Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Excitatory Postsynaptic Potentials”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 793 records · Page 44Linked to original sources
PubMed1991

Actions of (-)-baclofen on rat dorsal horn neurons.

The actions of a gamma-aminobutyric acid B (GABAB) agonist, (-)-baclofen, on the electrophysiological properties of neurons and synaptic transmission in the spinal dorsal horn (laminae I-IV) were examined by using intracellular recordings in spinal cord slice from young rats. In addition, the effects of baclofen on the dorsal root stimulation-evoked outflow of glutamate and aspartate from the spinal dorsal horn were examined by using high performance liquid chromatography (HPLC) with flourimetric detection. Superfusion of baclofen (5 nM to 10 microM) hyperpolarized, in a stereoselective and bicuculline-insensitive manner, the majority (86%) of tested neurons. The hyperpolarization was associated with a decrease in membrane resistance and persisted in a nominally zero-Ca2+, 10 mM Mg(2+)- or a TTX-containing solution. Our findings indicate that the hyperpolarizing effect of baclofen is probably due to an increase in conductance to potassium ions. Baclofen decreased the direct excitability of dorsal horn neurons, enhanced accommodation of spike discharge, and reduced the duration of Ca(2+)-dependent action potentials. Baclofen depressed, or blocked, excitatory postsynaptic potentials evoked by electrical stimulation of the dorsal roots. Spontaneously occurring synaptic potentials were also reversibly depressed by baclofen. Whereas baclofen did not produce any consistent change in the rate of the basal outflow of glutamate and aspartate, the stimulation-evoked release of the amino acids was blocked. The present results suggest that baclofen, by activating GABAB receptors, may modulate spinal afferent processing in the superficial dorsal horn by at least two mechanisms: (1) baclofen depresses excitatory synaptic transmission primarily by a presynaptic mechanism involving a decrease in the release of excitatory amino acids, and (2) at higher concentrations, the hyperpolarization and increased membrane conductance may contribute to the depressant effect of baclofen on excitatory synaptic transmission in the rat spinal dorsal horn.

Action Potentials↗
PubMedDate not supplied

[Long-term potentiation of the NMDA-dependent component of the EPSP in the hippocampus].

In the hippocampus, excitatory postsynaptic potential (EPSP) consists of two components, which are related to activation of different types of glutamate receptors. The first component is related to activation of receptors, sensitive to kainate and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA), and the second one to N-methyl-D-aspartate (NMDA) (AMPA- and NMDA-EPSP respectively). The components are differently changed after induction of long-term potentiation (LTP), which is a known model for cellular mechanisms of learning, memory and a number of pathological processes. Activation of NMDA-receptors is a necessary step of induction of LTP, whereas maintenance of LTP related mainly with increase of AMPA-EPSP. However, in some situations NMDA-EPSP could be also increased after tetanisation or other influences which induce LTP. The increase of NMDA-EPSP could be an important neural mechanism for learning and memory or for neurodegenerative processes, related to disfunction of memory. Recent experimental data and hypothesis about mechanisms of NMDA-EPSP LTP are reviewed.

Animals↗
PubMed2001

Spread of synaptic potentials through electrical synapses in Retzius neurones of the leech.

We studied the spread of excitatory postsynaptic potentials (EPSPs) through electrical synapses in Retzius neurones of the leech Haementeria officinalis. The pair of Retzius neurones in each ganglion is coupled by a non-rectifying electrical synapse. Both neurones displayed synchronous EPSPs of varying amplitudes and rise times. The kinetics of synchronous EPSPs was similar in 79 % of the EPSP pairs. In the remaining 21 %, one EPSP was smaller and slower than the other, suggesting its passive spread from the other neurone. The proportion of these events increased to 75 % in the presence of Mg(2+) in the bathing fluid. This spread of EPSPs from one neurone to another was tested by producing artificial EPSPs by current injection into the soma of one Retzius neurone. The artificial EPSPs were smaller and arrived more slowly at the soma of the coupled neurone. The coupling ratios for the EPSPs were proportional to the coupling ratio for long steady-state pulses in different neuronal pairs. Our results showed that EPSPs spread from one Retzius neurone to the other and support the idea that EPSP spread between electrically coupled neurones may contribute to the integration processes of neurones.

Animals↗
PubMed1998

Comparison of corticomotoneuronal EPSPs and macro-MUPs in amyotrophic lateral sclerosis.

We correlated the size of the corticomotoneuronal excitatory postsynaptic potential (CM-EPSP) arising in a single spinal motor neuron with the function of the target motor unit as measured by conventional and macro EMG in early amyotrophic lateral sclerosis (ALS). Macro motor unit potentials (macro-MUPs) were recorded from a surface electrode after spike-triggered averaging in the extensor digitorum communis muscle. The size of the CM-EPSP projecting to the same motor unit was measured from changes in the firing probability of single motor units induced by transcranial magnetic stimulation using peristimulus time histograms. In controls, the amplitudes of CM-EPSPs and macro-MUPs correlated inversely, probably reflecting a lower input resistance of larger spinal motoneurons. In ALS the amplitude of macro-MUPs did not correlate with that of CM-EPSPs and one third of normal ALS motor units had a reduced or temporally dispersed CM-EPSP. The findings indicate primary dysfunction of the corticomotoneuronal projection system in ALS that is independent of functional changes of spinal motoneurons.

Action Potentials↗
PubMed2004

Enhanced excitability compensates for high-pressure-induced depression of cortical inputs to the hippocampus.

High pressure (>1.0 MPa) induces the high-pressure neurological syndrome (HPNS) characterized by increased excitability of the CNS and cognitive impairments involving memory disorders. The perforant-path transfer of cortical information to the hippocampal formation is important for memory acquisition. High pressure may alter information transfer in this connection. We used rat corticohippocampal slices for studying the effect of pressure on the transfer function between synaptic inputs from the medial perforant path (MPP) and spike generation by granule cells (GC) of the dentate gyrus. High pressure (10.1 MPa) reduced single MPP field excitatory postsynaptic potential (fEPSP) amplitude and slope by nearly 50%. Field antidromic action potentials (AAPs) elicited by stimulation of GC axons, and population spike (PS) generation by the pressure-depressed MPP fEPSP were not significantly altered at hyperbaric conditions. Nevertheless the relationship PS/fEPSP increased at high pressure, indicating dendritic hyperexcitability in the GC. PSs elicited by paired-pulse MPP fEPSPs at 10- to 200-ms interstimulus intervals and PS generated by trains of five fEPSPs at 25 Hz were also not affected in spite of severe pressure-induced synaptic depression. Similarly, trains of AAPs at 25-50 Hz were not significantly changed. Trains of fEPSPs at higher frequency (50 Hz), however, induced additional spikes at high pressure, indicating pressure disruption of the regular low-pass filter properties of the DG. Such effect was closely mimicked by partial blockade of GABAA inhibition. High pressure depresses synaptic activity while increases excitability in the neuronal dendrites but not in the axons. This mechanism, allowing neuronal communication at low input signals, may partially cope with pressure effects at the low frequency range (<25 Hz) but losses reliability at higher frequencies (>50 Hz).

Action Potentials↗
PubMed1996

Block of glutamate decarboxylase decreases GABAergic inhibition at the crayfish synapses: possible role of presynaptic metabotropic mechanisms.

1. The cytosolic concentration of a neurotransmitter is believed to be an important factor determining its release. The effects of 3-mercaptopropionic acid (MP) and aminooxyacetic acid (AOAA), glutamate decarboxylase (GAD) blockers, on GABAergic postsynaptic and presynaptic inhibitory neurotransmission were examined in the crayfish (Procambarus clarkii) opener neuromuscular synapses. 2. Intracellular recordings of evoked excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs) as well as loose macropatch clamp measurements of excitatory postsynaptic currents (EPSCs) and inhibitory postsynaptic currents (IPSCs) were used to evaluate the effects of the drugs, which were applied exclusively to the nerve bundle. 3. Under normal conditions, a stimulus train to the inhibitor preceding the excitor stimulation elicited a large reduction in EPSP amplitude in a time interval-dependent manner. This inhibition is effected by postsynaptic as well as presynaptic processes. 4. Treatment with MP or AOAA decreased the IPSP amplitude and its altered conductance but had no effect on the IPSP reversal potential or the resting potential of the cell. They did, however, slightly increase the Rin of the fiber. 5. Quantal analysis of single IPSCs revealed that GAD blockers increased the number of failures and thus reduced quantal content (m), diminished the probability of release (p), but did not affect the quantum current (q) or the statistical parameter (n), believed to be the number of available active zones. 6. Quantal analysis of EPSCs, released after interaction with the inhibitor, revealed a reduction in m without any effect on q. GAD blockers greatly reduced the efficacy of this inhibition without affecting the EPSC q. 7. GAD blockers increased the output of the excitor release sites by the following mechanisms: 1) increased EPSC, 2) increased EPSC facilitation, or 3) enhancement of spontaneous activity (miniature EPSCs). 8. Short time incubation with picrotoxin and CGP-35348 eliminated IPSCs and evoked inhibition. However, longer exposure (90 min) increased the excitor responses, similarly to the effects of GAD blockers. 9. Baclofen, a gamma-aminobutyric acid-B (GABAB) agonist, antagonized AOAA effects on evoked inhibition. 10. These results demonstrate that GAD blockers decrease postsynaptic and presynaptic inhibition by reducing both tonic and evoked release, most likely by diminishing p. 11. The reduction in GABA synthesis and release revealed a complex mechanism for GABAergic metabotropic regulation of inhibition efficacy and the release from the excitor glutamatergic terminals.

3-Mercaptopropionic Acid↗
PubMed2006

Input-output relations in the entorhinal cortex-dentate-hippocampal system: evidence for a non-linear transfer of signals.

In the current study we analyzed the input-output relations in the entorhinal-dentate-hippocampal system, a major network involved in long-term memory. In anesthetized guinea pigs, the system was driven by activation of perforant path neurons in the entorhinal cortex (ENT), via presubicular fibers directly stimulated in the dorsal psalterium. Perforant path neuron discharge activated in parallel the dentate gyrus (DG) and hippocampal field CA2. Whereas the output from the DG activated hippocampal field CA3, the output from the sole field CA2 was sufficient for activation of field CA1. Signals from field CA3 operated in concert with CA2, likely contributing to discharge field CA1. These findings indicate the existence of two in parallel disynaptic systems: an ENT-CA2-CA1 and an ENT-DG-CA3 system. The convergence of the latter with the former gives origin the classical trisynaptic circuit, the ENT-DG-CA3-CA1 system. The input-output relations between the population excitatory postsynaptic potentials (pEPSP) evoked in the DG, CA3, CA2 and CA1 and the population spike (PS) evoked in the structure upstream (the input) were described by smooth sigmoid curves. In contrast, the input-output relations of the PS versus the pEPSP within each structure were described by steep sigmoid curves. The net input-output functions of the DG (ENT-DG system), field CA2 (ENT-CA2 system), field CA3 (ENT-DG-CA3 system) and field CA1 (ENT-CA2-CA1&ENT-DG-CA3-CA1 system) were described by sigmoid curves. While the DG and field CA2 exhibited steep sigmoids, fields CA3 and CA1 had less steep sigmoid functions. The present study demonstrates that all structures downstream to the ENT operate according to sigmoid input-output functions, characterized by specific parameters. These different behaviors may contribute to different memory processes. We additionally demonstrate that field CA1 can be activated by field CA2, independently from field CA3. This functional dissociation between CA3 and CA1 may subserve specific roles of each field in memory encoding/retrieval.

Action Potentials↗
PubMed2004

Synaptic integration in electrically coupled neurons.

Interactions among chemical and electrical synapses regulate the patterns of electrical activity of vertebrate and invertebrate neurons. In this investigation we studied how electrical coupling influences the integration of excitatory postsynaptic potentials (EPSPs). Pairs of Retzius neurons of the leech are coupled by a nonrectifying electrical synapse by which chemically induced synaptic currents flow from one neuron to the other. Results from electrophysiology and modeling suggest that chemical synaptic inputs are located on the coupled neurites, at 7.5 microm from the electrical synapses. We also showed that the space constant of the coupled neurites was 100 microm, approximately twice their length, allowing the efficient spread of synaptic currents all along both coupled neurites. Based on this cytoarchitecture, our main finding was that the degree of electrical coupling modulates the amplitude of EPSPs in the driving neurite by regulating the leak of synaptic current to the coupled neurite, so that the amplitude of EPSPs in the driving neurite was proportional to the value of the coupling resistance. In contrast, synaptic currents arriving at the coupled neurite through the electrical synapse produced EPSPs of constant amplitude. This was because the coupling resistance value had inverse effects on the amount of current arriving and on the impedance of the neurite. We propose that by modulating the amplitude of EPSPs, electrical synapses could regulate the firing frequency of neurons.

Action Potentials↗
PubMed1998

Glycine induces a novel form of long-term potentiation in the superficial layers of the superior colliculus.

1. The mammalian superior colliculus (SC) is a midbrain nucleus containing space maps of different sensory modalities which show various forms of age- and activity-dependent plasticity in vivo and in vitro. In the present study, we aimed to characterize the role of glycine (Gly) receptors in the SC, and we observed that application of glycine (Gly; 500 microM and 3 mM) for 7 min to SC slices of adult guinea-pigs caused a novel form of long-term potentiation (termed LTPgly) of evoked excitatory postsynaptic potentials recorded in the superficial layers. 2. The strength of potentiation was found to be concentration-dependent and partially independent from synaptic stimulation. 3. LTPgly did not involve NMDA receptor activation as proven by the lack of inhibition by 100 microM D,L-2-amino-5-phosphonovaleric acid (APV) and 10 microM MK-801. 4. LTPgly could only be masked but not prevented by strychnine (100 microM) and remained undisturbed in the presence of picrotoxin (100 microM). 5. Inhibition of carbonic anhydrase by acetazolamide (20 microM) had no effect on LTPgly suggesting that the excitatory action of Gly is not due to a differential breakdown of the Cl-/HCO3 gradients. 6. As indicated by the inhibition of LTPgly of the fEPSP slope by the L-type calcium channel blocker nifedipine (20 microM), voltage-dependent calcium channels are the source for Ca2+ elevation as the intracellular trigger. 7. Our data provide the first evidence for a role of Gly in SC synaptic transmission. They illustrate a so far unknown action of Gly which can lead to long-lasting changes of synaptic efficacy and which is not mediated via NMDA-related or strychnine-sensitive binding sites.

Animals↗
PubMed2001

Modulation of synaptic transmission in hippocampal CA1 neurons by a novel neurotoxin (beta-pompilidotoxin) derived from wasp venom.

We examined the effects of beta-pompilidotoxin (beta-PMTX), a neurotoxin derived from wasp venom, on synaptic transmission in the mammalian central nervous system (CNS). Using hippocampal slice preparations of rodents, we made both extracellular and intracellular recordings from the CA1 pyramidal neurons in response to stimulation of the Schaffer collateral/commissural fibers. Application of 5-10 microM beta-PMTX enhanced excitatory postsynaptic potentials (EPSPs) but suppressed the fast component of the inhibitory postsynaptic potentials (IPSPs). In the presence of 10 microM bicuculline, beta-PMTX potentiated EPSPs that were composed of both non-NMDA and NMDA receptor-mediated potentials. Potentiation of EPSPs was originated by repetitive firings of the presynaptic axons, causing summation of EPSPs. In the presence of 10 microM CNQX and 50 microM APV, beta-PMTX suppressed GABA(A) receptor-mediated fast IPSPs but retained GABA(B) receptor-mediated slow IPSPs. Our results suggest that beta-PMTX facilitates excitatory synaptic transmission by a presynaptic mechanism and that it causes overexcitation followed by block of the activity of some population of interneurons which regulate the activity of GABA(A) receptors.

2-Amino-5-phosphonovalerate↗
PubMed2000

AMPA receptor antagonists, GYKI 52466 and NBQX, do not block the induction of long-term potentiation at therapeutically relevant concentrations.

The involvement of alpha-amino-3-hydroxy-5-methylizoxazole-4-propionic acid (AMPA) receptors in induction of long-term potentiation (LTP) was examined in rat hippocampal slice preparation. Using conventional extracellular recording, excitatory postsynaptic potentials (EPSPs) and population action potentials (PSs), evoked by low-frequency stimulation of the Schaffer collateral-commissural fibres, were recorded in the CA1 region. The effects of a competitive AMPA receptor antagonist, 6-nitro-7-sulfamoylbenzo(f)quinoxaline-2, 3-dione (NBQX), and that of a non-competitive blocker, 1-(4-aminophenyl)-4-methyl-7,8-methylendioxy-5H-2,3-benzodiazepine (GYKI 52466) have been examined. 0.25-0.5 microM of NBQX and 20-40 microM of GYKI 52466 did not suppress the induction of LTP. LTP was attenuated only at the highest concentrations tested (1 microM NBQX or 80 microM GYKI 52466). These in vitro concentrations, however, exceed the brain levels needed for in vivo anticonvulsant action. Furthermore, even at the highest concentrations both compounds suppressed only the expression but not the induction of LTP. Namely after their washout LTP reappeared. Thus, at pharmacologically relevant concentrations these AMPA receptor antagonists apparently do not suppress LTP, a cellular mechanism underlying memory formation. These experiments suggest that in clinical practice AMPA receptor blockade may have some advantage over N-methyl-D-aspartate receptor antagonism, which is accompanied by severe memory impairment.

Animals↗
PubMed2005

Melatonin inhibits hippocampal long-term potentiation.

The goal of this study is to investigate the effect of the hormone melatonin on long-term potentiation and excitability measured by stimulating the Schaffer collaterals and recording the field excitatory postsynaptic potential from the CA1 dendritic layer in hippocampal brain slices from mice. Application of melatonin produced a concentration-dependent inhibition of the induction of long-term potentiation, with a concentration of 100 nm producing an approximately 50% inhibition of long-term potentiation magnitude. Long-duration melatonin treatments of 6 h were also effective at reducing the magnitude of long-term potentiation. Melatonin (100 nm) did not alter baseline evoked responses or paired-pulse facilitation recorded at this synapse. The inhibitory actions of melatonin were prevented by application of the melatonin (MT) receptor antagonist luzindole as well as the MT2 receptor subtype antagonist 4-phenyl-2-propionamidotetraline. These inhibitory actions of melatonin were lost in mice deficient in MT2 receptors but not those deficient in MT1 receptors. In addition, application of the protein kinase A inhibitor H-89 both mimicked the effects of melatonin and precluded further inhibition by melatonin. Finally, the application an activator of adenylyl cyclase, forskolin, overcame the inhibitory effects of melatonin on LTP without affecting the induction of long-term potentiation on its own. These results suggest that hippocampal synaptic plasticity may be constrained by melatonin through a mechanism involving MT2-receptor-mediated regulation of the adenylyl cyclase-protein kinase A pathway.

Animals↗
PubMed2006

Synaptic origin of the respiratory-modulated activity of laryngeal motoneurons.

To determine the synaptic source of the respiratory-related activity of laryngeal motoneurons, spike-triggered averaging of the membrane potentials of laryngeal motoneurons was conducted using spikes of respiratory neurons located between the Bötzinger complex and the rostral ventral respiratory group as triggers in decerebrate, paralyzed cats. We identified one excitatory and two inhibitory sources for inspiratory laryngeal motoneurons, and two inhibitory sources for expiratory laryngeal motoneurons. In inspiratory laryngeal motoneurons, monosynaptic excitatory postsynaptic potentials were evoked by spikes of inspiratory neurons with augmenting firing patterns, and monosynaptic inhibitory postsynaptic potentials (IPSPs) were evoked by spikes of expiratory neurons with decrementing firing patterns and by spikes of inspiratory neurons with decrementing firing patterns. In expiratory laryngeal motoneurons, monosynaptic IPSPs were evoked by spikes of inspiratory neurons with decrementing firing patterns and by spikes of expiratory neurons with augmenting firing patterns. We conclude that various synaptic inputs from respiratory neurons contribute to shaping the respiratory-related trajectory of membrane potential of laryngeal motoneurons.

Action Potentials↗
PubMed2005

Zonisamide at clinically relevant concentrations inhibits field EPSP but not presynaptic fiber volley in rat frontal cortex.

We investigated the effect of Zonisamide (ZNS), a newer anti-epileptic drug, on field potentials and neuropropagation in rat frontal cortex, with the aid of the 64-channel multi-electrode dish (MED64) system. The amplitude and propagation of field potentials were expressed dimensionally in the MED64 system. ZNS (3-100 microM) inhibited the amplitude and propagation of field excitatory postsynaptic potentials (fEPSP) in a concentration dependent manner. In contrast, ZNS could not suppress the amplitude and propagation of the presynaptic fiber volley (PrV) at clinically relevant concentrations (10-30 microM). Stimulating dependency with reduction fEPSP was seen in the presence of ZNS at clinically relevant concentrations, but not with PrV. The reduction of fEPSP amplitude was not accompanied by a change in paired-pulse facilitation. These data suggest that at clinically relevant concentrations of ZNS, the suppression of neuronal propagation is at least partially due to the postsynaptic mechanism, probably through alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors.

Action Potentials↗
PubMed2001

Excitatory synaptic inputs on myenteric Dogiel type II neurones of the pig ileum.

The synaptic input on myenteric Dogiel type II neurones (n = 63) obtained from the ileum of 17 pigs was studied by intracellular recording. In 77% of the neurones, electrical stimulation of a fibre tract evoked fast excitatory postsynaptic potentials (fEPSPs) with an amplitude of 6 +/- 5 mV (mean +/- S.D.) and lasting 49 +/- 29 ms. The nicotinic nature of the fEPSPs was demonstrated by superfusing hexamethonium (20 microM). High-frequency stimulation (up to 20 Hz, 3 seconds) did not result in a rundown of the fEPSPs, and did not evoke slow excitatory or inhibitory postsynaptic potentials. The effects of neurotransmitters, possibly involved in these excitatory responses, were investigated. Pressure microejection of acetylcholine (10 mM in pipette) resulted in a fast nicotinic depolarisation in 67%(18/27) of the neurones (13 +/- 9 mV, duration 7.0 +/- 7.2 seconds) as did 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP) application (10 mM; 14 +/- 10 mV, duration 4.1 +/- 2.8 seconds) in 76% of the cells. The fast nicotinic response to acetylcholine was sometimes (6/27) followed by a slow muscarinic depolarisation (8 +/- 4 mV; duration 38.7 +/- 10.8 seconds). Immunostaining revealed 5-hydroxytryptamine hydrochloride (5-HT)- and calcitonin gene-related peptide (CGRP)-positive neuronal baskets distributed around and in close vicinity to Dogiel type II neuronal cell bodies. Microejection of 5-HT (10 mM) resulted in a fast nicotinic-like depolarisation (12 +/- 6 mV, duration 3.0 +/- 1.3 seconds) in 4 of 8 neurones tested, whereas microejection of CGRP (20 mM) gave rise to a slow muscarinic-like depolarisation (6 +/- 2 mV, duration 56.0 +/- 27.5 seconds) in 8 of 12 neurones tested. In conclusion, myenteric Dogiel type II neurones in the porcine ileum receive diverse synaptic input. Mainly with regard to the prominent presence of nicotinic responses, these neurones behave contrary to their guinea pig counterparts.

Acetylcholine↗
PubMed1999

Histochemistry and electrophysiology of cultured adult rabbit pancreatic neurons.

Pancreatic neurons receive and integrate synaptic input from a wide variety of extrinsic nerves while providing the predominant innervation of pancreatic acini, ducts, and islets of Langerhans. Here we report the first primary cultures of adult rabbit pancreatic neurons, isolated from extrinsic nerves and secretory cells, and evaluate the neurochemical and electrical properties of these neurons. Pancreatic cultures consisted of single and clustered neurons, extended varicose processes after 3-4 days in culture, and formed interconnecting networks of neurons after 7-10 days. Isolated pancreatic islet cells, added to established neuron cultures, remained attached and viable for several weeks and received innervation by varicose nerve fibers. Histochemical staining revealed populations of neurons positive for acetylcholinesterase (75%), NADPH-diaphorase (62%), nitric oxide synthase (73%), and/or vasoactive intestinal peptide (VIP) (65%). Intracellular recordings revealed active and passive electrical properties comparable to those of neurons from intact ganglia. Several distinct populations of neurons were identified by their firing patterns (phasic vs. tonic) in response to prolonged depolarizing currents or the amplitude and duration of their after-spike hyperpolarizations. Low-amplitude, pacemaker-like potentials were observed in 25% of the neurons and, in older cultures with extensive networks of fibers, spontaneous fast excitatory postsynaptic potentials (EP-SPs) also occurred. Thus these cultures retained the salient neurochemical and electrophysiologic properties observed in pancreatic neurons from intact ganglia and offer a good model for studies of the intrinsic innervation of the pancreas.

Acetylcholinesterase↗
PubMed1987

Long-term potentiation involves enhanced synaptic excitation relative to synaptic inhibition in guinea-pig hippocampus.

1. Tetanization of hippocampal pyramidal cell afferents travelling in stratum radiatum of area CA1 induces both long-term potentiation (l.t.p.) of extracellularly recorded excitatory postsynaptic potentials (e.p.s.p.s), and an increase in the number of cells firing, as measured by the extracellular population spike, for a given sized field e.p.s.p. The mechanism of this latter change, known as e.p.s.p.-spike (E-S) potentiation, was investigated in the guinea-pig hippocampal slice preparation. 2. Plots of the E-S relation before and after tetanization were constructed from measures taken over a series of stimulus strengths. Tetanization of afferents in stratum radiatum decreased the spike threshold by 24%, while the gamma-aminobutyric acid antagonist picrotoxin (PTX) decreased spike threshold by 72%. Sequential administration of PTX and tetanization, in either order, resulted in no more change in the E-S threshold than did PTX application alone. 3. Extracellular synaptic potentials, matched for initial slope before and after tetanization by adjusting the stimulus strength, showed an increased peak amplitude and increased peak latency following tetanization. PTX produced similar but larger percentage changes. Tetanization in the presence of PTX, however, did not alter the field potential wave shape. 4. Intracellular postsynaptic potentials (p.s.p.s) were also matched for initial slope before and after tetanization. Tetanization induced p.s.p. shape changes similar to those observed extracellularly, i.e. in the direction of less inhibition. Such changes did not occur in the presence of PTX. 5. Inhibitory p.s.p.s (i.p.s.p.s) were studied in depolarized pyramidal cells with microelectrodes filled with QX-314. Tetanization of afferents in stratum radiatum produced i.p.s.p. increases in eight of nineteen cells. These increases were generally attributable to an increased activity in the recurrent inhibitory pathway. Tetanization of the alveus failed to produce any lasting increases in the i.p.s.p. amplitude. 6. Tetanization of afferents in stratum radiatum decreased the ratio of the intracellular i.p.s.p. to field e.p.s.p. over stimulus strengths below population spike threshold. Above population spike threshold, the ratio tended towards its pretetanization level. 7. The results indicate that E-S potentiation results from an increase in the level of depolarization reached by a synaptic potential of given initial slope. These findings support the hypothesis that tetanization induces greater l.t.p. of excitatory inputs onto pyramidal cells than of inputs onto feed-forward inhibitory interneurones.

Action Potentials↗
PubMed2005

Circadian regulation of hippocampal long-term potentiation.

The goal of this study is to investigate the possible circadian regulation of hippocampal excitability and long-term potentiation (LTP) measured by stimulating the Schaffer collaterals (SC) and recording the field excitatory postsynaptic potential (fEPSP) from the CA1 dendritic layer or the population spike (PS) from the soma in brain slices of C3H and C57 mice. These 2 strains of mice were of interest because the C3H mice secrete melatonin rhythmically while the C57 mice do not. The authors found that the magnitude of the enhancement of the PS was significantly greater in LTP recorded from night slices compared to day slices of both C3H and C57 mice. They also found significant diurnal variation in the decay of LTP measured with fEPSPs, with the decay slower during the night in both strains of mice. There was evidence for a diurnal rhythm in the input/output function of pyramidal neurons measured at the soma in C57 but not C3H mice. Furthermore, LTP in the PS, measured in slices prepared during the day but recorded during the night, had a profile remarkably similar to the night group. Finally, PS recordings were carried out in slices from C3H mice maintained in constant darkness prior to experimentation. Again, the authors found that the magnitude of the enhancement of the PS was significantly greater in LTP recorded from subjective night slices compared to subjective day slices. These results provide the 1st evidence that an endogenous circadian oscillator modulates synaptic plasticity in the hippocampus.

Animals↗