Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Synaptic 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 757 records · Page 42Linked to original sources
PubMed2006

Postsynaptic mechanisms are essential for forskolin-induced potentiation of synaptic transmission.

It has been demonstrated that stimulation of protein kinase A (PKA) results in enhanced synaptic transmission in the hippocampus and other brain areas. To investigate mechanisms of the PKA-mediated potentiation of synaptic transmission, we used rat hippocampal embryonic cultures. In low-density cultures, paired recordings under the perforated patch demonstrated that 15-min forskolin treatment produced long-lasting potentiation of evoked excitatory postsynaptic currents (eEPSCs) mediated by the cAMP/PKA pathway. eEPSC amplitudes increased to 240 +/- 10% of baseline after 15 min of forskolin treatment (early). After forskolin washout, eEPSCs declined to a potentiated level. Potentiation was sustained for > or = 85 min after forskolin washout and, 60 min after forskolin washout, constituted 152 +/- 7% of baseline (late potentiation). Disruption of presynaptic processes with the whole cell configuration and internal solution containing PKA inhibitor peptide did not affect forskolin-induced potentiation. Disruption of postsynaptic processes, in contrast, impaired early potentiation and abolished late potentiation. Study of mEPSCs confirmed the contribution of postsynaptic mechanisms. Forskolin-induced enhancement of mEPSC frequency observed under the perforated patch was attenuated by the whole cell configuration. Forskolin also induced an increase of mEPSC amplitudes in the perforated patch, but not in the whole cell, experiments. Potentiation of eEPSCs was not activity dependent, persisting in the absence of stimulation. NMDA receptor blockade did not abolish forskolin-induced potentiation. In summary, we demonstrate that forskolin-induced potentiation of eEPSCs was mediated by postsynaptic mechanisms, presumably by upregulation of AMPA receptors by phosphorylation.

Animals↗
PubMedDate not supplied

[Ultrastructural mechanism of the long-term potentiation of synaptic transmission].

A review. The data concerning the structural changes that accompany long-term potentiation (LTP) of synaptic transmission are analyzed. A bulk of morphological studies is aimed at searching for quantitative and qualitative structural LTP signs and elucidating the involvement of cytoskeleton in their formation. The role of cytoskeletal protein actin in synaptic structural and functional modification is discussed. On the basis of experimental evidence obtained by the authors a proposal is made that actin is involved into the LTP not only as a contractile protein but as a cable which strengthen the electrotonic properties of the synapses.

Actin Cytoskeleton↗
PubMed1974

Equilibrium potential for the postsynaptic response in the squid giant synapse.

The reversal potential for the EPSP in the squid giant synapse has been studied by means of an intracellular, double oil gap technique. This method allows the electrical isolation of a portion of the axon from the rest of the fiber and generates a quasi-isopotential segment. In order to make the input resistance of this nerve segment as constant as possible, the electroresponsive properties of the nerve membrane were blocked by intracellular injection of tetraethylammonium (TEA) and local extracellular application of tetrodotoxin (TTX). Thus, EPSP's could be evoked in the isolated segment with a minimal amount of electroresponsive properties. The reversal potential for the EPSP (EEPSP) was measured by recording the synaptic potential or the synaptic current during voltage clamping. The results indicate that EEPSP may vary from +15 to +25 mV, which is more positive than would be expected for a 1:1 conductance change for Na(+) and K(+) (approximately -15 mV) and too negative for a pure Na(+) conductance ((+)40 mV). This latter value (E(Na)) was directly determined in the voltage clamp experiments. The results suggest that the synaptic potential is probably produced by a permeability change to Na(+) to K(+) in a 4:1 ratio. No change in time-course was observed in the synaptic current at clamp levels of -100 and +90 mV. The implications of a variable ratio for Na(+)-K(+) permeability in subsynaptic-postsynaptic membranes are discussed.

Animals↗
PubMed1985

Muscarinic M1 and M2 receptors mediate depolarization and presynaptic inhibition in guinea-pig enteric nervous system.

Intracellular recordings were made from guinea-pig myenteric and submucous plexus neurones. Nicotinic excitatory post-synaptic potentials (fast e.p.s.p.s) and slow e.p.s.p.s were recorded in both plexuses; adrenergic inhibitory post-synaptic potentials (i.p.s.p.s) were recorded from submucous plexus neurones. The effects of muscarinic agonists and antagonists were examined on the synaptic potentials in those neurones in which these substances did not change the membrane potential. Muscarine, oxotremorine, methylfurmethide and McNeil A343 reversibly depressed the amplitude of the fast e.p.s.p. in a concentration-dependent way. Hyoscine, pirenzepine and 4-diphenylacetoxy-N-methyl-piperidine (4-DAMP) caused a parallel shift to the right of the agonist dose-response curves. These muscarinic antagonists themselves did not alter the amplitudes of fast e.p.s.p.s evoked by low frequency (0.05-0.1 Hz) stimulation. Antagonist pA2 values (the negative logarithm of the dissociation equilibrium constant) were determined while recording from individual neurones. pA2 values were: pirenzepine 7.0, hyoscine 8.9, and 4-DAMP 8.7. I.p.s.p.s in the submucous plexus were also depressed by muscarinic agonists, and this was competitively reversed by pirenzepine and 4-DAMP, with apparent pA2 values of 6.9 and 8.7 respectively. Muscarinic antagonists alone increased the amplitude of the i.p.s.p. evoked either by single or repeated stimuli. This enhancement was observed with low concentrations of antagonists and did not become greater when the concentrations were increased. Muscarinic agonists depolarized about one-quarter of myenteric and submucous plexus neurones. Low concentrations of pirenzepine antagonized these depolarizations; the pA2 value was 8.4. Cholinergic slow e.p.s.p.s recorded in some myenteric neurones were depressed or abolished by pirenzepine; concentrations that caused 50% inhibition (IC50) for this action ranged from 10 to 60 nM. It is concluded that presynaptic muscarinic receptors, activation of which inhibits the release of acetylcholine and noradrenaline, are the m2 type. Post-synaptic muscarinic receptors, activation of which depolarizes the membrane, are of the m1 type. The results also suggest that acetylcholine may exert a tonic inhibition of noradrenaline release in the submucous plexus through m2 receptors, and mediates the slow e.p.s.p. in the myenteric plexus through m1 receptors.

Action Potentials↗
PubMed1984

Ethanol-induced modulation of the membrane potential and synaptic activity of trigeminal motoneurons during sleep and wakefulness.

In the present study we investigated the direct actions of ethanol on the membrane properties and excitatory and inhibitory postsynaptic potentials of trigeminal motoneurons in chronic cats. During states of sleep and wakefulness, extracellular and intracellular recordings were carried out together with juxtacellular (somatic and dendritic) and intracellular pressure injections of 0.05-2.5 M ethanol solutions in femtoliter quantities. Juxtacellularly applied ethanol induced: a sequence of excitatory-inhibitory alterations in firing activity which were accompanied by depolarizing-hyperpolarizing shifts in the resting membrane potential; a decrease in the amplitude of action potentials; and a depression in excitatory and inhibitory postsynaptic potentials. Intracellular ethanol injections resulted in depolarization of the membrane potential and a decrease in the amplitude of action potentials as well as a reduction in the amplitude of excitatory and inhibitory postsynaptic potentials. Both juxtacellularly and intracellularly applied ethanol affected the membrane potential and synaptic activity in a fashion that was not dependent upon the animal's behavioral state of sleep or wakefulness.

Action Potentials↗
PubMed1983

Projection of single pulmonary stretch receptors to solitary tract region.

1. Central projections of single slowly adapting pulmonary stretch receptors were mapped in the medulla by the technique of spike-triggered averaging of extracellular field potentials. Discharge of pulmonary stretch receptors was recorded in continuity from the nodose ganglion; this activity provided the trigger for an averaging computer. 2. These pulmonary stretch receptors were characterized by a linear increase in firing rate in response to increases in transpulmonary pressure, an adaptation index, and peripheral axonal and intramedullary conduction velocities. 3. In accordance with the terminology used by Munson and Sypert (21), three types of electrical potentials were observed for the projection of a pulmonary stretch receptor in the medulla. Axonal potentials were recorded when the brain stem electrode was in the vicinity of the afferent axon. Terminal potentials were recorded when the electrode was adjacent to terminations of the afferent axon. Focal synaptic potentials were recorded when the electrode was near postsynaptic units receiving input from the pulmonary stretch receptor. Maxima of terminal potentials were recorded in a region 1 mm rostral to the obex in the medial nucleus of the tractus solitarius (six cases), in the ventrolateral nucleus of the tractus solitarius (three cases), and in an area just dorsolateral to the tractus solitarius (two cases). Focal synaptic potentials for five pulmonary stretch receptors were observed in a region 1 mm rostral to obex. Maxima of these potentials were recorded in the medial nucleus of tractus solitarius (two cases), in the ventrolateral nucleus of tractus solitarius (two cases), and in an area just dorsolateral to the tractus solitarius (one case). 4. Occasionally both terminal and focal synaptic potentials were observed for the same pulmonary afferent. The difference in the latencies of these potentials fell within the range previously reported for monosynaptic connections of muscle spindle Ia and group II afferents for alpha-motoneurons. This suggests that the afferents of pulmonary stretch receptors have monosynaptic connections with neurons in the medial nucleus of the tractus solitarius, in the ventrolateral nucleus of the tractus solitarius, and in an area dorsolateral to the tractus solitarius.

Action Potentials↗
PubMed2004

A cephalic projection neuron involved in locomotion is dye coupled to the dopaminergic neural network in the medicinal leech.

It is widely appreciated that the selection and modulation of locomotor circuits are dependent on the actions of higher-order projection neurons. In the leech, Hirudo medicinalis, locomotion is modulated by a number of cephalic projection neurons that descend from the subesophageal ganglion in the head. Specifically, descending brain interneuron Tr2 functions as a command-like neuron that can terminate or sometimes trigger fictive swimming. In this study, we demonstrate that Tr2 is dye coupled to the dopaminergic neural network distributed in the head brain. These findings represent the first anatomical evidence in support of dopamine (DA) playing a role in the modulation of locomotion in the leech. In addition, we have determined that bath application of DA to the brain and entire nerve cord reliably and rapidly terminates swimming in all preparations exhibiting fictive swimming. By contrast, DA application to nerve cords expressing ongoing fictive crawling does not inhibit this motor rhythm. Furthermore, we show that Tr2 receives rhythmic feedback from the crawl central pattern generator. For example, Tr2 receives inhibitory post-synaptic potentials during the elongation phase of each crawl cycle. When crawling is not expressed, spontaneous inhibitory post-synaptic potentials in Tr2 correlate in time with spontaneous excitatory post-synaptic potentials in the CV motor neuron, a circular muscle excitor that bursts during the elongation phase of crawling. Our data are consistent with the idea that DA biases the nervous system to produce locomotion in the form of crawling.

Action Potentials↗
PubMed1998

Acute intrahippocampal infusion of BDNF induces lasting potentiation of synaptic transmission in the rat dentate gyrus.

The effect of acute intrahippocampal infusion of brain-derived neurotrophic factor (BDNF) on synaptic transmission in the dentate gyrus was investigated in urethan-anesthetized rats. Medial perforant path-evoked field potentials were recorded in the dentate hilus and BDNF-containing buffer was infused (4 microl, 25 min) immediately above the dentate molecular layer. BDNF led to a slowly developing increase of the field excitatory postsynaptic potential (fEPSP) slope and population spike amplitude. The potentiation either reached a plateau level at approximately 2 h after BDNF infusion or continued to increase for the duration of experiment; the longest time point recorded was 10 h. Mean increases at 4 h after BDNF infusion were 62.2 and 224% for the fEPSP slope and population spike, respectively. No changes in responses were observed in controls receiving buffer medium only or buffer containing cytochrome C. BDNF-induced potentiation developed in the absence of epileptiform activity in the hippocampal electroencephalogram or changes in recurrent inhibition on granule cells as assessed by paired-pulse inhibition of the population spike. We conclude that exogenous BDNF induces a lasting potentiation of synaptic efficacy in the dentate gyrus of anesthetized adult rats.

Animals↗
PubMed1983

Effects of a spider toxin on the glutaminergic synapse of lobster muscle.

We studied the effect of neurotoxin (JSTX) separated from spider venom on the lobster neuromuscular junction. JSTX selectively suppressed excitatory post-synaptic potentials (e.p.s.p.s) without affecting the inhibitory post-synaptic potentials (i.p.s.p.s). The effect of JSTX was dose-dependent. The threshold dose for suppressing e.p.s.p.s corresponded to a small fraction of the toxin amount in a venom gland. At high concentration, JSTX irreversibly blocked e.p.s.p.s. The reduction in amplitude of extracellularly recorded e.p.s.p.s after JSTX application followed an exponential time course. The rate of suppression increased proportionally with the toxin concentration. JSTX blocked the glutamate potential in the post-synaptic membrane but it failed to affect the aspartate-induced depolarization. Kainic acid potentiated the glutamate-induced depolarization but it was without effect in the presence of JSTX. Depolarization produced by quisqualic acid is suppressed by the toxin. Our results suggest that the spider venom contains specific blockers of glutamate receptors in crustacean neuromuscular junctions.

Animals↗
PubMed2002

Activity-dependent expression of simultaneous glutamatergic and GABAergic neurotransmission from the mossy fibers in vitro.

GABAergic transmission in the mossy fiber (MF) projection of the hippocampus is not normally detected in the rat. However, seizures induce simultaneous glutamatergic and GABAergic transmission in this projection, which coincides with an overexpression of GAD(67) and vesicular GABA transporter (VGAT) mRNA in the dentate gyrus (DG) and MF. To test whether this plastic change could be induced in an activity-dependent fashion in the absence of seizures, I recorded intracellularly from slices/cells that served as their own control, before and after direct or synaptic kindling of the DG in vitro. As expected, synaptic responses of CA3 pyramidal cells to test pulse DG stimulation were blocked by perfusion of N-methyl-D-aspartate (NMDA) and non-NMDA receptors' antagonists. However, after kindling the perforant path (3 1-s trains of 0.1-ms pulses at 100 Hz, 1 min apart from each other every 15 min for 3 h), which potentiated synaptic responses without inducing epileptiform activity, the perfusion of glutamatergic antagonists blocked the excitatory synaptic potential and isolated a fast bicuculline-sensitive inhibitory synaptic potential. Immunohistochemical experiments confirmed the overexpression of GAD(67) in the kindled slices. If kindling stimulation was provided just for 1 h or if it was completed in the presence of the protein synthesis inhibitor, cycloheximide, the expression of the GABAergic potential was prevented. Alternatively, when control synaptic responses of a given cell were first blocked, the direct kindling stimulation over the same site during perfusion of glutamatergic antagonists resulted in the induction of fast GABAergic potentials after 16.6 +/- 0.9 kindling trials. Furthermore, a high spacial specificity of this phenomenon was evidenced by recording synaptic responses of a given pyramidal cell to two different MF inputs. After blockade of all synaptic responses with the perfusion of glutamatergic antagonists, one of the inputs was kindled, while synaptic responses between the kindling trials were monitored by applying test pulse stimulation to both inputs. After 17 +/- 1 trials, test pulse stimulation provided over the kindled site evoked GABAergic potentials, whereas test pulse stimulation delivered to the alternative nonkindled parallel MF input remained ineffective. The DG-evoked GABAergic responses were inhibited by the activation of GABA(B)R and mGluR, whereby activation of group III mGluR with L-2-amino-4-phosphonobutyric acid (L-AP4) was significantly more effective than the activation of group II mGluR with DCG-IV. These data demonstrate that GABAergic transmission from the MF projection has distinctive features in the adult rat, and that its induction is dependent on protein synthesis responding in an activity-dependent fashion.

2-Amino-5-phosphonovalerate↗
PubMed2003

Sleep and synaptic homeostasis: a hypothesis.

During much of sleep, the cerebral cortex is rippled by slow waves, which appear in the electroencephalogram as oscillations between 0.5 and 4.5 Hz. Slow waves are regulated as a function of previous wakefulness, being maximal at the beginning of sleep and then progressively returning to a baseline level. This paper discusses a hypothesis about the significance of slow-wave activity and its homeostatic regulation. The hypothesis is as follows: 1. Wakefulness is associated with synaptic potentiation in several cortical circuits; 2. Synaptic potentiation is tied to the homeostatic regulation of slow-wave activity; 3. Slow-wave activity is associated with synaptic downscaling; 4. Synaptic downscaling is tied to the beneficial effects of sleep on performance. The hypothesized link between sleep and synaptic homeostasis is supported by several lines of evidence and leads to testable predictions.

Animals↗
PubMed1987

Inhibition of neuromuscular transmission in the guinea-pig saphenous artery by atriopeptin II.

In the guinea-pig saphenous artery, stimulation of perivascular nerves elicited contraction and two types of synaptic potentials: the excitatory junction potential and the slow depolarization. The synaptic potentials were inhibited by atriopeptin II but not by sodium nitroprusside. Exogenous noradrenaline induced membrane depolarization and contraction, and both sodium nitroprusside and atriopeptin II inhibited the contraction but not the depolarization. These results suggest that atriopeptin II has an inhibitory effect both presynaptically at the nerve terminals and postsynaptically on the vascular smooth muscle cells.

Animals↗
PubMed1983

Electrophysiology of neurones of the inferior mesenteric ganglion of the cat.

Intracellular recordings were obtained from cells in vitro in the inferior mesenteric ganglia of the cat. Neurones could be classified into three types: non-spontaneous, irregular discharging and regular discharging neurones. Non-spontaneous neurones had a stable resting membrane potential and responded with action potentials to indirect preganglionic nerve stimulation and to intracellular injection of depolarizing current. Irregular discharging neurones were characterized by a discharge of excitatory post-synaptic potentials (e.p.s.p.s.) which sometimes gave rise to action potentials. This activity was abolished by hexamethonium bromide, chlorisondamine and d-tubocurarine chloride. Tetrodotoxin and a low Ca2+ -high Mg2+ solution also blocked on-going activity in irregular discharging neurones. Regular discharging neurones were characterized by a rhythmic discharge of action potentials. Each action potential was preceded by a gradual depolarization of the intracellularly recorded membrane potential. Intracellular injection of hyperpolarizing current abolished the regular discharge of action potential. No synaptic potentials were observed during hyperpolarization of the membrane potential. Nicotinic, muscarinic and adrenergic receptor blocking drugs did not modify the discharge of action potentials in regular discharging neurones. A low Ca2+ -high Mg2+ solution also had no effect on the regular discharge of action potentials. Interpolation of an action potential between spontaneous action potentials in regular discharging neurones reset the rhythm of discharge. It is suggested that regular discharging neurones were endogenously active and that these neurones provided synaptic input to irregular discharging neurones.

Action Potentials↗
PubMed1996

Dual-component excitatory amino acid-mediated responses in trigeminal motoneurons and their modulation by serotonin in vitro.

1. Intracellular recordings were made from guinea pig trigeminal motoneurons in brain stem slices. Monosynaptic excitatory postsynaptic potentials (EPSPs) were evoked in trigeminal motoneurons by focal stimulation of the mesencephalic nucleus of V (Mes V), a region containing cell bodies of primary afferent fibers of jaw muscle spindle and periodontal receptor origin. 2. The presence of N-methyl-D,L-aspartate (NMDA) and non-NMDA excitatory amino acid receptors (EAAs) was determined by iontophoretic application of NMDA and (+/-)-alpha-amino-3-hydroxy methylisoxazole-4-propionic acid (AMPA) from multi-barreled micropipettes. Application of either agonist in normal Mg(2+)-containing extracellular solutions produced a membrane depolarization or inward current from resting potential in current-or voltage-clamp modes, respectively. However, the voltage and current responses to NMDA and AMPA differed in their dependence on initial membrane potential. In voltage clamp between -70 and -50 mV, the peak current response to NMDA application increased whereas the response to AMPA application decreased as a function of holding potential. 3. Mes-V-induced synaptic potentials were examined for the presence of NMDA and non-NMDA components in extracellular solutions devoid of Mg2+. In the presence of DL-2-amino-5-phosphonopentanoic acid (30 microM), the peak amplitude and half-amplitude duration were decreased 52 and 36% (n = 2), respectively, compared with control. In the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10-15 microM), a specific non-NMDA antagonist, the mean decrease in evoked synaptic potential amplitude was 55% (n = 5), but the half-amplitude duration increased by a mean of 63% (n = 5). 4. The non-NMDA component of the evoked EPSP obtained in the presence of DL-2-amino-5-phosphonovaleric acid showed a linear decrease in peak amplitude as a function of holding potential. In contrast, the NMDA EPSP component obtained in the presence of CNQX increased in peak amplitude as a function of holding potential between -70 and -40 mV. The increase in EPSP peak amplitude was abolished by removal of Mg2+ from the extracellular media. 5. Bath application of serotonin (5-HT) (50-100 microM) increased the peak NMDA and non-NMDA EPSP components by 31% (n = 10) and 23% (n = 8), respectively, while producing a mean increase in half-amplitude duration of 67 and 88%, respectively. Concomitantly, 5-HT increased input resistance by approximately 40% and produced a membrane depolarization. 6. In the presence of tetrodotoxin, 5-HT enhanced both iontophoretic NMDA and AMPA voltage responses. In cells voltage clamped between -60 and -70 mV in Mg(2+)-free solutions, iontophoretic NMDA and AMPA peak currents were enhanced 27 and 32%, respectively, by 5-HT. 7. The enhancement of the iontophoretic NMDA and non-NMDA responses was mimicked by (+/-)-1-(2,5-dimethyoxy-4-iodophenyl)-2- aminopropane HCL and blocked by 3-[2-[4-(fluorobenzoyl)-1-piperdinyl]-2,4 (1H,3H)-quinazolinedione-tartrate and N'-[(8a)-1,6-dimethylergolin-8-yl]-N,N-dimethyl-sulfamide hydrochloride, suggesting 5-HT2 receptor involvement. 8. The results demonstrate that trigeminal motoneurons possess both NMDA and non-NMDA receptors that are activated during Mes-V-induced synaptic transmission. The data suggest that EAA-mediated responses in trigeminal motoneurons are substrates for modulation by 5-HT via changes in membrane resistance and modulation of the EAA-induced synaptic current.

Animals↗
PubMed2002

Pre- and postsynaptic inhibition mediated by GABA(B) receptors in cerebellar inhibitory interneurons.

The inhibitory interneurons in the molecular layer of the cerebellar cortex form a complex network, interconnected by both chemical and electrotonic synapses. Previous work, using voltage optical imaging in an isolated cerebellum, has indicated that these interneurons also form presynaptic inhibitory interconnections. Here we examine the participation of GABA(B) receptors in the proposed presynaptic inhibition by recording from the molecular layer interneurons (MLI) in cerebellar slices. The GABA(B) agonist, baclofen, profoundly depressed synaptic transmission; a concentration of 10 microM decreased the frequency of spontaneous inhibitory synaptic potentials by 82 +/- 15% and of miniature synaptic potentials by 75 +/- 13%. In simultaneous recording from two synaptically interconnected MLIs, baclofen (10 microM) increased the failure rate of synaptic transmission by a factor of 3, confirming a presynaptic mechanism, most likely mediated by a decrease in calcium conductance. A postsynaptic effect of baclofen was also found; 10 microM decreased the spontaneous firing rate by 55 +/- 19% even in the presence of synaptic blockers. One hundred micromolar baclofen induced an averaged hyperpolarization of 6 +/- 2 mV or an averaged 7.8 +/- 3 pA net outward current that can account for the decrease in firing rate. The outward current reflects a reduction in a tonic Ca(2+) current, since it was abolished by blocking Ca(2+) currents and remained unchanged in the presence of Ba(2+). Application of the specific GABA(B) blocker, CGP 55845A (1 microM), not only reversed the effects of baclofen but also increased the spontaneous firing rate and synaptic activity when applied alone. Thus in slice preparations, GABA(B) receptors are tonically activated by endogenous GABA. The temporal role of GABA(B) receptors was tested using the paired-pulse paradigm. Recording from two synaptically interconnected MLIs showed a 3.5 times lower probability of release for the second stimulus. In the isolated cerebellar preparation, a robust depression of the second inhibitory response was observed. This depression was partially blocked by CGP 55845A (2 microM). We conclude that both the pre- and postsynaptic effects of baclofen are mediated by GABA(B) receptors that decrease Ca(2+) currents. These can serve a modulatory role as well as participating in shaping the temporal interactions between consecutive inputs.

Animals↗
PubMed1997

Potentiation of synaptic transmission in the rat dentate gyrus in vitro by (S)-3,5-dihydroxyphenylglycine ((S)-DHPG).

The direct activation of metabotropic glutamate receptors (mGluRs) by 1S,3R-aminocyclopentane dicarboxylate (1S,3R-ACPD), has previously been shown to induce a relatively fast (maximum at 10 min) and slow (90 min) onset long-term potentiation (LTP) of synaptic transmission in the hippocampus. Here we report the first evidence for a relatively fast onset LTP of synaptic transmission in the immature male rat (50-100 g) dentate gyrus in vitro by application of the mGluR type I agonist, (S)-3,5-dihydroxyphenylglycine ((S)-DHPG; 20 microM). Bath application of (S)-DHPG caused a transient depression of the field excitatory postsynaptic potential (EPSP) slope, followed after washout by a relatively rapidly developing potentiation of synaptic transmission to a maximum increase at 12-15 min (161.1 +/- 11.4% compared to controls at 15 min; n = 8). This effect was not observed following perfusion with the enantiomer (R,S)-DHPG at the same dose. The (S)-DHPG potentiation occluded tetanically induced LTP and vice versa. The potentiation was antagonised by the non-specific mGluR antagonist (R,S)-alpha-methyl-4-carboxyphenylglycine ((R,S)-MCPG) at high doses (500-1000 microM) but was unaffected in the presence of the N-methyl-D-aspartate (NMDA) receptor blocker, D(-)-2-amino-5-phosphonopentanoic acid (D-AP5; 50 microM). Our results demonstrate a robust NMDA-independent LTP induced by (S)-DHPG that occludes tetanically induced LTP.

2-Amino-5-phosphonovalerate↗
PubMed2003

Direct chemically mediated synaptic transmission from mechanosensory afferents contributes to habituation of crayfish lateral giant escape reaction.

The neural mechanism of habituation of the crayfish lateral giant-mediated escape reaction was analyzed electrophysiologically and pharmacologically. Upon repeated stimulation of tailfan afferents (at 0.2-1 Hz) lateral giant showed rapid habituation and failed to spike. Upon low-intensity sensory stimulation, the lateral giant responded with two subthreshold excitatory post-synaptic potentials, the alpha and beta components. A third component, the alpha' component, was discriminated at the boundary of excitatory post-synaptic potentials between the late alpha and early beta components with stimulation just subthreshold or suprathreshold to evoke lateral giant spikes. This alpha' component increased in amplitude with hyperpolarizing current injected into the lateral giants, although the amplitude of both the alpha and beta components remained constant. Furthermore, bath application of the nicotinic antagonist, d-tubocurarine caused a rapid reduction in the amplitude of the alpha' component while the amplitude of the beta component was reduced gradually and that of the alpha component remained unchanged. Single-hair stimulation indicated that some sensory afferents made direct connections with the lateral giants mediated by chemical synapses and form the potential of alpha' component of the lateral giants. Since lateral giant inactivation was associated with a reduction of excitatory post-synaptic potential amplitude of the alpha' component, connection from these afferents could contribute, at least in part, to lateral giant habituation.

Animals↗
PubMed1967

Post-synaptic effects of cortical stimulation on forelimb motoneurones in the baboon.

1. The arm area of the baboon's precentral motor cortex was stimulated by brief surface-anodal pulses, and the post-synaptic potentials elicited in contralateral forelimb motoneurones were studied by intracellular recording.2. Strong cortical stimuli elicited a rapid series of excitatory and, in some cells, inhibitory post-synaptic potentials (EPSPs and IPSPs respectively). Comparisons with the simultaneously recorded response of the pyramidal tract indicated that these post-synaptic potentials were due to a repetitive discharge of fast pyramidal fibres. Thus, the later synaptic events were mostly due to a repetition of the early monosynaptic EPSP and early IPSP respectively.3. Inhibition was seen more often in cells whose monosynaptic EPSP had a small maximal size than in those whose monosynaptic EPSP was larger. The net depolarization produced by a strong cortical stimulus was related to the maximal size of the early monosynaptic EPSP.4. In the Discussion, an interpretation is suggested for previous findings concerning the spinal distribution of late synaptic effects elicited by cortical stimulation.

Action Potentials↗