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PubMed1986

Long-term potentiation of synaptic transmission in the hippocampus of the rat; effect of calmodulin and oleoyl-acetyl-glycerol on release of [3H]glutamate.

The effect of calmodulin (CaM) and oleyl-acetyl-glycerol (OAG, a synthetic analogue of diacylglycerol, DAG) on K+-induced release of radiolabelled glutamate (Glu), was examined in synaptosomes prepared from area CA3 of control rats and rats in which long-term potentiation (LTP) had been induced in vivo by a brief train of high-frequency stimulation. Both CaM and OAG significantly enhanced release from control tissue in a dose-dependent manner. Release of preloaded L-[3H]Glu was significantly greater in synaptosomes prepared from potentiated tissue than from control tissue but neither CaM nor OAG further enhanced release in potentiated preparations. The occlusion of the two effects suggests that CaM and endogenous DAG are likely to be involved in control of Glu release and the enhancement of release associated with LTP.

Animals↗
PubMed1993

Vasopressin induction of long-lasting potentiation of synaptic transmission in the dentate gyrus.

Vasopressin receptors are present in both the developing and mature dentate gyrus of the rat brain and are of the V1 vasopressor type. Because vasopressin has been shown to influence memory function when injected into the dentate gyrus, the influence of this peptide on an electrophysiological model of learning and memory using the field excitatory postsynaptic potential (EPSP) of the dentate gyrus was investigated. Results of these studies showed that nanomolar concentrations of [Arg8]-vasopressin induced a prolonged increase in the amplitude and slope of the evoked population response in the presence of 1.5 mM calcium. Moreover, the expression of the vasopressin-induced potentiation of the EPSP persisted following removal of vasopressin from the perfusion medium. The vasopressin-induced sustained increase has been termed long-term vasopressin potentiation (LTVP). The closely related neuropeptide oxytocin had no effect upon the EPSP of the dentate gyrus. Preincubation of hippocampal slices in a selective V1 antagonist blocked the expression of LTVP. The ability of the V1 antagonist to block LTVP demonstrates that the potentiation induced by vasopressin is receptor-specific. In the presence of 2.5 mM calcium, the effect of vasopressin was opposite to that observed in 1.5 mM calcium. Under the conditions of 2.5 calcium, vasopressin induced a prolonged depression in the amplitude and slope of the EPSP. Expression of both potentiation and depression appeared within 5 minutes of application and persisted for the length of the observation, 60 minutes. These experiments demonstrate that vasopressin can induce long-lasting changes in the excitability of dentate gyrus neurons that are both calcium-dependent and receptor-specific.

Animals↗
PubMed1982

Responses of primate spinothalamic neurons located in the sacral intermediomedial gray (Stilling's nucleus) to proprioceptive input from the tail.

Extracellular an intracellular recordings were obtained from 24 spinothalamic neurons located in the intermediomedial gray (Stilling's nucleus) in the S2 and S3 spinal segments of anesthetized adult monkeys (Macaca fascicularis). Most units were spontaneously active. They lacked cutaneous receptive fields but could be excited by subcutaneous receptors. Bending the tail to one side of the animal's body axis excited cells located on the contralateral side of the cord an inhibited ipsilateral cells. The firing rate of each cell was a reproducible function of the angle of the portion of the tail distal to the innervated segment. Cells responded with a burst of spikes to electrical stimulation of low threshold ipsilateral primary afferent fibers in the homosegmental dorsal root. The latency of the underlying synaptic potential was 0.5-0.7 ms from the time of arrival of the afferent volley at the cord, indicating monosynaptic input. Low intensity stimulation of the contralateral homosegmental dorsal root inhibited back-ground activity. The latency of the underlying inhibitory synaptic potential was 0.8-1.1 ms, suggesting crossed disynaptic inhibition. We conclude that sacral spinothalamic tract neurons located in the intermediomedial gray participate in signalling the spatial orientation of the animal's tail.

Animals↗
PubMed1995

Motor neuron disease. Studies of the corticospinal excitation of single motor neurons by magnetic brain stimulation.

The responses to magnetic brain stimulation of 57 motor units (MUs) in the first dorsal interosseous muscle of 33 patients with sporadic motor neuron disease (MND), and 44 MUs of 15 healthy control subjects have been compared. Thresholds for MU excitation both in the resting state and during tonic activity have been measured and the modulation of MU discharge by series of magnetic stimuli has been determined from peristimulus time histograms (PSTHs). Abnormalities in the MND MUs have been correlated with the physical signs of impaired hand muscle function. Motor units from hands showing pure lower motor neuron (LMN) signs fired at increased frequency when recruited, had normal or reduced thresholds for activation by magnetic scalp stimuli and had normal or large primary excitatory peaks with normal inter-subpeak intervals on PSTHs. Occasionally muscles with pure LMN signs also had fasciculations that could be driven by cortical stimuli. In contrast, MUs from hands showing pure upper motor neuron (UMN) signs fired at reduced frequency when recruited, had raised thresholds for excitation by cortical stimuli, had prolonged primary peaks with wide inter-subpeak intervals and had large secondary peaks on PSTHs. The rise times and amplitudes of the underlying post-synaptic potentials released by cortical stimuli in spinal motor neurons have been deduced from measurements of the peaks in PSTHs. This analysis suggests that in some MUs from muscles showing pure LMN signs, stimuli evoke larger than normal excitatory post-synaptic potentials (EPSPs), probably resulting from abnormalities in central motor fibres. It is proposed that a major cause of the changes found in MND MUs from hands showing either pure UMN or pure LMN signs may be an abnormality in the motor cortex leading to faulty initiation of the descending corticospinal volley from magnetic stimuli.

Adult↗
PubMed1995

GABAergic suppression prevents the appearance and subsequent fatigue of an NMDA receptor-mediated potential in neocortex.

We have investigated the regulation of an N-methyl-D-aspartate (NMDA) receptor-mediated synaptic potential by gamma-aminobutyric acid (GABA)-mediated inhibition using extracellular and whole-cell voltage clamp recordings in rat auditory cortex in vitro. Single afferent stimulus pulses at low intensity elicited a slow extracellular negativity (Component C) that was mediated by NMDA receptors. At higher intensities, Component C was suppressed by recruitment of GABAergic inhibition. To understand the actions of GABAergic inhibition on Component C, we determined the effects of: (i) paired-pulse stimulation, which depresses GABAergic inhibition; (ii) pharmacological antagonism of GABA receptors; and (iii) afferent stimulation in slices from neonatal rats prior to the development of cortical inhibition. The results indicate that GABAergic inhibition prevents Component C from occurring, thereby preventing its reduction upon repeated stimulation. Whole-cell voltage clamp recordings were used to test the hypothesis that GABAergic suppression occurred by way of membrane hyperpolarization. At hyperpolarized holding potentials no NMDA receptor-mediated synaptic current was elicited, even with paired-pulse stimulation. At depolarized holding potentials a significant NMDA synaptic current was elicited despite the presence of GABAergic synaptic currents. We conclude that membrane hyperpolarization by GABAergic inhibition prevents the appearance and subsequent fatigue of an NMDA receptor-mediated synaptic potential. Reduction of inhibition can act as a 'switch' to fully release the NMDA potential as frequently as once every 10-20 s.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1992

Age-dependence of effects of A1 adenosine receptor antagonism in rat hippocampal slices.

1. Population excitatory postsynaptic potentials (EPSPs) and population spikes evoked in area CA1 of hippocampal slices from aged Fischer 344 rats were significantly smaller in amplitude than responses obtained in slices from young Fischer 344 rats. 2. The A1 adenosine receptor antagonist 8-cyclopentyltheophylline (8-CPT) produced a concentration-dependent increase in synaptic potentials in slices from both young and aged rats. Low concentrations (1 nM) of 8-CPT were effective in producing increases in both population spike amplitudes and population EPSP slopes in young and aged rat slices. Response increases were maximized by 100 nM 8-CPT in slices from rats of both age groups. 3. Adenosine antagonism produced greater average increases in synaptic responses in hippocampal slices from aged rats at all concentrations tested (1.0 nM-1.0 microM). A qualitative age-related difference in the response to 8-CPT was also observed; 8-CPT produced a late component, consisting of multiple population spikes, in evoked responses in slices obtained from aged but not young rats. 4. Adenosine antagonism significantly increased the maximum evocable response (both spike amplitude and EPSP slope) in slices from aged rats, relative to increases observed in slices from young rats. This suggested that smaller synaptic potentials seen in slices from aged rats were in part due to greater levels of "tonic" adenosinergic inhibition. 5. Slices from young and aged rats were incubated in the adenosine reuptake inhibitor soluflazine (R64719; 1.0, 10, and 100 microM) and the inhibition of population EPSPs was observed for 60 min. No difference was observed in the rate of inhibition or the maximal level of inhibition produced by soluflazine, in slices from rats of either age group. 6. Application of (+)-5-methyl-10,11-dihydro-5H-dibenzo-[a,d]cyclo-hepten- 5,10-imine hydrogen maleate (MK-801) and 2-amino-5-phosphonopentanoic acid (2-AP5), antagonists of N-methyl-D-aspartate (NMDA) excitatory amino acid (EAA) receptors, reduced the late multiple population spike component in slices from aged rats incubated in 8-CPT. A smaller direct effect of the NMDA antagonists was observed in slices from aged rats in the absence of 8-CPT treatment at maximal response levels. No effect of NMDA receptor antagonism was observed in slices from young rats under either condition. 7. Hippocampal tissue, from young and old rats utilized in the electrophysiological experiments, was assayed for A1 adenosine binding site density with a saturating concentration of radiolabeled agonist and antagonist. Guanine nucleotide modulation of agonist binding was also measured.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed2000

Is pharmacological neuroprotection dependent on reduced glutamate release?

BACKGROUND AND PURPOSE: The aim of this study was to determinate the possible role of the ionotropic glutamate receptor in the expression of irreversible electrophysiological changes induced by in vitro ischemia and to test whether the neuroprotective action of various neurotransmitter agonists and drugs of clinical interest is related to a presynaptic inhibitory action at glutamatergic synapses. METHODS: Intracellular and extracellular recordings have been performed in a rat corticostriatal slice preparation. Different pharmacological compounds have been tested on corticostriatal glutamatergic transmission in control conditions and in an in vitro model of ischemia (oxygen and glucose deprivation). RESULTS: In vitro ischemia lasting 10 minutes produced an irreversible loss of the field potential recorded from striatal slices after cortical stimulation. Preincubation of the slices with 3 micromol/L 6-cyano-7-nitroquinoxaline-2,3-dione (an alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid [AMPA] receptor antagonist) allowed a significant recovery of the field potential amplitude (P<0.05, n=6), whereas incubation with 30 micromol/L aminophosphonovaleric acid (an N-methyl-D-aspartate receptor antagonist) did not produce a significant recovery after 10 minutes of ischemia (P>0.05, n=7). Bath application of 3 mmol/L glutamate for 5 minutes produced a complete but reversible inhibition of the field potential amplitude. When a similar application was coupled with a brief period of ischemia (5 minutes), which produced, per se, only a transient inhibition of the field potential, it caused an irreversible loss of this parameter. We also tested the possible neuroprotective effect of neurotransmitter agonists reducing the release of glutamate from corticostriatal terminals. Agonists acting on purinergic (adenosine), muscarinic (oxotremorine), and metabotropic glutamate receptors (L-serine o-phosphate [L-SOP]) significantly (P<0.001, n=8 for each agonist) reduced glutamatergic synaptic potentials, with each showing different potencies. The EC(50) was 26.4 micromol/L for adenosine, 0. 08 micromol/L for oxotremorine, and 0.89 micromol/L for L-SOP. Concentrations of these agonists producing the maximal inhibition of the synaptic potential were tested on the ischemia-induced irreversible loss of field potential. Adenosine (P<0.05, n=9) and oxotremorine (P<0.05, n=8) showed significant neuroprotective action, whereas L-SOP was ineffective (P>0.05, n=10). Similarly, putative neuroprotective drugs significantly (P<0.001, n=10 for each drug) reduced the amplitude of corticostriatal potential, with different EC(50) values (phenytoin, 33.5 micromol/L; gabapentin, 96.8 micromol/L; lamotrigine, 26.7 micromol/L; riluzole, 6 micromol/L; and sipatrigine, 2 micromol/L). Concentration of these drugs producing maximal inhibition of the amplitude of corticostriatal potentials showed a differential neuroprotective action on the ischemic electrical damage. Phenytoin (P<0.05, n=10), lamotrigine (P<0.05, n=10), riluzole (P<0.05, n=9), and sipatrigine (P<0.001, n=10) produced a significant neuroprotection, whereas gabapentin (P>0.05, n=11) was ineffective. The neuroprotective action of transmitter agonists and clinical drugs was not related to their ability in decreasing glutamate release, as detected by changes in the paired-pulse facilitation protocol. CONCLUSIONS: Ionotropic glutamate receptors, and particularly AMPA-like receptors, play a role in the irreversible loss of field potential amplitude induced by ischemia in the striatum. Drugs acting by reducing glutamatergic corticostriatal transmission may show a neuroprotective effect. However, their efficacy does not seem to be directly related to their capability to decrease glutamate release from corticostriatal terminals. We suggest that additional modulatory actions on voltage-dependent conductances and on ischemia-induced ion distribution at the postsynaptic site may also exert a crucial role.

Action Potentials↗
PubMed1998

In vivo electrophysiological investigations into the role of histamine in the dentate gyrus of the rat.

Drugs acting at the three known classes of histamine receptors were injected intracerebroventricularly into the rat. The effects of these drugs upon synaptic potentials recorded from the dentate gyrus of the freely-moving rat were determined. Population spikes and field excitatory postsynaptic potentials were recorded from the granule cell layer of the dentate gyrus following stimulation of the perforant path. Drugs, dissolved in 0.9% NaCl were applied into the lateral cerebral ventricle in a volume of 5 microl over a period of 6 min. The histamine H1 receptor antagonist mepyramine (0.4 or 0.8 microg) had no significant effect on population spikes or field excitatory postsynaptic potentials. In contrast the H2 receptor antagonist cimetidine (3.25, 6.5 or 13 microg) showed a biphasic effect. At the lower doses (3.25 or 6.5 microg) a small (15%) depression of the field excitatory postsynaptic potentials and population spikes was observed beginning about 1 h following the infusion. At the highest dose tested (13 microg) a marked increase of the population spike was observed beginning immediately following the infusion and lasting for 90 min. Application of the H3 receptor agonist R-alpha-methylhistamine (0.2 microg) depressed the field excitatory postsynaptic potentials (15% at 4 h post-injection) and even more strongly the population spike (50%). Surprisingly, at higher doses (0.4 and 0.8 microg) no effect was seen. The H3 receptor antagonist thioperamide (0.41 and 0.82 microg) did not cause an increase in synaptic potentials but rather at the highest dose a small depression occurred at later time points (2-4 h following the infusion). At the lower dose (0.41 microg) thioperamide blocked the effect of R-alpha-methylhistamine (0.2 microg). These results show that the histaminergic system modulates information flow through the dentate gyrus in a complex manner involving both histamine H2 and H1 receptors.

Animals↗
PubMed1992

Synaptic mechanisms in sympathetic preganglionic neurons.

Intracellular recordings from sympathetic preganglionic neurons (SPNs) in adult cat and neonatal rat spinal cord slices reveal four types of synaptic potentials, namely, excitatory postsynaptic potentials (EPSPs), inhibitory postsynaptic potentials (IPSPs), and slow EPSPs in both preparations, and a slow IPSP in cat SPNs. Pharmacological studies show that glutamate or a related excitatory amino acid and glycine are the probable mediators of EPSPs and IPSPs. There may be heterogenous mediators of slow EPSPs; substance P, serotonin, norepinephrine, and epinephrine are all probable mediators of slow EPSPs in subpopulations of SPNs. In the case of slow IPSPs, norepinephrine appears to be the likely transmitter. Finally, stimulation of ventral roots elicits a synaptic potential that appears to be caused by glutamate released from afferent fibers in the ventral roots. Our results indicate that a multitude of synaptic mechanisms exist in the rat SPNs by means of which inputs arising from sensory and supraspinal neurons are processed in a timely and orderly manner, thus ensuring highly organized but differentiated outputs to multiple peripheral target cells.

Animals↗
PubMed1990

Pharmacologic analysis of inhibition produced by last-order intermediate nucleus interneurons mediating nonreciprocal inhibition of motoneurons in cat spinal cord.

1. The aim of this study was to investigate the effects of drugs blocking glycinergic and GABAergic transmission on the postsynaptic inhibition of hindlimb motoneurons produced by activation of last-order laminae V-VI interneurons, which are coexcited by muscle and cutaneous afferents and have axonal branches projecting to the Clarke's column. 2. In anesthetized cats with right spinal cord hemisected and both dorsal columns cut between L4 and L5 segments, stimulation of the Clarke's column (CC) at L3-L4 level produced a short-latency, presumably monosynaptic, inhibitory potential that could be recorded either from L7 or S1 ventral rootlets by means of the sucrose-gap technique (iVRP) or intracellularly from hindlimb motoneurons (IPSP). These potentials have been attributed to antidromic activation of a population of last-order interneurons mediating nonreciprocal inhibition of motoneurons. 3. The early iVRP and IPSP produced by CC stimulation was practically abolished 10-20 s after the intravenous injection of strychnine (0.1 mg/kg) and replaced by an excitatory synaptic potential followed by delayed, slow, strychnine-resistant inhibitory potential. 4. Monosynaptic reflexes (MSR) elicited by stimulation of group I gastrocnemius (GS) afferents were inhibited during the occurrence of the CC-iVRP. This inhibition was significantly reduced after intravenous strychnine. On the other hand, the inhibition of the GS-MSR, produced by conditioning stimulation of the posterior biceps and semitendinosus (PBSt) nerve with trains of pulses applied 25-35 ms before the test stimulus, was practically unchanged after the intravenous injection of strychnine. 5. The CC-iVRP and the associated inhibition of GS-MSRs were not significantly affected after the intravenous injection of 0.1 mg/kg of picrotoxin, which clearly reduced the dorsal root potentials (DRP), the late component of the iVRP, and the inhibition of MSRs produced by PBSt volleys. 6. The effect of strychnine and picrotoxin was tested on the monosynaptic iVRP elicited by single intermediate nucleus interneurons that were antidromically activated from the CC and responded both to low-threshold cutaneous fibers and to group I or group II afferents. In three experiments where the interneuronal activity could be kept after the drug injection, it was possible to show that strychnine abolished the interneuronally elicited iVRP, which was replaced by an excitatory synaptic potential with onset preceding the interneuronal activity. In another experiment, it was possible to show that the interneuronally elicited iVRP was not affected by an intra-aortic injection of picrotoxin (0.5 mg/kg) that reduced to one-half the DRP and the iVRP produced by group I PBSt volleys.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

Propagating dendritic action potential mediates synaptic transmission in CA1 pyramidal cells in situ.

1. The events leading to the Schaffer collateral-induced discharge of CA1 pyramidal neurons were investigated in the hippocampus of anesthetized rats by current source-density (CSD) analysis. 2. The earliest evoked currents detected shortly after a stimulus were a sink in the zone where synapses are known to be located (300-350 microns ventral to the somatic layer) flanked by two smaller sources in the distal portion of the apical dendrites and in the somatic layer. This synaptic sink (SyS) extended over 75-100 microns; it lasted for 15-20 ms, and it reached its maximum amplitude some milliseconds after the population spike (PS) and remained in the same location. Stimuli submaximal and supramaximal for evoking a PS yielded the same pattern of current distribution for the SyS. Presynaptic fiber volleys were not detected in these recordings. 3. During the rising phase of the SyS a second sink appeared in a more proximal portion of the apical dendrites. This late dendritic sink (LS) extended over 50-75 microns and was centered 100-150 microns ventral to the somatic layer. This proximal dendritic sink was of amplitude comparable with the SyS; it outlasted the latter and was not necessarily followed by a somatic PS. The LS was extinguished with the appearance of a PS, whereas the SyS persisted regardless of the presence of a PS. 4. After maximal stimuli the LS grew until it exceeded a threshold amplitude, and then, it started to move somatopetally as a continuously propagating sink (PrS). The average speed of propagation was approximately 0.2 m/s. In 0.5-0.7 ms the PrS reached the cell-body layer displacing the passive source that moved into the basal dendrites. The PrS then became the intensive sink corresponding to the main (negative) phase of the somatic PS. This was followed by the development of an active source in the soma layer, probably corresponding to the repolarization phase of the PS. 5. From these observations it appears that the LS and PrS are active dendritic responses. It may be inferred that, shortly after the synaptic currents enter the dendrites, depolarization of adjacent membranes causes the opening of low-threshold, voltage-dependent, slowly inactivating channels that generate the LS. If the depolarization resulting from the LS current is intense enough, another population of channels open that are also voltage-dependent but of higher threshold and faster inactivation.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMedDate not supplied

Electrophysiological analysis of the convergence of peripheral inputs onto neurons of the coeliac ganglion in the guinea pig.

The convergence of intestinofugal axons from different intestinal regions onto individual neurons in the coeliac ganglion of the guinea pig was investigated using intracellular recording methods in vitro. Peripheral nerve trunks from the distal ileum, the most proximal colon and the colon near the colonic flexure were electrically stimulated along with preganglionic fibres running in the splanchnic nerve. Fast cholinergic excitatory synaptic potentials (EPSPs) were seen in ganglion cells in response to stimulation of each nerve trunk. Roughly half of 78 neurons impaled received inputs from stimulation of peripheral nerves, and almost all of these received input from the proximal colon. Most cells responded to stimulation of more than one peripheral nerve indicating that coeliac neurons receive converging inputs from intestinofugal neurons located in more than one intestinal region. In a second series of experiments, segments of intestine were left attached to the ganglion and distended with saline to stimulate peripheral mechanosensory input to the coeliac ganglion. In each experiment, two segments were stimulated. A subgroup of ganglion cells exhibited spontaneous fast EPSPs and the frequency of these potentials was increased by distension of one or other of the attached intestinal segments. However, few neurons responded to distension of both of the attached intestinal segments suggesting that some of the intestinofugal inputs to the coeliac ganglion identified by electrical stimulation may be sensitive to sensory modalities other than distension. Hexamethonium (0.5 mM) applied to the intestine, and not to the coeliac ganglion, reduced the frequency of the spontaneous synaptic potentials seen in coeliac ganglion cells, but did not abolish the response to distension of the colon (n = 8). When the Ca2+ concentration of the solution bathing the proximal colon was reduced to block all synaptic transmission in the enteric plexuses the background synaptic input was further depressed, but again the response to distension was little changed (n = 4). This suggests that at least some of the neurons projecting from the colon to the coeliac ganglion are first order mechanosensory neurons.

Animals↗
PubMed1980

Intrinsic cholinergic excitation in the rat neostriatum: nicotinic and muscarinic receptors.

An in vitro slice technique was employed to study the receptors involved in intrinsic cholinergic excitation in the rat neostriatum. The locally evoked synaptic potentials were suppressed by antinicotinic agents, mecamylamine (10 muM), d-tubocurarine (3 muM) or hexamethonium (100 muM), but not by the antimuscarinic agent atropine (100 muM). If the slices were exposed to an acetylcholinesterase (AChE)-inhibitor (paraoxon 1--20 muM, physostigmine 0.1--0.5 muM), the synaptic potentials were potentiated. The amplitude of the orthodromic population spike increased, and it was further facilitated when the stimulus frequencies were raised from 1--3 Hz to 10--30 Hz. The frequency facilitation following exposure to an AChE-inhibitor was blocked by atropine (1--100 muM). Intracellular recording indicated that a slow depolarizing potential caused the frequency potentiation of the orthodromic discharges. Apparently rat neostriatum is similar to cholinergic systems in sympathetic ganglia and spinal Renshaw cells, in that nicotinic receptors mediate fast excitation and muscarinic receptors mediate slow excitation.

Acetylcholinesterase↗
PubMed1986

Projection of Ia and Ib afferents from forelimb muscles to the C3-C4 segments of the cat spinal cord.

Group Ia muscle spindle afferents were activated separately by small stretches applied to the tendons of antibrachial muscles in the forelimb in the cat. Group Ib tendon organ afferents were stimulated electrically after a selective increase of the threshold of the Ia afferents. Recordings of focal synaptic potentials were made in the C3-C4 segments in the medial part of the base of the dorsal horn. It has been found that both Ia and Ib afferents have monosynaptic connections with neurones in this medial region. Quantitatively, these two groups of afferents produced focal synaptic potentials of approximately the same size. The connections may be to inhibitory interneurones projecting to the C3-C4 propriospinal neurones, which are known to receive disynaptic IPSPs from group I muscle afferents.

Afferent Pathways↗
PubMed1972

Transmitter release from insect excitatory motor nerve terminals.

1. Intracellular and extracellular electrodes were used to study spontaneous and impulse-linked release of transmitter at locust retractor unguis nerve-muscle synapses.2. At most extracellular recording sites the amplitude distributions of the excitatory post-synaptic potentials (e.p.s.p.s) were apparently non-Poisson. However, interpretation of these amplitude distributions was complicated by the effect on the extracellular recordings of the complex structural organization of the retractor unguis nerve terminal with its spatially distinct transmitter release sites extending over distances of 15-30 mum.3. The spontaneous miniature excitatory post-synaptic potentials (min e.p.s.p.s) did not occur at random intervals, bursts of min e.p.s.p.s being frequently recorded. As a result the spontaneous release of transmitter rarely approximated a Poisson process.4. For a period of at least 390 msec following a conditioning nerve impulse a test e.p.s.p. was facilitated and the probability of spontaneous transmitter release was enhanced. A large primary phase of facilitation of impulse-linked and spontaneous release was invariably followed by one or more secondary phases of smaller magnitude.

Animals↗
PubMed1997

NMDA-glutamate receptors regulate phosphorylation of dendritic cytoskeletal proteins in the hippocampus.

Most forms of synaptic potentiation need the activation of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors which generate changes in dendritic morphology of postsynaptic neurons. Since microtubule proteins have an essential role in dendritic morphology, they may be involved and regulated during the modifications of dendritic morphology associated with synaptic potentiation. The phosphorylation of the microtubule-associated proteins (MAPs) has been analyzed in situ after activation or blockade of NMDA-glutamate receptors in hippocampal slices. The phosphorylation of MAP1B and MAP2 has been studied by using several antibodies raised against phosphorylation-sensitive epitopes. Whereas antibodies 125 and 305 recognize phosphorylated epitopes on MAP1B and MAP2, respectively, Ab 842 recognizes a phosphorylatable sequence on MAP1B only when it is dephosphorylated. NMDA treatment decreased the phosphorylation state of the epitope recognized by the antibody 305 on MAP2 and caused a slight dephosphorylation of MAP1B sequences recognized by Ab 125 and 842. Moreover, exposure to APV (an antagonist of NMDA-glutamate receptors) counteracted the effect of NMDA and induced an increase in the phosphorylation state of these sequences in MAP2. Since phosphorylation regulates the interaction of MAPs with cytoskeleton, the results suggest that the modulation of the phosphorylated state of MAP2 by NMDA-glutamate receptors may be implicated in dendritic plasticity.

2-Amino-5-phosphonovalerate↗
PubMed1975

Co-ordinating interneurones of the locust which convey two patterns of motor commands: their connexions with flight motoneurones.

1. Some flight motoneurones receive two superimposed rhythms of depolarizing synaptic potentials when the locust is not flying; a slow rhythm which is invariably linked to the expiratory phase of ventilation, and a fast rhythm with a period of about 50 ms which is similar to the wingbeat period in flight. 2. By recording simultaneously from groups of motoneurones, the synaptic potentials which underly these rhythms have been revealed in 30 flight motoneurones in the three thoracic ganglia. The inputs occur in elevator motoneurones and some depressors but are of lower amplitude in the latter. The inputs have not been found in leg motoneurones. 3. The rhythmic depolarizations are usually subthreshold but sum with sensory inputs to evoke spikes in flight motoneurones at intervals equal to or multiples of the wingbeat period in flight. 4. Both rhythms originate in the metathoracic ganglion and are mediated by the same interneurones. They can be adequately explained by supposing that there are two symmetrical interneurones which each make widespread connexions with left and right flight motoneurones in the three ganglia. 5. The slow rhythm is coded in the overall burst of interneurone spikes during expiration and the fast rhythm in the interval between the spikes of a burst.

Action Potentials↗
PubMed2000

Backpropagation of the delta oscillation and the retinal excitatory postsynaptic potential in a multi-compartment model of thalamocortical neurons.

Uniform and non-uniform somato-dendritic distributions of the ion channels carrying the low-threshold Ca(2+) current (I(T)), the hyperpolarization-activated inward current (I(h)), the fast Na(+) current (I(Na)) and the delayed rectifier current (I(K)) were investigated in a multi-compartment model of a thalamocortical neuron for their suitability to reproduce the delta oscillation and the retinal excitatory post-synaptic potential recorded in vitro from the soma of thalamocortical neurons. The backpropagation of these simulated activities along the dendritic tree was also studied. A uniform somato-dendritic distribution of the maximal conductance of I(T) and I(K) (g(T) and g(K), respectively) was sufficient to simulate with acceptable accuracy: (i) the delta oscillation, and its phase resetting by somatically injected current pulses; as well as (ii) the retinal excitatory postsynaptic potential, and its alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionate and/or N-methyl-D-aspartate components. In addition, simulations where the dendritic g(T) and g(K) were either reduced (both by up to 34%) or increased (both by up to 15%) of their respective value on the soma still admitted a successful reproduction of the experimental activity. When the dendritic distributions were non-uniform, models where the proximal and distal dendritic g(T) was up to 1.8- and 1. 2-fold larger, respectively, than g(T(s)) produced accurate simulations of the delta oscillation (and its phase resetting curves) as well as the synaptic potentials without need of a concomitant increase in proximal or distal dendritic g(K). Furthermore, an increase in proximal dendritic g(T) and g(K) of up to fourfold their respective value on the soma resulted in acceptable simulation results. Addition of dendritic Na(+) channels to the uniformly or non-uniformly distributed somato-dendritic T-type Ca(2+) and K(+) channels did not further improve the overall qualitative and quantitative accuracy of the simulations, except for increasing the number of action potentials in bursts elicited by low-threshold Ca(2+) potentials. Dendritic I(h) failed to produce a marked effect on the simulated delta oscillation and the excitatory postsynaptic potential. In the presence of uniform and non-uniform dendritic g(T) and g(K), the delta oscillation propagated from the soma to the distal dendrites with no change in frequency and voltage-dependence, though the dendritic action potential amplitude was gradually reduced towards the distal dendrites. The amplitude and rising time of the simulated retinal excitatory postsynaptic potential were only slightly decreased during their propagation from their proximal dendritic site of origin to the soma or the distal dendrites. These results indicate that a multi-compartment model with passive dendrites cannot fully reproduce the experimental activity of thalamocortical neurons, while both uniform and non-uniform somato-dendritic g(T) and g(K) distributions are compatible with the properties of the delta oscillation and the retinal excitatory postsynaptic potential recorded in vitro from the soma of these neurons. Furthermore, by predicting the existence of backpropagation of low-threshold Ca(2+) potentials and retinal postsynaptic potentials up to the distal dendrites, our findings suggest a putative role for the delta oscillation in the dendritic processing of neuronal activity, and support previous hypotheses on the interaction between retinal and cortical excitatory postsynaptic potentials on thalamocortical neuron dendrites.

Action Potentials↗