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PubMed1987

Vestibular effects in long C3-C5 propriospinal neurones.

The effects of stimulation of the vestibular nerve and of regions in and around the vestibular nuclei on long C3-C5 propriospinal neurones (PNs) were investigated with intracellular recording. Disynaptic excitatory postsynaptic potentials were evoked from the contralateral (co) or ipsilateral (i) vestibular nerve in many long PNs but mainly in crossed PNs from the co and in uncrossed from the i nerve. Disynaptic inhibitory postsynaptic potentials were evoked more rarely, mainly from the i vestibular nerve. Threshold mapping revealed an excitatory relay from the co nerve in the medial vestibular nucleus (MVN) and also that the excitatory MVN neurones projecting to the long PNs send collaterals to the abducens and interstitial nucleus of Cajal. Excitation from the i vestibular nerve was relayed in the lateral vestibular nucleus (LVN) and in the MVN. Also, non-second order LVN neurones project to the long PNs. Monosynaptic IPSPs were evoked from the i MVN and i LVN.

Brain Mapping↗
PubMed1989

Projections from inspiratory neurons of the nucleus retroambigualis to phrenic motoneurons in the cat.

The connection between the inspiratory neurons of the nucleus retroambigualis and the phrenic motoneurons was examined using the techniques of antidromic mapping to discover collaterals and spike-triggered averaging to detect postsynaptic potentials. Axon collaterals within the region of the C5 phrenic nucleus were found for 17 of 26 (65%) inspiratory neurons and 6 of these 17 (35%) were shown to generate excitatory postsynaptic potentials in at least one phrenic motoneuron. It was concluded that these results demonstrate a strong connection for those inspiratory neurons of the nucleus retroambigualis with a collateral within the phrenic nucleus.

Animals↗
PubMed1990

Neuromuscular actions of sodium selenite on chick biventer cervicis nerve-muscle preparation.

Sodium selenite was found to be toxic to chicks, with an LD50 of 8.5 micrograms/g, which was increased to 16.3 micrograms/g by NaCN. The major symptoms of chicks, treated with selenite, were sedation and then dyspnea and paralysis. The cause of death by selenite was apparently due to the respiratory failure. The possible mechanism of toxicity was explored in the isolated chick biventer cervicis nerve-muscle preparation. Selenite initially increased the amplitude of the twitch, reversed the suppression of the twitch caused by d-tubocurarine, Mg2+, Cd2+ or Mn2+ and significantly increased the quantal content and amplitude of endplate potentials. Subsequently, selenite depressed the amplitude of the twitch, blocked the axonal conduction and inhibited excitatory postsynaptic potentials. Both NH4+ and K+ enhanced the action of selenite in depressing the twitches. In addition, selenite induced a sustained contracture of the muscle, which was partially inhibited by removal of external Ca2+ and markedly blocked by EGTA. Entry of Ca2+ and release of the internal Ca2+ were considered to be responsible for inducing contracture by selenite. Pretreatment with trypsin, glutathione (GSH) and cyanide profoundly inhibited the effects of selenite, indicating that the site of action of selenite was on the outer membrane and the binding of selenite to the sulfhydryl groups of membrane proteins was proposed to be an essential step for selenite-induced contracture and neuromuscular action. These findings suggest that neuromuscular blockade and tetanic spasm, produced by selenite in chicks, may play a role in causing respiratory failure in vivo.

Animals↗
PubMed1997

Interleukin-6 inhibits long-term potentiation in rat hippocampal slices.

The effects of recombinant human interleukin-6 (rhIL-6) on long-term potentiation (LTP) induced in the Schaffer collateral/commissural-CA1 pathway were examined using rat hippocampal slices. Field excitatory postsynaptic potential was recorded in the stratum radiatum of the CA1 region. Ten-min applications of rhIL-6 (50-2000 U/ml), started 5 min before the tetanus, significantly inhibited the induction of LTP, and in high doses of rhIL-6 also inhibited short-term potentiation (over 200 U/ml) and post-tetanic potentiation (over 500 U/ml). The effects of rhIL-6 (500 U/ml) were completely abolished by the preincubation of the slices with monoclonal anti-IL-6 receptor antibody (16 microg/ml) for 2 h. Heat-inactivated rhIL-6 had no effect on the synaptic potentiation. RhIL-6 affected neither the previously established LTP nor the basal synaptic transmission. These findings indicated that rhIL-6 modulated synaptic potentiation through the IL-6 receptor-mediated process in the hippocampus, probably by affecting post- and presynaptic sites in the CA1 region. The possible mechanisms of the IL-6-induced suppression of the synaptic potentiation were discussed.

Action Potentials↗
PubMed1998

Nerve growth factor improves evoked potentials and long-term potentiation in the dentate gyrus of presenile rats.

Chronic infusion of nerve growth factor (NGF, 1.2 microg/day) for 14 days to presenile rats (17 months at the beginning of treatment) that showed an initial cognitive impairment led to an improved long-term potentiation in the dentate gyrus. Both the relative increase of the slope of the population excitatory postsynaptic potential and that of the population spike were enhanced by NGF pretreatment after long-term potentiation induction at 400 Hz. The treatment was also able to increase the diminished baseline amplitude of the population spike, an effect not seen when the treatment was applied to older animals [Bergado, J., Fernández, C.I., Gómez-Soria, A., González, O., 1997a. Chronic intraventricular infusion with NGF improves LTP in old cognitively-impaired rats. Brain Res. 770, 1-9] stressing the importance of an early start of trophic therapy to achieve better results.

Animals↗
PubMed1986

Mechanism of long-term potentiation of transmitter release induced by adrenaline in bullfrog sympathetic ganglia.

A mechanism of the long-term potentiation of transmitter release induced by adrenaline (ALTP) was studied by recording intracellularly the fast excitatory postsynaptic potentials (fast EPSPs). The ALTP was produced during the blockade of K+ channels at the presynaptic terminals by tetraethylammonium (TEA). The synaptic delay, possibly reflecting a relative change in the duration of an action potential at the presynaptic terminal, was not changed during the course of the ALTP. By contrast, it was significantly lengthened by TEA and other K+ channel inhibitors (4-aminopyridine and Cs+) that markedly enhanced the evoked release of transmitter. The magnitude of facilitation of the fast EPSP, induced by a conditional stimulus to the preganglionic nerve, was decreased during the generation of the ALTP, but was unchanged during the potentiation of transmitter release caused by TEA. These results, together with theoretical considerations applying the residual Ca2+ hypothesis to the facilitation, suggest that the enhancement of transmitter release during the ALTP is not caused by an increased Ca2+ influx during a presynaptic impulse owing to the blockade of K+ channel or the modulation of Ca2+ channel, but presumably is induced by a rise in the basal level of free Ca2+ in the presynaptic terminal.

Animals↗
PubMed1993

Declining inhibition elicited in cat lumbar motoneurons by repetitive stimulation of group II muscle afferents.

1. The aim of the present experiments was to verify whether group II inputs from gastrocnemius medialis (GM) muscle could elicit declining inhibitions similar to those observed during GM contractions in a variety of lumbar motoneurons of the cat spinal cord. Motoneurons were recorded intracellularly in chloralose- or pentobarbitone-anesthetized preparations during electrical stimulation of GM nerve with repetitive trains. 2. With strengths in the group I range, repetitive stimulation evoked the usual Ia excitation in homonymous motoneurons and excitatory postsynaptic potential (EPSP) amplitudes remained constant throughout the stimulation sequence. In synergic plantaris motoneurons lacking an excitatory connection with Ia afferents from GM, the same stimulation, kept at a constant strength throughout the stimulation sequence, elicited rapidly decreasing inhibitory potentials reminiscent of those evoked by GM contractions. 3. In motoneurons of pretibial flexors, quadriceps, and posterior biceps-semitendinosus, the stimulation strength required to observe declining inhibitions resembling those produced by GM contractions was 4-8 times group I threshold, engaging group II in addition to group I fibers. 4. These results show that input from GM group II plus group I afferents can elicit inhibitory effects in a variety of motoneurons. Such observations support the hypothesis that messages from spindle secondary endings and/or nonspecific muscle receptors activated during contraction might contribute to the widespread inhibition caused by GM contractions. 5. Inasmuch as constant input in group II and group I afferents evoked declining inhibitory potentials, the origin of the decline must be central, which suggests that the rapid reduction of contraction-induced inhibitions also depended on a central mechanism.

Afferent Pathways↗
PubMed1994

Altered desensitization produces enhancement of EPSPs in neocortical neurons.

1. Neocortical brain slices were prepared from rats (35-50 days of age) and maintained in vitro. Intracellular recordings were obtained from neurons in cortical layers II/III. The effect of bath application of cyclothiazide (CYZ), a potent blocker of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor desensitization, on evoked synaptic activity and passive membrane properties was investigated. 2. Bath application of CYZ did not significantly affect resting membrane potential, input resistance, or repetitive firing. CYZ increased both the amplitude and duration of evoked excitatory postsynaptic potentials (EPSPs). Polysynaptic responses were also augumented. These effects persisted after the blockade of N-methyl-D-aspartate (NMDA) receptors with D-2-amino-5-phosphonovaleric acid (D-APV). The magnitude of these effects appeared to vary directly with stimulation intensity and presumably, amount of glutamate release. 3. Epileptiform activity was induced by bath application of bicuculline methiodide. The amplitude and duration of evoked paroxysmal discharges were increased by CYZ. Similar results were seen in presence of D-APV. 4. These results indicate that CYZ has significant effects on synaptic transmission. Desensitization of non-NMDA receptors may be an important mechanism for determining the time course of EPSPs and in curtailing epileptiform responses in the rat neocortex.

2-Amino-5-phosphonovalerate↗
PubMed1995

Relative contributions of thalamic reticular nucleus neurons and intrinsic interneurons to inhibition of thalamic neurons projecting to the motor cortex.

1. Intracellular responses to stimulation of the cerebral cortex (Cx) and cerebellum were analyzed in thalamocortical neurons (TCNs) in the ventroanterior-ventrolateral (VA-VL) complex of the thalamus and neurons in the thalamic reticular nuclei (RNs) of anesthetized cats, and the contribution of reticular nucleus neurons (RNNs) and thalamic interneurons (TINs) to cerebral and cerebellar inhibition of TCNs was determined. 2. Single TCNs projecting to area 4 or 6 received convergent monosynaptic excitatory and disynaptic inhibitory inputs from both the dentate nucleus (DN) and the interpositus nucleus (IN). These TCNs also received monosynaptic excitatory postsynaptic potentials (EPSPs) and disynaptic inhibitory postsynaptic potentials (IPSPs) from the pericruciate cortex (areas 4 and 6). Each TCN received the strongest excitatory and inhibitory inputs from the cortical area to which that TCN projected, and weaker inhibitory inputs from adjacent cortical areas. 3. RNNs were identified morphologically by intracellular injection of horseradish peroxidase (HRP). Stimulation of the brachium conjunctivum (BC) evoked disynaptic EPSPs with a long decay phase in RNNs in the anterior ventrolateral part of the RN. Single RNNs received convergent disynaptic excitatory inputs from both the DNA and the IN. Stimulation of the Cx produced monosynaptic long-lasting EPSPs with two different latencies in these RNNs: early EPSPs with latencies of 0.9-2.1 ms and late EPSPs with latencies of 1.8-3.5 ms. Collision experiments with BC- and Cx-evoked EPSPs in RNNs indicated that BC-evoked disynaptic EPSPs and Cx-evoked early EPSPs were produced by axon collaterals of TCNs to RNNs. The latencies of the Cx-evoked late EPSPs in RNNs were almost identical to those of Cx-evoked monosynaptic EPSPs in TCNs, indicating that corticothalamic neurons (CTNs) exert monosynaptic excitatory effects on RNNs and TCNs. 4. Stimulation of the Cx produced IPSPs in TCNs with short latencies of 1.8-2.7 ms and longer latencies of > or = 2.8 ms. The Cx-evoked early IPSPs with latencies of 1.8-2.7 ms were mediated by RNNs. The origin of Cx-evoked late IPSPs with latencies of > or = 2.8 ms in TCNs was twofold, Cx-induced early IPSPs in TCNs were facilitated by conditioning cortical stimulation that induced late IPSPs in the TCNs. The same conditioning cortical stimulation also facilitated BC-evoked disynaptic IPSPs. The time course of this facilitatation indicated that CTNs produce long-lasting excitation in TINs. These results indicated that Cx-evoked IPSPs with latencies of > 2.7 ms were mediated at least in part by RNNs and inhibitory TINs in the VA-VL complex.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

[Reversal potential of the EPSP of frog motoneurons].

The current-chop technique has shown that I-V characteristic of the membrane are nonlinear in lumbar motoneurons of isolated perfused frog spinal cord. Input resistance of the membrane decreased with depolarization when constant current was applied during 0.1-1.0 s. However, injection of current 40-60 nA during 1-2 min led to an increase of the membrane resistance to the initial value. As a result the membrane potential could be shifted to the positive level up to +50 mV and more. Monosynaptic excitatory postsynaptic potentials evoked by stimulation of the brainstem or by microstimulation of ventrolateral tract fibres were found to reverse completely at a positive level of the membrane potential. In most cases the reversal potentials ranged between 0 mV and -10 mV.

Animals↗
PubMed1991

Excitation and inhibition of trigeminal motoneurons by palatal stimulation.

Excitation and inhibition of jaw-closing motoneurons (Masseteric and Temporal Motoneurons, Mass. and Temp. Mns) during transient jaw closing, the so-called jaw-closing reflex, and prolonged jaw opening elicited by palatal stimulation were studied. By pressing the anterior palatal surfaces sustained jaw opening was elicited, suggesting that sustained jaw opening results from inhibition of tonic background activity of jaw-closing motoneurons by inhibitory postsynaptic potentials (IPSPs) elicited by mechanical stimulation of the anterior palatal mucosa. Recordings showed that the onset of IPSPs was 80 ms earlier than the onset of jaw opening. Application of diffuse pressure stimulation to the posterior palatal surfaces elicited bursts of spikes triggered on excitatory postsynaptic potentials (EPSPs), suggesting that mechanosensory receptors from the posterior palatal mucosa send excitatory synaptic inputs to jaw-closing motoneurons. Furthermore, it is suggested that mechanosensory inputs from the posterior palatal mucosa may excite neurons in the central pattern generator and provide the motor patterns responsible for jaw closure during the jaw-closing reflex. We have demonstrated that excitation of Mass. Mns innervating the deep masseter muscle mainly contributed to maintaining the occlusal phase of jaw closure during the jaw-closing reflex. However, the onset of EPSPs was 100 to 160 ms (n = 27) earlier than the onset of jaw closure. In studies on spontaneously occurring jaw closure it was demonstrated that there was a proportional increase in the number of spikes of the Temp. Mn and the mechanical response (jaw closure).

Animals↗
PubMedDate not supplied

[Shape and amplitude of stimulating postsynaptic potentials in a neuronal model with an N-shaped volt-ampere characteristic of the dendritic membrane].

We developed a model of a neuron with N-shaped current--voltage characteristic of dendritic membrane and studied the change of shape and amplitude of excitatory postsynaptic potentials (EPSP) when changing the place of synapses on dendrites. Local EPSP can activate slow inward current. Consequently, the EPSP amplitude does not always diminish when the rise- and decay-time increases. In some cases the rise- and decay-time of a more distant synapse may become shorter than that of the more approximate one. The common method of judging about the location of synapses by means of the shape of EPSPs may be wrong.

Cell Membrane↗
PubMed1985

Electrical stimulation of mesencephalic cell groups (A9-A10) produces monosynaptic excitatory potentials in rat frontal cortex.

Electrical stimulation of the ventral tegmental area and substantia nigra produces monosynaptic and polysynaptic excitatory postsynaptic potentials in rat frontal neurons that can be recorded intracellularly. The electrophysiological characteristics of the monosynaptic responses and the possibility that dopamine (DA) mediates these events are discussed.

Animals↗
PubMed1995

Enhancement of NMDA receptor mediated synaptic potentials of rat hippocampal neurones in vitro by thyrotropin releasing hormone.

The effects of thyrotropin releasing hormone (TRH) on excitatory postsynaptic potentials (EPSPs) evoked by electrical stimulation of Schaffer collaterals on CA1 neurones of the adult rat hippocampal slice preparation were investigated using intracellular recording under current clamp conditions. At resting membrane potential and in the presence of extracellular Mg2+, TRH (10-20 microM) largely potentiated NMDA receptor-mediated EPSPs while leaving those mediated by non-NMDA receptors unaffected. This phenomenon had a brief duration (approximately 2 min) and was not accompanied by changes in resting membrane potential or input conductance. It is suggested that TRH provided a transient upregulation of synaptic responses due to NMDA receptor activation.

Action Potentials↗
PubMed1996

Ageing potentiates anaesthetic-induced synaptic depression in hippocampal slices.

The effects of the volatile anaesthetic isoflurane on dendritic field excitatory postsynaptic potentials (fEPSP) were compared in hippocampal slices taken from young mature and old Fisher 344 rats. Application of isoflurane (1% v/v) to young brain slices produced minimal effects on the recorded fEPSPs. On the contrary, the same anaesthetic concentration depressed field responses obtained from old hippocampal slices by 42 +/- 6.8% compared with baseline values. Such increased sensitivity to anaesthetic action in the old slices was consistently observed with administration of higher isoflurane concentrations. The presynaptic afferent volley was unaffected by application of low or high anaesthetic concentration, suggesting that age-induced changes in nerve fibre conduction and probably nerve ending excitability are not involved in the increased vulnerability of old synapses to anaesthetic action. Other synaptic sites are probably involved in the mechanisms of age-dependent potentiation of anaesthetic suppression of synaptic transmission.

Aging↗
PubMed1992

Presynaptic dopamine D1 receptors attenuate excitatory and inhibitory limbic inputs to the shell region of the rat nucleus accumbens studied in vitro.

1. Intracellular recordings were made from the shell region of the nucleus accumbens in an in vitro slice preparation. The mean resting membrane potential, input resistance, and action potential amplitude of these neurons were -76 +/- 1 mV, 87 +/- 5 M omega and 94 +/- 2 mV (N = 108), respectively. A sample of these neurons (N = 18) was identified as medium spiny neurons with the use of the biocytin-avidin labeling technique. 2. Electrical stimulation of the fornix, subcortical fibers, or neuropil within the nucleus accumbens shell itself elicited a depolarizing postsynaptic potential (PSP). Dopamine (10-100 microM) attenuated PSPs elicited by stimulation of all of these sites. In a paired-pulse stimulation protocol, dopamine was observed to enhance the facilitation of the test response with respect to the conditioning response. 3. The suppressive effect of dopamine was mimicked by the D1 receptor agonist SKF 82958 (10-30 microM), whereas the D2 receptor agonist quinpirole (10-30 microM) was ineffective. The action of dopamine was antagonized by the D1 receptor antagonist Sch 23390 (10-30 microM), but not by the D2 receptor antagonist sulpiride (10-50 microM) or various adrenergic receptor antagonists. 4. The PSP was usually composed of an excitatory postsynaptic potential (EPSP)-inhibitory postsynaptic potential (IPSP) sequence. Dopamine equally attenuated the excitatory and inhibitory component of the synaptic response. The attenuation of both EPSP and IPSP did not depend on membrane potential. 5. Dopamine effects on the resting membrane potential and input resistance were variable and did not correlate with changes in the PSP. Two further indications were found in favor of a presynaptic locus of dopaminergic modulation. First, the time course of the PSP was not altered during dopamine application. Second, dopamine did not attenuate depolarizations induced by bath-applied L-glutamate. In extracellular recordings, it was found that dopamine reduced the population spike but not the presynaptic fiber volley. 6. These findings strongly indicate that dopaminergic modulation of synaptic responses in neurons located in the accumbens shell region is mediated by presynaptic D1 receptors. Notably, dopamine does not exert a purely inhibitory effect on synaptic excitability in the nucleus accumbens, because it suppresses both the excitatory and inhibitory component of the synaptic response.

Afferent Pathways↗
PubMed1989

Development of inhibitory synapses among striatal neurons in vitro.

The development of excitatory and inhibitory synaptic connections has been studied in postnatal neurons from the caudate and putamen maintained in tissue culture. Excitatory postsynaptic potentials which were sensitive to the glutamate antagonist CNQX (6-cyano-7-nitroquinoxaline-2,3-dione) appeared between 4 and 8 d in vitro. This is the first indication that glutamatergic excitatory neurons may be intrinsic to the striatum. Spontaneous inhibitory postsynaptic currents appeared at approximately the same time, several days after process outgrowth. Antibodies to glutamic acid decarboxylase (GAD), the synthetic enzyme for GABA, labeled neurons which produce bicuculline-sensitive, inhibitory postsynaptic currents. GAD immunoreactivity and immunoreactivity to synapsin I, a synaptic vesicle-associated protein, became localized to discrete sites along neurites 4-8 d after plating. It is concluded that the punctate GAD immunoreactivity identified possible sites of presynaptic transmitter release.

Acetylcholinesterase↗
PubMed1983

The vestibulo-ocular reflex arc in the newborn kitten. An electrophysiologic investigation.

Field potentials and postsynaptic potentials were recorded in the vestibular and abducens nuclei and neurons following vestibular nerve stimulation in anesthetized newborn kittens (within 72 h after birth). Stimulation of the ipsilateral vestibular nerve evoked an initial P wave and an N1 field potential in the vestibular nuclei. No N2 potential was evoked. Latencies of the peak of the P wave, the onset and the peak of the N1 potential were 0.99 +/- 0.16 ms, 1.66 +/- 0.18 ms, and 2.51 +/- 0.23 ms, respectively. Ipsilateral vestibular nerve stimulation evoked monosynaptic excitatory postsynaptic potentials (EPSPs) and polysynaptic inhibitory postsynaptic potentials (IPSPs) in vestibular nuclear neurons. Stimulation of the contralateral vestibular nerve evoked polysynaptic IPSPs in vestibular nuclear neurons. In abducens motoneurons, ipsilateral vestibular nerve stimulation evoked monosynaptic EPSPs and disynaptic IPSPs; contralateral vestibular nerve stimulation produced disynaptic EPSPs. We conclude that short circuit pathways of the vestibulo-vestibular and vestibulo-ocular reflex arc are present in the kitten already at birth.

Abducens Nerve↗