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PubMed1981

Oligosynaptic excitation of motoneurones by impulses in group Ia muscle spindle afferents in the cat.

1. Intracellular recording from hind-limb motoneurones was used to investigate whether di- and trisynaptic (oligosynaptic) excitatory post-synaptic potentials (e.p.s.p.s) are evoked from group Ia muscle spindle afferents in those motoneurones in which such potentials are evoked from Ib tendon organ afferents or entire group I afferents. Ia afferents of triceps surae and plantaris were activated either selectively by single brief stretches of these muscles, or together with Ib afferents by electrical stimuli applied to the nerves.2. Muscle stretches below threshold for Ib afferents (10-35 mum) evoked e.p.s.p.s which appeared with latencies compatible with disynaptic and trisynaptic coupling between the afferents and the motoneurones. The latencies of a majority of these e.p.s.p.s were too short to allow their mediation by group II afferents, if any were activated by the applied stretches. They were also too short to be compatible with effects attributable to dorsal root reflexes. These e.p.s.p.s are thus attributed to oligosynaptic actions of Ia afferents.3. Stretch-evoked di- and trisynaptic Ia e.p.s.p.s were found in 83% of motoneurones in which e.p.s.p.s were evoked by stimuli which activated both Ia and Ib afferents; in five motoneurone species they were found in more than 90%. These observations lead to the conclusion that group Ia muscle spindle afferents evoke not only inhibitory but also excitatory actions in parallel with group Ib tendon organ afferents.4. The distribution of Ia oligosynaptic stretch-evoked excitation from ankle and toe extensor muscles was compared with the distribution of Ia non-reciprocal inhibition as described by Jankowska, McCrea & Mackel (1981b). Excitation pre-dominated in posterior biceps-semitendinosus motoneurones and inhibition in other species of motoneurones investigated, except those of intrinsic foot muscles (tibial motoneurones); similar proportions of the latter showed excitation and inhibition.5. Occurrence of oligosynaptic e.p.s.p.s as well as inhibitory post-synaptic potentials (i.p.s.p.s) of Ia origin in some motoneurone species, and in particular in individual motoneurones, is indicative of a number of reflex pathways between group I afferents and these motoneurones. Furthermore, the disappearance of some of the e.p.s.p.s evoked by near-threshold electrical stimulation following stronger stimuli indicates interactions between various functional groups of interneurones mediating group I actions.

Animals↗
PubMed1992

Synaptic excitation produces a long-lasting rebound potentiation of inhibitory synaptic signals in cerebellar Purkinje cells.

Persistent changes in synaptic efficacy are thought to underlie the formation of learning and memory in the brain. High-frequency activation of an afferent excitatory fibre system can induce long-term potentiation, and conjunctive activation of two distinct excitatory synaptic inputs to the cerebellar Purkinje cells can lead to long-term depression of the synaptic activity of one of the inputs. Here we report a new form of neural plasticity in which activation of an excitatory synaptic input can induce a potentiation of inhibitory synaptic signals to the same cell. In cerebellar Purkinje cells stimulation of the excitatory climbing fibre synapses is followed by a long-lasting (up to 75 min) potentiation of gamma-aminobutyric acid A (GABAA) receptor-mediated inhibitory postsynaptic currents (i.p.s.cs), a phenomenon that we term rebound potentiation. Using whole-cell patch-clamp recordings in combination with fluorometric video imaging of intracellular calcium ion concentration, we find that a climbing fibre-induced transient increase in postsynaptic calcium concentration triggers the induction of rebound potentiation. Because the response of Purkinje cells to bath-applied exogenous GABA is also potentiated after climbing fibre-stimulation with a time course similar to that of the rebound potentiation of i.p.s.cs, we conclude that the potentiation is caused by a calcium-dependent upregulation of postsynaptic GABAA receptor function. We propose that rebound potentiation is a mechanism by which in vivo block of climbing fibre activity induces an increase in excitability in Purkinje cells. Moreover, rebound potentiation of i.p.s.cs is a cellular mechanism which, in addition to the long-term depression of parallel fibre synaptic activity, may have an important role for motor learning in the cerebellum.

Animals↗
PubMed1985

Electrophysiology of identified neurosecretory and non-neurosecretory cells in the cockroach pars intercerebralis.

Two cell types can be distinguished with intracellular recording from the pars intercerebralis of the American cockroach (Periplaneta americana). The first type, which corresponds morphologically to the medial neurosecretory cell, always had spontaneously occurring, overshooting action potentials. These action potentials are probably endogenously produced. Tetrodotoxin experiments revealed that sodium is the dominant ion of the action potential. The action potentials are followed by a relatively long after-hyperpolarization. The input resistance of these cells ranged from 120 to 390 M omega. A mathematical model, based on cellular morphology and response to current pulses, revealed a membrane time constant of about 100 msec and an axonal:somatic conductance ratio of approximately 13. Area-specific membrane resistance was estimated at 33 k omega cm2. These cells also often had reversible and spontaneous inhibitory postsynaptic potentials. The second cell type, which is non-neurosecretory, never produced spontaneous action potentials and rarely had synaptic potentials. Action potentials could be evoked by current injection into the cell body or by extracellular stimulation of their axons in the posteroventral portion of the the protocerebrum. These action potentials also depend on sodium ions. Their input resistance ranged from 16 to 35 M omega. They had a membrane time constant of approximately 15 msec and an axonal:somatic conductance ratio of about 9. Their area specific membrane resistance was estimated at 14 k omega cm2.

Action Potentials↗
PubMed1987

Diffusion approximation of the neuronal model with synaptic reversal potentials.

The stochastic neuronal model with reversal potentials is approximated. For the model with constant postsynaptic potential amplitudes a deterministic approximation is the only one which can be applied. The diffusion approximations are performed under the conditions of random postsynaptic potential amplitudes. New diffusion models of nerve membrane potential are devised in this way. These new models are more convenient for an analytical treatment than the original model with discontinuous trajectories.

Mathematics↗
PubMed1997

Activation of muscarinic receptors modulates NMDA receptor-mediated responses in auditory cortex.

The present study examines the ability of muscarinic receptor activation to modulate glutamatergic responses in the in vitro rat auditory cortex. Whole-cell patch-clamp recordings were obtained from layer II-III pyramidal neurons and responses elicited by either stimulation of deep gray matter or iontophoretic application of glutamate receptor agonists. Iontophoresis of the muscarinic agonist acetyl-beta-methylcholine (MCh) produced an atropine-sensitive reduction in the amplitude of glutamate-induced membrane depolarizations that was followed by a long-lasting (at least 20 min) response enhancement. Glutamate depolarizations were enhanced by MCh when elicited in the presence of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)/kainate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) or 2,3-dihydroxy-6-nitro-7-sulfamoyl, benzo(F)quinoxaline (NBQX) but not the NMDA antagonists D-2-amino-5-phosphonovaleric acid (APV) or MK-801 hydrogen maleate. The magnitude of enhancement was voltage-dependent with the percentage increase greater at more depolarized membrane potentials. An involvement of NMDA receptors in these MCh-mediated effects was tested by using AMPA/kainate receptor antagonists to isolate the NMDA-mediated slow excitatory postsynaptic potential (EPSP) from other synaptic potentials. The slow EPSP and iontophoretic responses to NMDA were similarly modified by MCh, i.e., both being reduced during and enhanced (15-55 min) following MCh application. Cholinergic modulation of NMDA responses involves the engagement of G proteins, as enhancement was prevented by intracellular infusion with the nonhydrolyzable GDP analog guanosine-5'-O-(2-thiodiphosphate) trilithium salt (GDPbetaS). GDPbetaS was without effect on the early MCh-induced response suppression. Our results suggest that acetylcholine, acting at muscarinic receptors, produces a long-lasting enhancement of NMDA-mediated neurotransmission in auditory cortex, and that this modulatory effect is dependent upon a G protein-mediated event.

Acetylcholine↗
PubMed1996

In vitro hippocampal dentate frequency potentiation induction as model to detect electrophysiological correlates of some cognitive impairments in striatally-lesioned rats.

1. Hippocampal frequency potentiation, a form of short-term potentiation of hippocampal electrical synaptic potentials that is related to mnemonic and learning processes, is typically damped in aged rats and in certain rat strains with impaired place learning performance. 2. In vitro induction of hippocampal dentate frequency potentiation has been found decreased in striatally-lesioned rats with impaired place learning performance in water maze test. 3. The results demonstrate that also in brain-lesioned rats the poor performances in place learning of the animals are associated with a selective dentate frequency potentiation impairment. Thus in vitro induction of dentate frequency potentiation might be regarded as a model to detect the electrophysiological counterpart of the cognitive impairment in rats with altered place learning.

Animals↗
PubMed1992

Thermal influences on nervous system function.

The various effects of temperature change are only partially predictable. Temporal measures relevant to membrane activity, action potentials, synaptic transmission, and evoked potentials are all consistently increased with cooling and decreased by warming. However, the various measures of amplitude at different levels, and even within similar preparations, are contradictory: Some laboratories report increased amplitudes with cooling and others report decreased amplitudes under similar conditions. Emphasis is given to identifying factors that may resolve the differences. These include: (a) the rate of temperature change, (b) sites of cooling, stimulation and recording, (c) stimulus characteristics, and (d) fundamental differences in temperature sensitivities of different neural tissue. Other factors that may affect the ability to predict thermal influences on neural function from existing formulations are: relative ion permeabilities, metabolic ion pumps, the resting potential at the onset of cooling, and an animal's acclimated temperature at sacrifice.

Animals↗
PubMed2003

Myasthenic syndrome caused by mutation of the SCN4A sodium channel.

In a myasthenic syndrome associated with fatigable generalized weakness and recurrent attacks of respiratory and bulbar paralysis since birth, nerve stimulation at physiologic rates rapidly decremented the compound muscle action potential. Intercostal muscle studies revealed no abnormality of the resting membrane potential, evoked quantal release, synaptic potentials, acetylcholine receptor channel kinetics, or endplate ultrastructure, but endplate potentials depolarizing the resting potential to -40 mV failed to excite action potentials. Pursuing this clue, we sequenced SCN4A encoding the skeletal muscle sodium channel (Nav1.4) and detected two heteroallelic mutations involving conserved residues not present in 400 normal alleles: S246L in the S4/S5 cytoplasmic linker in domain I, and V1442E in the S3/S4 extracellular linker in domain IV. The genetically engineered V1442E-Na channel expressed in HEK cells shows marked enhancement of fast inactivation close to the resting potential, and enhanced use-dependent inactivation on high-frequency stimulation; S246L is likely a benign polymorphism. The V1442E mutation in SCN4A defines a novel disease mechanism and a novel phenotype with myasthenic features.

Adult↗
PubMed2000

Is anesthesia caused by potentiation of synaptic or intrinsic inhibition? Recent insights into the mechanisms of volatile anesthetics.

Volatile anesthetics modulate synaptic (GABAA receptor-mediated) and intrinsic (K+ channel-controlled) neuronal inhibition. GABAA receptor activity is enhanced, leading to increased charge transfer and prolonged synaptic inhibition, and members of the two pore domain family of potassium channels are activated, leading to neuronal hyperpolarization and reduced excitability. These effects may underlie different components of the complex anesthetic state.

Anesthetics, Inhalation↗
PubMed2005

Bradykinin produces pain hypersensitivity by potentiating spinal cord glutamatergic synaptic transmission.

Bradykinin, an inflammatory mediator, sensitizes nociceptor peripheral terminals reducing pain threshold. We now show that the B2 kinin receptor is expressed in rat dorsal horn neurons and that bradykinin, a B2-specific agonist, augments AMPA- and NMDA-induced, and primary afferent-evoked EPSCs, and increases the frequency and amplitude of miniature EPSCs in superficial dorsal horn neurons in vitro. Administration of bradykinin to the spinal cord in vivo produces, moreover, an NMDA-dependent hyperalgesia. We also demonstrate that nociceptive inputs result in the production of bradykinin in the spinal cord and that an intrathecal B2-selective antagonist suppresses behavioral manifestations of central sensitization, an activity-dependent increase in glutamatergic synaptic efficacy. Primary afferent-evoked central sensitization is, in addition, reduced in B2 receptor knock-out mice. We conclude that bradykinin is released in the spinal cord in response to nociceptor inputs and acts as a synaptic neuromodulator, potentiating glutamatergic synaptic transmission to produce pain hypersensitivity.

Animals↗
PubMed1986

Voltage dependence of 5-hydroxytryptamine release at a synapse between identified leech neurones in culture.

The release of 5-hydroxytryptamine (5-HT) from presynaptic terminals has been studied by the voltage-clamp technique at synapses made by isolated Retzius and pressure (P) sensory neurones dissected from the leech C.N.S. and maintained in tissue culture. At these synapses facilitation, depression and modulation of release occur with action potentials and with voltage-clamp pulses. Depolarization of Retzius cells from a constant holding potential by steps of varying amplitude (5 ms in duration) caused graded release of 5-HT. The steep transfer function for release using these short test pulses resembled that seen at the giant synapse of the squid: synaptic potentials increased markedly with presynaptic depolarizations beyond -25 mV and decreased with large depolarizing pulses beyond +40 mV. When the steady holding potential of voltage-clamped Retzius cells was suddenly displaced to a new value within the range of -40 mV to -85 mV, there followed a slow but smaller change of the post-synaptic P-cell membrane potential in the same direction. After an initial delay of about 40 ms, the post-synaptic potential reached its new level with an exponential time course and a time constant of 0.7 s. Since Retzius and P cells are not electrically coupled, these effects can be accounted for by alterations in tonic release of transmitter. Changes of presynaptic holding potential to a more depolarized level resulted in an increase in voltage noise recorded in the P cell. Conversely, hyperpolarization from a depolarized level reduced noise. Noise analysis showed that these changes could be accounted for by quantal events with a mean amplitude of about 0.15 mV. This value is similar to that for spontaneous miniature potentials and quantal fluctuations observed at synapses between Retzius and P cells. Changes in steady holding potential also had marked effects upon the transfer function observed with brief depolarizing pulses of the Retzius cell. The post-synaptic responses evoked by depolarizations to 0 mV with pulses of 5 ms duration were reduced in amplitude as the holding potential of the Retzius cell was increased from the resting value of -45 to -75 mV. For example, depolarization to 0 mV starting from -45 mV evoked synaptic potentials as much as ten times larger than those evoked by depolarizations to 0 mV starting from -75 mV.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed2001

Voltage-dependent sodium channels are expressed in nonspiking retinal bipolar neurons.

Retinal bipolar neurons transmit visual information by means of graded synaptic potentials that spread to the synaptic terminal without sodium-dependent action potentials. Although action potentials are not involved, voltage-dependent sodium channels may enhance subthreshold depolarizing potentials in the dendrites and soma of bipolar cells, as they do in other CNS neurons. We report here that voltage-dependent sodium currents are observed in a subset of bipolar neurons from goldfish retina. Single-cell reverse transcriptase-PCR identified four different sodium channel alpha subunits in goldfish bipolar cells, putatively corresponding to the mammalian voltage-gated sodium channels Na(v)1.1, Na(v)1.2, Na(v)1.3, and Na(v)1.6. The amount of sodium current was largest in cells with smaller synaptic terminals, which probably represent cone bipolar cells. Localization of sodium channel immunoreactivity in goldfish retina confirmed the expression of voltage-gated sodium channels in cone bipolar cells of both ON and OFF types. Both immunocytochemical and physiological evidence suggests that the sodium channels are localized to the soma and dendrites where they may play a role in transmission of synaptic signals, particularly in the long, thin dendrites of cone bipolar cells.

Animals↗