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PubMed2026

Altered Excitation-Inhibition Balance and mGluR1/5-Driven Plasticity in the Motor Cortical Surface in a Rat Model of Parkinson's Disease.

Parkinson's disease (PD) is characterized by progressive dopaminergic degeneration and maladaptive motor cortical plasticity. However, the cellular pathways underlying cortical surface activity in the primary motor cortex (M1) remain unclear, despite serving as a potential target for electrotherapy. We investigated the excitatory-inhibitory (E-I) balance and synaptic plasticity of superficial M1 circuits in a unilateral 6-hydroxydopamine (6-OHDA)-induced rat model of PD. Using extracellular local field potential and whole-cell patch recordings from the contralateral and ipsilateral M1 hemispheres of hemi-parkinsonian rats, we observed a significantly elevated field excitatory postsynaptic potential (fEPSP) input-output function but unchanged intrinsic neuronal excitability in the M1 superficial layer. An altered relative contribution between alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)- and N-methyl-D-aspartate receptor (NMDAR)-mediated transmission was reflected by a significantly increased AMPA/NMDA ratio. Markedly reduced inhibitory synaptic tone was also evidenced by the decreased amplitude and frequency of spontaneous inhibitory postsynaptic currents (sIPSCs), supporting an E-I imbalance favoring excitation in PD. Furthermore, group I metabotropic glutamate receptor (mGluR1/5)-dependent long-term depression (LTD) was abolished in the ipsilateral PD hemisphere, whereas NMDAR-dependent LTD remained intact. In summary, dopamine depletion appears to enhance network excitation and disrupt mGluR1/5-mediated control of M1 surface circuitry. Our findings identify altered cortical surface mGluR-dependent plasticity in the hemi-parkinsonian model; however, the relationship between these electrophysiological alterations and individual motor outcomes remains to be determined.

Animals↗

PubMed1976

Frequency facilitation and post-tetanic potentiation of a unitary synaptic potential in Aplysia californica are limited by different processes.

Post-tetanic potentiation (PTP) of the monosynaptic and unitary excitatory postsynaptic potential (EPSP) recorded in cell R15 of the abdominal ganglion of Aplysia californica was observed after repetitive stimulation of the right visceropleural connective. PTP at this synapse developed after a few pulses (about 20) and after trains of low frequency stimulation (1/2 sec) under normal physiological conditions of media and temperature. No phase of post-tetanic depression was observed. Evidence is presented that the PTP is due to an increase in transmitter release. The amplitude of the PTP was a function of the frequency and number of stimuli in the preceding train. The PTP was observed to decay, with a single exponential time course, to the size of an isolated EPSP. The rate constant of PTP decay depended upon both the frequency and number of stimuli in the preceding train. The magnitude of the various types of synaptic plasticities seen at this junction, i.e., synaptic depression, frequency facilitation and PTP, correlated with the size of an isolated EPSP as well as with each other. Based on the analysis of the data in terms of a flow model of transmitter release, it is concluded that: (a) during a train of repetitive stimulation the net rate of transmitter supply into the immediately available pool (net transmitter mobilization) increases, the efficiency of the release mechanism (fractional release) increases, and the pool of immediately available transmitter depletes; (b) upon the cessation of the train, as the peak amplitude of PTP is approached, the increased but diminishing rate of net transmitter mobilization refills the available pool to its equilibrium size, while the fractional release is still elevated; (c) during the PTP period after the peak potentiation, the elevated fractional release slowly decays with a single exponential time course; (d) the size of the facilitated EPSPs during the train is limited by the net rate of transmitter supply, although the efficiency of release is also increased; while the size of the EPSPs during the falling phase of the PTP period is determined solely by an increased efficiency of the release mechanism; and (e) the rising phase of the PTP observed in the period shortly after termination of the train is produced by the refilling of the depleted pool of available transmitter in the presence of an elevated release efficiency.

Animals↗

PubMed1979

Effects of ACTH4-10 on synaptic transmission in frog sympathetic ganglion.

The influence of ACTH4-10, a behaviourally active fragment of adrenocorticotropic hormone (ACTH) devoid of endocrine activity, on synaptic transmission in the paravertebral sympathetic ganglion of the frog was investigated. Postsynaptic potentials evoked by electrical stimulation of pregnanglionic nerves were recorded using a sucrose gap method. Fast excitatory postsynaptic potentials (EPSPs), which are mediated via nicotinic cholinergic synapses, were not affected by 10(-6) M ACTH4-10. Application of ACTH4-10 in a concentration as low as 10(-8) M for 60 min caused a marked augmentation of the amplitude of slow inhibitory postsynaptic potentials (IPSPs) which are mediated via dopaminergic synapses. The increase in amplitude developed gradually after a latency of 60--90 min and outlasted the application of the peptide. In addition, ACTH4-10 at 10(-6) M increased the hyperpolarising response of the ganglion to exogenous dopamine, as studied by a micro-application method. There was no significant effect of ACTH4-10 on the muscarinic cholinergic depolarising response of the ganglion towards exogenous acetylcholine. The behaviourally active vasopressin fragment DG-LVP (10(-6) M) had no effect on slow IPSPs. The results demonstrate that ACTH4-10 specifically affects slow synaptic inhibition in frog sympathetic ganglion, probably by acting upon the postsynaptic membrane. The possibility is discussed that ACTH4-10 affects one of the intermediate steps between dopaminergic receptor interaction and generation of the slow IPSP.

Acetylcholine↗

PubMed1978

Postnatal development of visually evoked activity within motor cortex of cat.

1. The development of visually evoked activity within motor cortex was studied in chloralose-anesthetized kittens of 3, 4, and 5 mo of age and adult cats. 2. The slow-wave response from motor cortex of the adult cat is a triphasic negative-positive-negative wave. In 3-mo-old kittens the response is only a long-duration negative wave, while at 4 mo the positive and late negative waves emerge, and at 5 mo of age the adult form of the response is present. 3. Single neurons in the adult respond to the light during the positive component of the slow-wave response. When only the negative wave is present in kittens of 3 and 4 mo of age, neurons do not respond to the photic stimulus. At 5 mo of age the correlation between unit activity and the positive component of the response is identical to the adult. 4. The laminar analysis of the positive component of the response suggests that it originates relatively superficially in cortex and migrates down toward the deeper layers. Its correlation with unit activity indicates that the positive component represents excitatory postsynaptic potentials. 5. These results are consistent with an excitatory drive on neurons within motor cortex undergoing development change until the 5th mo of life.

Aging↗

PubMed1977

Presynaptic modulating effects of GABA on depression, facilitation, and posttetanic potentiation of a cholinergic synapse in Aplysia californica.

The effects of gamma-aminobutyric acid (GABA) have been studied on the synaptic depression, frequency facilitation, and posttetanic potentiation (PTP) of a unitary, monosynaptic, and presumably cholinergic excitatory postsynaptic potential (EPSP). This EPSP, produced by minimal stimulation of the right visceropleural connective, was recorded in cell R 15 of Aplysia californica. Perfusion with GABA (10(-4)-10(-3) M) reduces the size of all EPSPs produced by a train of 100 stimuli at 1/s. It also reduced the synaptic depression and PTP, and increases the frequency facilitation seen during the train. GABA does not significantly effect the membrane resistance (mean 102%) but it slightly depolarizes (mean 6 mV) the postsynaptic cell. GABA does not reduce an acetylcholine iontophoretic potential produced on R15. The effects of GABA are reduction when chloride is replaced by acetate but they remain significant. Picrotoxin and bicuculline fail to antagonize GABA. Addition of sodium azide or dinitrophenol does not reduce the action of GABA and even prolongs it. The effects of GABA are attributed to two sites of action: a postsynaptic one, responsible for the small change in potential and partially responsible for the reduction of EPSP size; and a presynaptic one, responsible for a further reduction of EPSP size and the changes of depression, facilitation, and PTP.

Acetylcholine↗

PubMed1978

Presynaptic modulation of voltage-dependent Ca2+ current: mechanism for behavioral sensitization in Aplysia californica.

Behavioral sensitization of the gill-withdrawal reflex of Aplysia is the result of a prolonged increase in transmitter release from the presynaptic terminals of sensory neurons. Earlier work suggested that this presynaptic facilitation might be mediated by a serotonin-sensitive adenylate cyclase in the sensory neuron terminals. Here we present evidence that presynaptic facilitation results from a cyclic AMP-dependent increase in the calcium current that underlies action potentials in the sensory neurons. The action potentials of sensory neuron cell bodies have, in addition to a sodium current, a calcium current that is enhanced by blocking the opposing potassium current with tetraethylammonium. Under these conditions, the action potentials show a slowly repolarizing plateau that follows the Nernst potential for a calcium electrode and serves as a sensitive assay for changes in calcium current. Stimulation of the pathway that mediates sensitization, incubation with serotonin or phosphodiesterase inhibitors, or intracellular injection of cyclic AMP produces an increase in the calcium plateau in the presence of tetraethylammonium. In addition, both before and after sensitizing stimulation, the duration of the plateau potential parallels transmitter release as measured by the amplitude of monosynaptic excitatory postsynaptic potentials evoked in the motor neurons by intracellular stimulation of single sensory neurons. These results are consistent with the idea that presynaptic facilitation is caused by a cyclic AMP-mediated increase in a voltage-sensitive calcium current in sensory neuron presynaptic terminals. This synaptic action is novel in that it can produce little or no change in the resting potential, is of long duration, and exerts its influence directly on a conductance triggered by the action potential, rather than on non-voltage-sensitive conductances, as is typical of conventional synaptic actions.

Action Potentials↗

PubMed1976

Synaptic transmission: long-lasting potentiation by a postsynaptic mechanism.

Slow decreases of ionic conductance across neuronal cell membranes, which generate slow synaptic potentials, can increase the effectiveness of synaptic transmission. Slow conductance decreases sufficient magnitude increase the amplitude of monosynaptic fast excitatory postsynaptic potentials in B cells of the bullfrog sympathetic ganglion. By this postsynaptic mechanism, activation of one synaptic pathway can cause an increase in transmission, lasting several minutes, across another synapse. This may provide an important mechanism for synaptic integration and control of neuronal interaction.

Animals↗

PubMed1978

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

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

Action Potentials↗

PubMed1979

Orthodromic activation of hippocampal CA1 region of the rat.

(1) The posterior alveus (PA), the anterior alveus (AA) and the Schaffer collaterals (SCH) evoked field potential components which were organized as parasagittal strips of various widths. Spatially continuous and interactive lamellae are suggested. (2) By correlation with unit activities, the early postsynaptic components evoked by PA, AA and SCH were inferred to be extracellular excitatory postsynaptic potentials (EPSPs) and the late, long-duration components, the inhibitory postsynaptic potentials (IPSPs). The hypothesis that interneurons as well as pyramidal cells generate the field is proposed and discussed. (3) One- and two-dimensional profiles of deep evoked potentials and current source-sink analysis revealed excitatory synapses in stratum oriens for the PA and AA inputs and in stratum radiatum for the SCH input. The late dipole field evoked by PA and AA possessed current sources in strata radiatum and pyramidale, the sites of the inhibitory synapses. The late dipole field evoked by SCH had another component possibly generated by recurrent activity, afterpotentials or relayed activity through CA3.

Animals↗

PubMed1979

Effects of some divalent cations on motoneurones in cats.

In cats under Dial, Co, Mn, La, and Sr were injected extracellularly near lumbosacral motoneurones. All tended to improve intracellular recording, but when the membrane potential was initially stable, Mn, and especially Co, had a moderate and reproducible depolarizing action. Both Mn and Co depressed excitatory postsynaptic potentials evoked by dorsal root stimulation. The prominent after-hyperpolarization (a.h.p.), which normally follows the motoneuronal action potential, was consistently and reversibly depressed by Mn and Co (as well as La), the underlying conductance increase being also diminished, but there was no significant reduction in the after-depolarization. By contrast, Sr tended to potentiate the a.h.p., especially when this was depressed by a previous injection of Co or Mn. Unlike the other cations, Co had a marked depressant effect on the action potential, particularly its rate of rise. Since the action potential could be immediately restored by hyperpolarization or by an injection of Sr (in the absence of depolarization), Co may enhance Na inactivation.

Action Potentials↗

PubMed1979

Modification of synaptic facilitation and bursting patterns in Aplysia californica by hyperbaric air.

We have studied the effects of air pressure to 10 atmospheres absolute on several electrophysiological characteristics of identified neurons in Aplysia californica. These pressures did not affect the resting potential, rates of polarization, amplitude, or duration of action potentials in cell R2. Repetitive stimulation of the right pleurovisceral connective nerve produced a frequency-dependent train of unitary excitatory postsynaptic potentials (PSPs) in cell R15 which showed marked facilitation near the end of the train. The amount of facilitation of the last four PSPs increased significantly (approximately 20%) at 9 ATA air pressure. The amplitude of the first PSP was not altered by pressure. Changes in extracellular [Ca2+] or oxygen tension did not influence these pressure effects. Increases in air pressure also reduced the number of action potentials per burst, burst duration, and interburst interval of cell R15 but left the overall firing frequency unchanged. These results indicate that fundamental neurophysiological processes can be altered by increased gas tensions similar to those confronting animals experiencing narcotic symptoms at less than 300 ft of seawater.

Action Potentials↗

PubMed1979

Spontaneous electrical activity and interaction of large and small cells in cardiac ganglion of the crab, Portunus sanguinolentus.

1. Semi-isolated preparations of the nine-celled cardiac ganglion of the crab, Portunus sanguinolentus, were studied electrophysiologically, using simultaneous recording from extracellular and two or three intracellular electrodes. Nine penetrations of small cells were achieved. 2. Three large (80 x 120 micron) cells lie near the anterior end of the 5-mm main trunk; two large and four small (less than 50 micron) cells at the posterior end. Large-cell axons pass along the main trunk and then exit to innervate cardiac muscle; small-cell axons do not leave the ganglion. 3. The semi-isolated ganglion produces spontaneous electrical activity organized into regularly patterned, rhythmic bursts of large- and small-cell impulses recurring at rates of 0.3-0.6/s and lasting 500-800 ms. Small impulse activity commences and ends each burst. Small cells fire trains during the burst, but impulses are not synchronized among them. Large-cell trains are synchronous, are at about one-half the frequency, and have fewer impulses than small-cell trains. 4. Intracellular recordings from small cells show a slow, pacemaker depolarization from a maximum membrane potential of -54 mV leading with only a slight inflection at ca. -50 mV to a depolarized plateau at ca. -40 mV; nonovershooting impulses are superimposed on this but cease before it repolarizes. Impulses, therefore, arise at a site distant from the soma and do not invade it. Deflections suggesting synaptic potentials are not seen. 5. Intracellular recordings from large cells show complex depolarizations corresponding to extracellularly recorded bursts. These represent excitatory postsynaptic potentials (EPSPs) corresponding with individual small-cell impulses, attenuated, non-overshooting spikes, and an underlying slow depolarization; usually no pacemaker depolarization is apparent between bursts. Chemically mediated transmission is probable for the EPSPs because they show delay, increase in amplitude with hyperpolarization, sometimes show facilitation, and are reduced in saline having one-third Ca, 3 x Mg. 6. EPSPs, impulses, and the slow depolarization occur synchronously among the large cells. Potentials recorded from posterior cells are attenuated and slower than those of the anterior cells. This is interpreted to reflect sites of occurrence more distant from the soma in the posterior than in the anterior cells. Impulses do not invade the somata. 7. Intracellular recordings from large-cell axons 4 mm from the soma show overshooting action potentials arising sharply from a base line. EPSPs are absent or highly attenuated and there is little underlying depolarization (less than 2 mV). 8. Current passing with electrodes intracellular to two cells has established directly that all large cells are electrotonically coupled and that an anterior cell and a small cell are coupled. Changes of burst rate during current passing into any large cell indicate that all large cells and small cells are electrotonically coupled. 9...

Animals↗

PubMed1975

Voltage transients in neuronal dendritic trees.

An analytical method is outlined for calculating the passive voltage transient at each point in an extensively branched neuron model for arbitrary current injection at a single branch. The method is based on a convolution formula that employs the transient response function, the voltage response to an instantaneous pulse of current. For branching that satisfies Rall's equivalent cylinder constraint, the response function is determined explicitly. Voltage transients, for a brief current injected at a branch terminal, are evaluated at several locations to illustrate the attenuation and delay characteristics of passive spread. A comparison with the same transient input terminal input, the fraction of input charge dissipated by various branches in the neuron model is illustrated. These fractions are independent of the input time course. For transient synaptic conductance change at a single branch terminal, a numerical example demonstrates the nonlinear effect of reduced synaptic driving potential. The branch terminal synaptic input is compared with the same synaptic conductance input applied to the soma on the basis of excitatory postsynaptic potential amplitude at the soma and charge delivered to the soma.

Action Potentials↗

PubMedDate not supplied

[Responses of hippocampal neurons during prolonged posttetanic potentiation].

Unit responses to stimulation of septo-fimbrial area or fascia dentata were recorded in hippocampus of unanaesthetized rabbits with extra- and intracellular microelectrodes. Neuronal discharge index was found to increase or latency to decrease in 10 out of 28 neurones recorded as long as 3 min to 2.5 hours after tetanization (20/sec, 10 sec). Posttetanic increase in amplitude of excitatory postsynaptic potentials (EPSP) was fo-nd in 8 of 24 neurones recorded intra- and quasi-intracellularly. EPSP latencies were as short as 2 msec in two of these neurones suggesting the monosynaptic origin of the EPSPs. Decrease in excitability was found shortly after tetanization in two neurones tested with intracellular current injections. A tendency to long-lasting posttetanic hyperpolarizing shifts was noted. Thus a long-lasting post-tetanic potentiation (PTP) was revealed at the level of hippocampal single neurone responses. Intracellular analysis suggests an increase in effectiveness of excitatory synapses as a main mechanism of the PTP. No significant adequate changes at the postsynaptic level were found to explain the long-lasting hippocampal PTP.

Animals↗

PubMed1979

Curare has a voltage-dependent blocking action on the glutamate synapse.

The skeletal muscle of members of Orthoptera and Diptera receives an innervation which is probably glutaminergic. Recent study of the ventral muscle fibres in the larvae of the beetle, Tenebrio molitor, has revealed that the transmitter action can be mimicked by the iontophoretic application of L-glutamate to the junctional sites at which the extracellular excitatory postsynaptic potentials (e.p.s.ps) could be recorded (D.Y. and H.W., unpublished observation). Contrary to the evidence favouring glutamate as a transmitter of junctional excitation in insects, some investigators have found that curare (+)tubocrarine, TC), a classic acetylcholine (ACh) antagonist, suppresses the neurally evoked muscle potentials in the fly Sacophaga, and Tenebrio. Here, we have analysed the action of curare on the neuromuscular junction of Tenebrio larvae and found that curare blocked the glutaminergic transmission by antagonising the transmitter at the postsynaptic site.

Action Potentials↗

PubMed1979

Depolarization of neurones in the isolated olfactory cortex of the guinea-pig by gamma-aminobutyric acid.

1 Effects of gamma-aminobutyric acid (GABA) on single neurones in slices of guinea-pig olfactory cortex maintained in vitro were recorded with single intracellular microelectrodes. The average resting potential of 52 cells was -75 mV and apparent input resistance ranged from 20 to 200 MOmega.2 Superfusions of GABA over the slice invariably depolarized the neurones and reduced their input resistance. The minimum effective concentration was 50 to 200 muM.3 The reversal potential for the depolarization produced by 0.1 mM GABA (E(g)) was -66 +/- 2 mV. At concentrations >0.1 mM the reversal potential became progressively more positive (-55 to -50 mV).4 Reduction of external chloride, with isethionate as the substitute anion, increased the amplitude of the depolarization.5 GABA reduced the amplitude of the excitatory postsynaptic potential produced by lateral olfactory tract stimulation, and occluded or reversed the subsequent depolarizing recurrent inhibitory postsynaptic potential.6 Action potentials elicited by injection of depolarizing current or by focal antidromic stimulation were slowed and reduced in amplitude by GABA.7 The effects of GABA on membrane conductance (potency = 1) were duplicated by 3-aminopropanesulphonic acid (potency = 20), beta-alanine (0.5), beta-amino-n-butyric acid (0.5), glycine (0.3) and L-2,4-diaminobutyric acid (0.2). For a given conductance change, 3-aminopropanesulphonic acid, glycine and beta-alanine produced less depolarization than did GABA.8 It is concluded that the action of GABA on the neurones is compatible with a role in mediating recurrent postsynaptic inhibition.

Action Potentials↗

PubMed1976

Modulation of synaptic transmitter release by repetitive postsynaptic action potentials.

The effect of repetitive action potentials in the postsynaptic axon on the release of synaptic transmitter from the presynaptic terminal was investigated at the squid giant synapse. Repetitive antidromic stimulation of the postsynaptic axon resulted in a reduction in the excitatory postsynaptic potential (EPSP). The reduction in transmitter release was accompanied by a decrease in the presynaptic spike after-hyperpolarization (AH). Increasing the concentration of extracellular potassium ions also reduced the EPSP and decreased the amplitude of the presynaptic spike AH. The reduction in transmitter release resulting from repetitive postsynaptic impulses is attributed to the accumulation of extracellular potassium ions. It is proposed that the accumulation of extracellular potassium ions resulting from repetitive postsynaptic activity may modulate synaptic transmission and function as an integrative mechanism in the nervous system.

Action Potentials↗

PubMed1978

Reticulospinal excitation and inhibition of neck motoneurons.

Responses of neck motoneurons to electrical stimulation of the pontomedullary reticular formation were recorded intracellularly in cerebellectomized cats anesthetized with chloralose. Stimulation of nucleus reticularis (n.r.) ventralis and the dorsal part of n.r. gigantocellularis evoked short latency, monosynaptic inhibitory postsynaptic potentials (IPSPs) in the majority of motoneurons supplying the ipsilateral splenius, biventer cervicis and complexus muscles and in 25% of motoneurons projecting in the ipsilateral spinal accessory nerve. Monosynaptic IPSPs were also evoked by stimulating the medial longitudinal fasciculus (MLF) but lesion and collision experiments indicated that these IPSPs were independent of those evoked by reticular stimulation. Monosynaptic IPSPs were also occasionally observed following stimulation of the contralateral reticular formation, especially of the dorsal part of n.r. gigantocellularis. Monosynaptic excitatory postsynaptic potentials (EPSPs) were evoked in all classes of neck motoneurons studied by stimulation of n.r. pontis caudalis, gigantocellularis and ventralis. Each reticular nucleus appeared to contribute to this excitation. The excitation was bilateral but large monosynaptic EPSPs were most often seen in motoneurons ipsilateral to the stimulus site. Data indicated that pontine EPSPs were mediated by ventromedial reticulospinal fibers while medullary EPSPs were mediated by ventrolateral reticulospinal fibers. Neck motoneurons thus receive at least three distinct direct reticulospinal inputs, two excitatory and one inhibitory.

Accessory Nerve↗