of the lidocaine derivative QX-314, as well as by extracellular tetrodotoxin (TTX). INaP was much more sensitive to QX-314 than was the height and rate of rise of the spike. This observation and the results in paragraph 3 above are best explained by separate INaP and spike sodium channels. After blockade of INaP and sodium spikes, Ca2+ spikes could be evoked only if potassium currents were first depressed. The Ca2+-dependent nature of the regenerative potentials was indicated by their disappearance when Co2+ or Mn2+ was substituted for Ca2+ in the perfusate and by the appearance of greatly enhanced potentials of similar form when Ba2+ was substituted for Ca2+. Ba2+ substitution greatly enhanced evoked and spontaneous synaptic potentials. Prolonged-plateau action potentials could be evoked in the presence of TTX and Ba2+. Ca2+ spike threshold was 30-40 mV positive to RP, which is significantly more positive than sodium spike threshold. Results of voltage clamp in the normal perfusate and in the presence of Ca2+-blockers or Ba2+ indicated that little or no Ca2+ conductance is activated in the voltage range 25 mV positive to RP where INaP is the dominant ionic current.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1997

Realistic simulation of the Aplysia siphon-withdrawal reflex circuit: roles of circuit elements in producing motor output.

The circuitry underlying the Aplysia siphon-elicited siphon-withdrawal reflex has been widely used to study the cellular substrates of simple forms of learning and memory. Nonetheless, the functional roles of the different neurons and synaptic connections modified with learning have yet to be firmly established. In this study we constructed a realistic computer simulation of the best-understood component of this network to better understand how the siphon-withdrawal circuit works. We used an integrate-and-fire scheme to simulate four neuron types (LFS, L29, L30, L34) and 10 synaptic connections. Each of these circuit components was individually constructed to match the mean or typical example of its biological counterpart on the basis of group measurements of each circuit element. Once each cell and synapse was modeled, its free parameters were fixed and not subject to further manipulation. The LFS motor neurons respond to sensory input with a brief phasic burst followed by a long-lasting period of tonic firing. We found that the assembled model network responded to sensory input in a qualitatively similar fashion, suggesting that many of the interneurons important for producing the LFS firing response have now been identified. By selectively removing different circuit elements, we determined the contribution of each of the LFS firing pattern. Our first finding was that the monosynaptic sensory neuron to motor neuron pathway contributed only to the initial brief burst of the LFS firing response, whereas the polysynaptic pathway determined the overall duration of LFS firing. By making more selective deletions, we found that the circuit elements responsible for transforming brief sensory neuron discharges into long-lasting LFS firing were the slow components of the L29-LFS fast/slow excitatory postsynaptic potentials. The inhibitory L30 neurons exerted a significant braking action on the flow of excitatory information through the circuit. Interestingly, L30 lost its ability to reduce the duration of LFS firing at high stimulus intensities. This was found to be due to the intrinsic nature of L30's current-frequency relationship. Some circuit elements, including interneuron L34, and the electrical coupling between L29 and L30 were found to have little impact when subtracted from the network. These results represent a detailed dissection of the functional roles of the different elements of the siphon-elicited siphon-withdrawal circuit in Aplysia. Because many vertebrate and invertebrate circuits perform similar tasks and contain similar information processing elements, aspects of these results may be of general significance for understanding the function of motor networks. In addition, because several sites in this network store learning-related information, these results are relevant to elucidating the functional significance of the distributed storage of learned information in Aplysia.

Animals↗
PubMed1996

Fimbria-fornix lesion impairs long-term potentiation in the dentate gyrus of the rat.

Bilateral aspiration lesions of the fimbria-fornix were performed in 10 male Sprague Dawley rats weighing 240-300 g under chloral hydrate narcose (420 mg/kg). Another 9 animals were operated in the same way, but no aspiration was carried out to constitute a control group. A week after surgery recording and stimulation electrodes were lowered to the dentate gyrus and the perforant path respectively, using the same narcose. After tetanic stimulation (10 trains at 400 Hz) a potentiation of the population spike develops in both groups, but the slope of the excitatory postsynaptic potential showed no potentiation in the lesioned group. Acetylcholinesterase histochemistry confirmed a severe reduction of the cholinergic innervation to the hippocampal formation, suggesting a causal relationship to the deficits seen in long-term potentiation. This impaired potentiation could be related to the memory deficits reported for fimbria-fornix lesioned rats. Such pattern of potentiation deviates from what has been described for aged, memory deficient rats, but closely corresponds to the changes described in infantile rats.

Acetylcholinesterase↗
PubMed1992

Cholinergic interneurons in the feeding system of the pond snail Lymnaea stagnalis. II. N1 interneurons make cholinergic synapses with feeding motoneurons.

The N1 neurons are a population of interneurons active during the protraction phase of the feeding rhythm. All the N1 neurons are coupled by electrical synapses which persist in a high Mg/low Ca saline which blocks chemical synapses. Individual N1 spikes produce discrete electrotonic postsynaptic potentials (PSPS) in other N1 cells, but the coupling is not strong enough to ensure 1:1 firing. Bursts of N1 spikes generate compound PSPS in the feeding motoneurons. The sign (excitation or inhibition) of the N1 input corresponds with the synaptic barrage recorded during the protraction phase. Discrete PSPS are only resolved in a Hi-Di saline. Their variation in latency and number can be explained by variation in electrotonic propagation within the electrically coupled network of N1 cells. The excitatory postsynaptic potentials (ESPS) in the 1 cell are reduced by 0.5 mM antagonists hexamethonium (HMT), atropine (ATR), curare (d-TC) and by methylxylocholine (MeXCh), all of which block the excitatory cholinergic receptor (Elliott et al. (Phil. Trans. R. Soc. Lond. 336, 157-166 (Preceding paper.) (1992)). The 1 cell EPSPS were transiently blocked by phenyltrimethylammonium (PTMA), which is both an agonist and antagonist at the 1 cell excitatory acetylcholine (ACh) receptor (Elliott et al. 1992). The inhibitory postsynaptic potential (IPSP) in the 3 cell is blocked by bath applications of MeXCh and PTMA, which both abolish the response of the 3 cell to ACh (Elliott et. al. 1992). The effects of the cholinergic antagonists on the response of 4 cluster and 5 cells to N1 stimulation matches their response to ACh (Elliott et al. 1992). It is concluded that the population of N1 cells are multiaction, premotor cholinergic interneurons.

Acetylcholine↗
PubMed1990

Alpha 2-adrenoceptors mediate the inhibition of cholinergic transmission in parasympathetic ganglia of the rabbit urinary bladder.

Intracellular recordings were made from neurons of vesical parasympathetic ganglia (VPG) isolated from the rabbit urinary bladder and maintained, in vitro. Bath-application of norepinephrine (NE, 500 nM-5 microM) caused a hyperpolarizing response at the postsynaptic membrane of VPG neurons in a concentration-dependent manner. NE blocked the action potential elicited by an orthodromic stimulation of preganglionic (pelvic) nerve fibers. At a relatively low concentration (5-100 nM), NE depressed the fast excitatory postsynaptic potential (EPSP), without producing the hyperpolarization. NE (100 nM) produced 49 +/- 17% (N = 5) decrease in the amplitude of the fast EPSP. NE did not depress the acetylcholine (ACh) potential produced by iontophoretic application of ACh to the ganglion cells. NE did not affect the amplitude of the miniature EPSP, while it reduced the frequency of miniature EPSPs. These results suggest that NE inhibits the nicotinic transmission in the rabbit VPG, probably reducing the ACh release from presynaptic nerve terminals. Epinephrine (1 microM) was more potent than NE (1 microM) in producing the hyperpolarization as well as the blockade of the fast EPSP amplitude. Isoproterenol was ineffective as an agonist for these inhibitory adrenoceptors. Clonidine mimicked the effect of NE on the fast EPSP. Yohimbine and idazoxan antagonized both the inhibition of the fast EPSP and the hyperpolarization produced by NE. These results suggest that alpha 2-adrenoceptors are responsible for the inhibition of the neuronal activity in parasympathetic ganglia of the rabbit urinary bladder. Immunohistochemical study demonstrated the presence of tyrosine hydroxylase (TH)-labelled neuronal elements in the VPG. They were a small proportion of principal neurons, their dendrites, and many varicose fibers.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1988

A persistent postsynaptic modification mediates long-term potentiation in the hippocampus.

Long-term potentiation (LTP) is a long-lasting enhancement of synaptic transmission that can be induced by brief repetitive stimulation of excitatory pathways in the hippocampus. One of the most controversial points is whether the process underlying the enhanced synaptic transmission occurs pre- or postsynaptically. To examine this question, we have taken advantage of the novel physiological properties of excitatory synaptic transmission in the CA1 region of the hippocampus. Synaptically released glutamate activates both NMDA and non-NMDA receptors on pyramidal cells, resulting in an excitatory postsynaptic potential (EPSP) with two distinct components. A selective increase in the non-NMDA component of the EPSP was observed with LTP. This result suggests that the enhancement of synaptic transmission during LTP is caused by an increased sensitivity of the postsynaptic neuron to synaptically released glutamate.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1978

Depression of spinal monosynaptic transmission by diethyl ether: quantal analysis of unitary synaptic potentials.

The site at which diethyl ether impairs transmission in the spinal monosynaptic pathway was studied by intracellular recording from lumbosacral motoneurons. The drug was administered by inhalation to spinal cats, in concentrations which produce surgical anesthesia. Ether had no significant effect on resting potential or input resistance of the cell membrane. It decreased the electrical excitability in some but not all motoneurons. This action may contribute to the depressant effects of ether. Monosynaptic excitatory postsynaptic potentials evoked by impulses in a single Ia afferent fiber (unitary EPSPs) of the triceps surae nerve were recorded from homonymous motoneurons. They were measured and their amplitude distribution was analyzed by a computer-aided procedure. The mean amplitude of the unitary EPSPs was 0.15 to 0.31 mV, and the mean number of transmitter quanta released by each impulse ranged from 1.5 to 4.1 before drug administration. Both values were decreased during inhalation of ether but recovered toward normal after the drug was discontinued. The mean amplitude of the EPSPs produced by one transmitter quantum was 0.08 to 0.15 mV and was not depressed during ether administration. It is concluded that either in anesthetic concentrations depresses synaptic potentials presynaptically by decreasing the amount of excitatory transmitter released, while leaving the chemosensitivity of the postsynaptic membrane unchanged.

Action Potentials↗
PubMed1995

Expression of LTP by AMPA and/or NMDA receptors is determined by the extent of NMDA receptors activation during the tetanus.

1. We have tested, in CA1 hippocampal slices, the hypothesis that the expression of long-term potentiation (LTP) by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and/or N-methyl-D-aspartate (NMDA) receptors depends on the degree of NMDA receptors activation during the tetanus. 2. Slices were perfused in an artificial cerebrospinal fluid (ACSF) containing glycine (1 microM), bicuculline (5 microM) and a low Mg2+ concentration (0.3 mM). To measure the AMPA and NMDA receptor-mediated field excitatory postsynaptic potential (fEPSPA and fEPSPN, respectively), we have used the following procedure: control fEPSPA was first measured, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM) was then added, and fEPSPN was evoked. CNQX was washed, and once control fEPSPA was recorded, the Schaffer collaterals were tetanized at a weak or a strong intensity. The slope of fEPSPA was measured for 30-45 min followed by that of fEPSPN after the application of CNQX. 3. At a weak intensity (TW, which corresponds to a fEPSPA of approximately 0.3 mV of amplitude and no fEPSPN), the tetanic stimulation generated LTP of fEPSPA (58.7 +/- 8.1% mean +/- SE, n = 9) but no significant potentiation of the fEPSPN (11.2 +/- 2.2%, n = 9). These values were significantly different (P < 0.05, analysis of variance, Fisher test). 4. In 9 of 13 slices, tetanic stimulation of strong intensity (Ts, intensity corresponding to a fEPSPN of approximately 0.3 mV of amplitude) generated LTP of fEPSPN (89.1 +/- 17.2%) but not of fEPSPA (9.44 +/- 2.8%). In the four remaining slices the tetani induce LTP of both fEPSPA and fEPSPN (81.7 +/- 14.7% and 101 +/- 35.6%, respectively, both values were not significantly different). 5. We then examined the effects of decreasing fEPSPN by 50% in LTP generated by Ts and Tw. In the presence of 7-Chlorokynurenate (7Cl(-)-Kyn; 6 microM; n = 6), an antagonist of the allosteric glycine site of the NMDA receptors, Ts generated LTP of fEPSPA (63.2 +/- 8.2%) but not of fEPSPN (12.6 +/- 4.0%). Both values were significantly different. Tw still evoked LTP of fEPSPA but of smaller magnitude (29.8 +/- 6.3%, n = 8) than the one obtained in the absence of the antagonist (58.7 +/- 8.1%). Both values were significantly different. 6. The present observation suggests that l) LTP of fEPSPA has a lower threshold than that of fEPSPN, i.e., stronger activation of NMDA receptors during the tetani is required to induce LTP of fEPSPN than the one required for inducing LTP of fEPSPA; and 2) there is a bell-shaped relationship between the degree of activation of NMDA receptors during the tetani and the magnitude of LTP of the fEPSPA: tetani that generate LTP of fEPSPN have a low probability to induce LTP of fEPSPA. We suggest that AMPA and NMDA components are potentiated through two different presumably postsynaptic processes.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1997

Electrophysiological studies of rat substantia nigra neurons in an in vitro slice preparation after middle cerebral artery occlusion.

We studied sequential changes in electrophysiological profiles of the ipsilateral substantia nigra neurons in an in vitro slice preparation obtained from the middle cerebral artery-occluded rats. Histological examination revealed marked atrophy and neurodegeneration in the ipsilateral substantia nigra pars reticulata at 14 days after middle cerebral artery occlusion. Compared with the control group, there was no significant change in electrical membrane properties and synaptic responses of substantia nigra pars reticulata neurons examined at one to two weeks after middle cerebral artery occlusion. On the other hand, there was a significant increase in the input resistance and spontaneous firing rate of substantia nigra pars compacta neurons at 13-16 days after middle cerebral artery occlusion. Furthermore, inhibitory postsynaptic potentials evoked by stimulation of the subthalamus in substantia nigra pars compacta neurons was suppressed at five to eight days after middle cerebral artery occlusion. At the same time excitatory postsynaptic potentials evoked by the subthalamic stimulation was increased. Bath application of bicuculline methiodide (50 microM), a GABA(A) receptor antagonist, significantly increased the firing rate of substantia nigra pars compacta neurons from intact rats. These results strongly suggest that changes in electrophysiological responses observed in substantia nigra pars compacta neurons is caused by degeneration of GABAergic afferents from the substantia nigra pars reticulata following middle cerebral artery occlusion. While previous studies indirectly suggested that hyperexcitation due to deafferentation from the neostriatum may be a major underlying mechanism in delayed degeneration of substantia nigra pars reticulata neurons after middle cerebral artery occlusion, the present electrophysiological experiments provide evidence of hyperexcitation in substantia nigra pars compacta neurons but not in pars reticulata neurons at the chronic phase of striatal infarction.

Animals↗
PubMed2003

Long-term potentiation as an electrophysiological assay for morphine dependence and withdrawal in rats: an in vitro study.

Using a long-term potentiation (LTP) method, we attempted to establish an electrophysiological assay for morphine dependence and withdrawal in rats in vitro. The field excitatory postsynaptic potential (fEPSP) and orthodromic population spikes (OPS) were recorded from stratums radiatum and pyramidale, respectively, of area CA1 following stimulation of Schaffer collaterals in control and morphine-dependent slices. To induce LTP, a 100 Hz primed-burst stimulation protocol was used. Although morphine exposure had excitatory effects on control slices, namely, an increase in the amplitude of primary population spikes (PSs) and appearance of extra PSs, slices taken from dependent rats demonstrated tolerance to morphine. LTP of the fEPSP was not changed in slices from dependent animals although dependent slices did show an enhanced OPS LTP compared to control ones, which was attenuated by morphine exposure. In the presence of morphine, naloxone caused a withdrawal phenomenon; apparent as a robust enhanced OPS LTP in dependent slices. So we propose morphine-naloxone withdrawn slices as a suitable in vitro withdrawal-like model. Such an in vitro preparation could provide a convenient practical experimental tool for examination of the probable molecular and cellular mechanisms involved in withdrawal states.

Animals↗
PubMed1986

The pathway for the slow inhibitory postsynaptic potential in bullfrog sympathetic ganglia.

Intracellular and sucrose gap recording techniques were used to examine synaptically evoked potentials and the response of neurons in bullfrog paravertebral sympathetic ganglia to muscarinic agonists. These neurons were defined as either B or C cells on the basis of the conduction velocity of antidromically evoked action potentials. Following stimulation of preganglionic C-fibers in the rostral portion of the VIIIth spinal nerve, a fast nicotinic excitatory postsynaptic potential (EPSP) and a slow atropine-sensitive inhibitory postsynaptic potential (IPSP) could be recorded intracellularly in C cells of the IXth and Xth paravertebral ganglia treated with 70 microM d-tubocurarine chloride (dTC). Under these conditions, local iontophoretic application of acetylcholine (ACh) could produce a slow hyperpolarization of C cell membrane potential. ACh hyperpolarizations or slow IPSPs were not detected in ganglionic B cells. Stimulation of the preganglionic B-fibers in the sympathetic chain produced a fast nicotinic EPSP and a slow muscarinic EPSP in ganglionic B cells. A small population of C cells also received cholinergic B-fiber innervation from the sympathetic chain and exhibited a slow IPSP upon tetanic stimulation of this pathway. When curarized ganglia were examined by means of sucrose gap recording, superfusion of the muscarinic agonist, methacholine (MCh), produced an initial hyperpolarization (MChH) followed by a depolarization (MChD). Both responses were blocked by atropine and therefore presumably reflect the activation of muscarinic receptors involved in the generation of the slow IPSP and the slow EPSP, respectively. Although synaptic transmission was blocked by Ringer solution containing 4 mM Co2+, neither this solution nor 10 microM tetrodotoxin reduced the amplitude of the MChH. The MChH was slightly reduced by Ringer solution containing 0.1 mM Ca2+, however, the response could be restored by the addition of 6 mM Mg2+. These results indicate that the MChH in curarized bullfrog sympathetic ganglia results from a direct muscarinic action on ganglionic cells. This suggests that the slow IPSP is mediated by ACh released from cholinergic preganglionic fibers that make synaptic contact with ganglionic C cells.

Acetylcholine↗
PubMed1995

Ethanol enhances muscarinic cholinergic neurotransmission in rat hippocampus in vitro.

Previous studies from our laboratory showed that ethanol enhances muscarinic excitatory responses in rat hippocampal neurons in vivo and, like muscarinic agonists, reduces the M-current (IM) in these neurons in vitro. Therefore, we used extracellular and intracellular recording techniques in the hippocampal slice preparation to examine the mechanisms underlying this ethanol-muscarinic interaction. Surprisingly, superfusion or local application of low concentrations of acetylcholine (ACh), carbachol (CCh) or muscarine reduced the amplitudes of CA1 field potentials evoked by stratum radiatum (SR) stimulation. This effect was blocked by 1 microM atropine but was independent of the method of agonist application, the site of application or the SR stimulus paradigm. In intracellular and extracellular single unit recordings, cholinergic depressions of field potentials were correlated with: (1) depolarization of pyramidal neurons; (2) spike discharge increases; (3) reduction of amplitudes of postsynaptic potentials and (4) reduction of late afterhyperpolarizations (AHPs). Superfusion of low ethanol concentrations (11-22 mM) alone had little effect on SR-evoked field potentials but enhanced (by 10-90%) both the depressions of evoked field potentials and depolarizations elicited by the muscarinic agonists. Ethanol (22-44 mM) also enhanced both the amplitude and duration of the muscarinic slow excitatory postsynaptic potentials (sEPSPs) recorded intracellularly in CA1 and CA3 neurons. This effect was enhanced by eserine and blocked by atropine, verifying involvement of muscarinic receptors. These results suggest that: (1) caution be used in interpreting results of field potential studies regarding drug-induced excitability changes; and (2) ethanol in just-intoxicating concentrations enhances endogenous muscarinic synaptic transmission as well as responses to exogenous muscarinic agonists.

Acetylcholine↗
PubMed1987

Effect of a spider toxin (JSTX) on excitatory postsynaptic current at neuromuscular synapse of spiny lobster.

1. We studied the blocking properties of a spider (Nephila clavata) toxin (JSTX) purified from venom on the spiny lobster neuromuscular junction. 2. When a small amount of JSTX was applied to the neuromuscular junction, the excitatory postsynaptic potential (EPSP) was partially suppressed. The amplitude of EPSPs remained at a steady level for several hours during the washing of the preparation, showing that the action of JSTX is irreversible. 3. We recorded the excitatory postsynaptic current (EPSC) from synaptic site using a macro-patch electrode. The amplitude of EPSC increased linearly with hyperpolarization of the membrane potential in the presence and absence of JSTX. 4. The decay phase time constant of EPSC and spontaneous EPSC was decreased by hyperpolarizing the membrane potential both in the absence and in the presence of JSTX. The relationship between the decay time constant and the membrane potential was not modified by JSTX. 5. It is suggested that JSTX irreversibly blocks EPSC by acting on the site that is apart from the ionic channel of the glutamate receptor molecule.

Animals↗
PubMed1991

Synaptic plasticity at crayfish neuromuscular junctions: facilitation and augmentation.

Simultaneous intracellular recordings from presynaptic nerve terminals and postsynaptic muscle fibers were used to investigate the extent to which changes in presynaptic voltage may contribute to short-term facilitation and augmentation of transmitter release at neuromuscular junctions of the crayfish (Procambarus simulans) opener muscle. Presynaptic nerve terminals have an average resting membrane potential of about -80 mV, single action potentials have an average foot-to-peak amplitude of about 98 mV, and single action potentials are followed by a depolarizing after potential (DAP) of about 10 mV. During stimulus trains of 9-16 impulses at 100 Hz, amplitudes of excitatory postsynaptic potentials (EPSPs) continuously facilitate up to 100-fold. This dramatic facilitation is associated with only slight increases in the peak voltage and duration of APs for the first 2-4 pulses in such a stimulus train. Foot-to-peak total amplitude of APs usually decreases after the first pulse in a stimulus train. The data strongly suggest that short-term facilitation is not due to changes in the amplitude or duration of APs invading the presynaptic terminal. Upon cessation of a longer stimulus train, the presynaptic terminal exhibits a hyperpolarizing after potential (HAP) up to 16 mV in amplitude depending upon the frequency (10-100 Hz) and duration (1-10 sec) of the tetanic stimulation. This post-tetanic HAP decays with a time constant of 10-20 sec, which is approximately equal to the third time constant of decay in EPSP amplitude (augmentation) following tetanic stimulation. Hence, presynaptic voltage changes and/or processes associated with these voltage changes (e.g., accumulation of ions, changes in ionic conductances, etc.) may be partly responsible for augmentation of EPSP amplitudes.

Animals↗
PubMed1995

Electrophysiological characterization of dopaminergic and non-dopaminergic neurones in organotypic slice cultures of the rat ventral mesencephalon.

The aim of the present study was to characterize electrophysiologically neurones in organotypic cultures of the rat ventral mesencephalon and to compare these results with results published for the same neurones in other types of preparation. Intracellular recordings were obtained in 3- to 8-week-old organotypic slice cultures of the ventral mesencephalon prepared from new-born rats. Dopaminergic neurones were distinguished from non-dopaminergic neurones by staining with the autofluorescent serotonin analogue 5,7-dihydroxytryptamine and briefly viewing the preparation with short exposures to ultraviolet (UV) light (365 nm). Short exposures to UV light did not affect the electrophysiological properties. There were no significant differences between dopaminergic and non-dopaminergic neurones with regard to resting membrane potential or action potential threshold and amplitude, and in both types of neurone spontaneous burst activity and glutamatergic excitatory postsynaptic potentials were seen. There were differences in the following parameters, which can be used to distinguish between the two types of neurone. Dopaminergic neurones had broad action potentials (2-9 ms), high input resistance (mean 81 M omega), were silent or fired spontaneously at a low frequency (0-9 Hz), and no spontaneous GABAA-ergic inhibitory postsynaptic potentials or inward rectification were present. In contrast, non-dopaminergic neurones had fast action potentials (0.6-3.2 ms), low input resistance (mean 32 M omega), were silent or fired spontaneously at relatively high firing frequency (0-28 Hz), and sometimes inhibitory postsynaptic potentials and inward rectification were seen. In the presence of 1 microM tetrodotoxin and 10 mM tetraethylammonium, Ca2+ spikes could be evoked in both dopaminergic and non-dopaminergic neurones. Dopaminergic neurones in 3- to 8-week-old organotypic slice cultures have a number of distinguishing electrophysiological characteristics similar to those recorded in other types of acute or cultured preparations. However, some intrinsic regulatory mechanisms, namely the slow oscillatory potentials, inward rectification and the K+ current, IA, seem to be missing in the cultured neurones.

5,7-Dihydroxytryptamine↗
PubMed1986

Phorbol ester promotes growth of synaptic plasticity.

Iontophoretic application of the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) to the intact rat hippocampus enhances potentiation produced by subsequent high frequency stimulation of the perforant path. The decay of the enhanced population spike amplitude recorded in the hilar dentate gyrus was prevented in animals receiving ejections of TPA, as compared to controls which decayed to baseline values within 2 h following high frequency stimulation. In fact, growth of the potentiated response was observed beginning at 45 min. Similar results were observed with the population excitatory postsynaptic potential slope, a measure of the synaptic response. Since tumour-promoting phorbol esters are known to translocate and activate protein kinase C (PKC) and PKC is translocated to the membrane following hippocampal potentiation, a role for membrane-associated PKC in the regulation of synaptic plasticity is suggested.

Action Potentials↗