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PubMed1984

Inhibition from the brain stem of inhibitory interneurones of the cat's dorsal lateral geniculate nucleus.

Brain-stem control of inhibitory circuits in the dorsal lateral geniculate nucleus (d.l.g.n.) of the cat was studied with extracellular recordings from functionally identified interneurones and with intracellular recordings from principal cells. Perigeniculate neurones, the recurrent inhibitory interneurones of the d.l.g.n., were inhibited by low-threshold stimulation within a wide bilateral field of the brainstem reticular formation extending from the rostral mesencephalon to the caudal medulla oblongata. The inhibition had a latency of 10-12 ms for stimulation sites in the mesencephalon and a duration of about 100 ms. The brain-stem stimulation evoked large hyperpolarizing potentials in intracellularly recorded perigeniculate neurones, indicating that the effect was due to post-synaptic inhibition. Intrageniculate interneurones, the feed-forward inhibitory interneurones of the d.l.g.n., were inhibited with a similar time course from the same region of the brain stem. Both feed-forward and recurrent inhibitory post-synaptic potentials (i.p.s.p.s) in principal cells were depressed by a preceding stimulation of brain-stem sites effective for the interneurones. The depression had about the same time course as the inhibition of the interneurones and it occurred without a concomitant change in the membrane potential of the recorded principal cells. A small depolarizing potential, with a latency of 10-20 ms, was observed in some principal cells after brain-stem stimulation. The potential reversed polarity when i.p.s.p.s were reversed by current injection into the recorded cell indicating that it was due to disinhibition of the principal cells. The possible neuronal pathway for the inhibition of the d.l.g.n. in interneurones is considered and it is proposed that the effect is mediated by a group of neurones located in the caudal mesencephalon and the rostral pons close to the fibres of the brachium conjunctivum.

Action Potentials↗
PubMedDate not supplied

[The generation of action potentials in the terminals of the Schaffer collaterals during long-term potentiation in the CA1 region of the hippocampus].

Experiments were performed in rat hippocampal slices. Activity of individual CA3 pyramidal neurons and field potentials in the CA1 areas were recorded extracellularly. The collision technique was applied to detect the antidromic origin of the background action potentials in the somata of CA3 neurons. Threshold stimulation of terminals of the Schaffer collaterals in the stratum radiatum of the CA1 area was applied to study their excitability during the CA1 long-term potentiation. During the long-term potentiation, antidromic action potentials appeared in the somata of the CA3 neurons. The obtained evidence suggests that the synaptic potentiation is accompanied by an enhancement of axon terminal excitability resulting in generation of the action potentials.

Action Potentials↗
PubMed1997

Cardiac inhibitory neurons in gastropod snail Achatina fulica.

Two inhibitory heart motor neurons (HI-1, HI-2) were identified in the visceral ganglion of the snail Achatina fulica. Both motor neurons were connected monosynaptically with the myocardium. Irregular action potentials composed a typical pattern of neuronal spontaneous electrical activity. The neurons shared common excitatory synaptic inputs, and were connected through electrical synapses. Neuronal endings of these cells responded to tactile stimulation and to cardiac stretching when the chemical synapses were blocked. HI-1 and HI-2 neurons both elicited inhibitory post synaptic potentials in the myocardium with a constant delay and thereby modulated cardiac spikes frequency and amplitude. Staining with the dye Lucifer yellow revealed that these two neurons were unipolar cells which had dendrites only in the visceral ganglion.

Action Potentials↗
PubMed1995

Currents caused by the spontaneous release of quanta of acetylcholine onto chromaffin cells in guinea-pig adrenal medulla.

Membrane potentials were recorded from chromaffin cells in isolated bisected adrenal glands from guinea-pigs. Spontaneous excitatory synaptic potentials (SESPs) were recorded whose frequency was increased following brief (up to 10 s) periods of presynaptic nerve stimulation at 10-30 Hz. The single electrode voltage-clamp method was used to record the currents underlying all but the largest SESPs. Spontaneous excitatory synaptic currents (SESCs) decayed according to a single exponential with a time constant of about 8 ms at 30 degrees C. Thus the neuronal nicotinic receptor-channels giving rise to SESCs in chromaffin cells are probably very similar to those that are opened by quanta of acetylcholine in sympathetic ganglion cells.

Acetylcholine↗
PubMed1990

A voltage-clamp study of the electrophysiological characteristics of the intramural neurones of the rat trachea.

1. The electrophysiological characteristics of intramural neurones from the paratracheal ganglia of 14- to 18-day-old rats were studied in vitro using intracellular, single-electrode current- and voltage-clamp techniques. 2. Resting membrane potentials ranged between -50 and -73 mV. In 50-60% of all neurones, random and occasionally patterned bursts of spontaneous, fast synaptic potentials were observed. In all cases, superfusion with either hexamethonium (100 microM), or Ca2(+)-free, high-magnesium-containing solutions abolished all synaptic activity. 3. Two distinct patterns of spike discharge were observed in response to prolonged intrasomal current injection. Most cells (65-75%) fired rhythmic, high-frequency (50-90 Hz) bursts of action potentials, with interburst intervals of between 300 and 500 ms, throughout the period of current stimulation. A further 10-15% of cells fired tonically at low frequencies (10-15 Hz) for the duration of the applied stimulus. In both cell types, trains of action potentials were followed by a pronounced calcium-dependent after-hyperpolarization which persisted for up to 3 s. The magnitude of the after-hyperpolarization following a single spike in tonic-firing cells was considerably larger than in burst-firing cells. Both the action potential and the after-hyperpolarization in all cells displayed a calcium-dependent, tetrodotoxin-resistant component which was abolished by the removal of the extracellular calcium. 4. The spike after-hyperpolarization resulted from activation of an outward calcium-dependent potassium current which reversed at -86.5 mV. This value was shifted by 63.6 mV for a 10-fold increase in extracellular potassium concentration. 5. All of the cells studied exhibited marked outward rectification when depolarized. This resulted from activation of a time- and voltage-dependent M-current. The slow inward current relaxations associated with the M-current became faster at more negative potentials and reversed around -85 mV. Raising the extracellular potassium concentration shifted the reversal potential for the current relaxations to more depolarized potentials in a manner predicted by the Nernst equation for a current carried by potassium ions. Both the outward current at depolarized potentials and the slow current relaxations were potently inhibited by extracellular BaCl2 (1 mM) but were unaffected by CsCl (1-3 mM). 6. Inward rectification at hyperpolarized potentials was a characteristic of all cells. Membrane hyperpolarization revealed inward rectification in the 'instantaneous' current-voltage relationship at membrane potentials greater than -80 mV.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1986

Mechanisms of action of acetylcholine in the guinea-pig cerebral cortex in vitro.

The mechanisms of action of acetylcholine (ACh) in the guinea-pig neocortex were investigated using intracellular recordings from layer V pyramidal cells of the anterior cingulate cortical slice. At resting membrane potential (Vm = -80 to -70 mV), ACh application resulted in a barrage of excitatory and inhibitory post-synaptic potentials (p.s.p.s) associated with a decrease in apparent input resistance (Ri). ACh, applied to pyramidal neurones depolarized to just below firing threshold (Vm = -65 to -55 mV), produced a short-latency hyperpolarization concomitant with p.s.p.s and a decrease in Ri, followed by a long-lasting (10 to greater than 60 s) depolarization and action potential generation. Both of these responses were also found in presumed pyramidal neurones of other cortical regions (sensorimotor and visual) and were blocked by muscarinic, but not nicotinic, antagonists. The ACh-induced hyperpolarization possessed an average reversal potential of -75.8 mV, similar to that for the hyperpolarizing response to gamma-aminobutyric acid (GABA; -72.4 mV) and for the i.p.s.p. generated by orthodromic stimulation (-69.6 mV). This cholinergic inhibitory response could be elicited by ACh applications at significantly greater distance from the cell than the slow depolarizing response. Blockade of GABAergic synaptic transmission with solution containing Mn2+ and low Ca2+, or by local application of tetrodotoxin (TTX), bicuculline or picrotoxin, abolished the ACh-induced inhibitory response but not the slow excitatory response. In TTX (or Mn2+, low Ca2+) the slow excitatory response possessed a minimum onset latency of 250 ms and was associated with a voltage-dependent increase in Ri. Application of ACh caused short-latency excitation associated with a decrease in Ri in eight neurones. The time course of this excitation was similar to that of the inhibition seen in pyramidal neurones. Seven of these neurones had action potentials with unusually brief durations, indicating that they were probably non-pyramidal cells. ACh blocked the slow after-hyperpolarization (a.h.p.) following a train of action potentials, occasionally reduced orthodromically evoked p.s.p.s, and had no effect on the width or maximum rate of rise or fall of the action potential. It is concluded that cholinergic inhibition of pyramidal neurones is mediated through a rapid muscarinic excitation of non-pyramidal cells, resulting in the release of GABA. In pyramidal cells ACh causes a relatively slow blockade of both a voltage-dependent hyperpolarizing conductance (M-current) which is most active at depolarized membrane potentials, and the Ca2+-activated K+ conductance underlying the a.h.p.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1986

Responses of phrenic motoneurones of the cat to stimulation of medullary raphe nuclei.

Responses of phrenic motoneurones to stimulation of the three medullary raphe nuclei (raphe magnus (r. magnus), raphe obscurus (r. obscurus) and raphe pallidus (r. pallidus] were recorded in anaesthetized and decerebrated cats. Stimulation of r. magnus or r. obscurus depressed phrenic motoneurones. Stimulation at 100 Hz reduced action potential frequency within each inspiratory burst, without appreciable changes in inspiratory duration, or number of inspiratory bursts per unit time. The depression was proportional to the stimulus intensity (40-160 microA) and frequency (12-100 Hz) and lasted throughout the period of stimulation. Intracellular recording revealed concomitant depression of central respiratory drive potentials (c.r.d.p.s) and increased membrane input resistance during r. obscurus or r. magnus stimulation. In motoneurones which discharged action potentials during expiratory as well as inspiratory phases following intracellular chloride injection, stimulation of r. magnus or r. obscurus depressed cell firing during both phases. Both c.r.d.p.s and reversed inhibitory post-synaptic potentials (i.p.s.p.s) were depressed. These findings indicate that the depression is not related to post-synaptic inhibition of phrenic motoneurones. Stimulation (100 Hz) of r. pallidus produced discharges of action potentials in phrenic motoneurones. Stimulation lengthened the duration of each inspiratory discharge in proportion to stimulus intensity. Continuous firing occurred throughout the period of stimulation with maximal intensities. Intracellular recordings revealed sustained depolarization and reduction in membrane input resistance during the discharge. Responses were recorded extracellularly from medullary inspiratory neurones of the dorsal respiratory group (d.r.g.) and ventral respiratory group (v.r.g.) and from vagal axons which fired in phase with phrenic nerve activity. Responses to raphe stimulation were similar to those recorded from phrenic motoneurones. Evidence is presented that the responses are not related to stimulation of decussating bulbo-spinal axons from d.r.g. or v.r.g. neurones. It is suggested that medullary respiratory neurones receive inhibitory and excitatory synaptic inputs from medullary raphe neurones. Hypercapnia (5% CO2 in O2) or hypoxia (15% O2 in N2) reduced markedly the inhibition produced during stimulation of r. obscurus or r. magnus, and restored expiratory-linked silent periods during stimulation of r. pallidus. Activation of Hering-Breuer or baroreceptor reflexes did not alter responses to r. pallidus stimulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1985

Kainic acid and penicillin: differential effects on excitatory and inhibitory interactions in the CA1 region of the hippocampal slice.

The effects of kainic acid (KA, 0.05-1.0 microM), and penicillin (PN, 3.4 mM) were studied in the CA1 region of rat hippocampal slices. Three components of the overall input/output function were taken: (1) the amplitude of the presynaptic compound action potential (prevolley) vs stimulation current applied to Schaffer collaterals, (2) the magnitude of the focally recorded synaptic potential (population EPSP) vs prevolley amplitude; and (3) the amplitude of the focally recorded population spike vs population EPSP magnitude. Recurrent inhibition was measured using the antidromic-orthodromic paired pulse method. KA caused a significant and reversible enhancement of all 3 component input/output functions while having no effect on paired pulse inhibition. PN caused a left shift in the EPSP-population spike relationship and decreased or abolished paired pulse inhibition; the other two measures of excitability were not changed. These results suggest that PN and KA differ fundamentally in the mechanisms by which they produce seizures: PN by removing inhibition while not affecting neuronal excitability per se; KA by exerting a generalized excitatory effect on neural membranes and on synaptic function while leaving recurrent inhibition unchanged.

Animals↗
PubMed1975

Physiological properties of junctions between nerve and muscle developing during salamander limb regeneration.

1. Physiological properties of developing nerve-muscle junctions were studied in regenerating limbs of adult salamanders. 2. During the period of synapse formation the muscle fibres had diameters of 4-10 mum, resting potentials of minus 90 to minus 100 mV and input resistances of 10-50 Momega. Some, but not all, pairs of adjacent muscle fibres were electrically coupled. 3. At the stage when muscle fibres could first be identified, some of them were not innervated, at least as determined by electrophysiological criteria. 4. During muscle innervation the neuromuscular synapses were encountered in several intermediate phases of maturity. (i) At the least mature junctions small spontaneous synaptic potentials occurred, but stimulation of the motor nerve trunk did not evoke synchronous transmitter release. (ii) At other junctions maximal nerve stimulation evoked only a single end-plate potential of low quantum content. (iii) More mature fibres received synaptic input from as many as four motor neurons, which could be distinguished by their discrete stimulus thresholds. 5. During this period of synapse development the fibres lacked an action potential but often showed a prolonged response to depolarization. 6. Fibres in normal adult muscles had from one to three synaptic inputs, were not electrically coupled, and responded to depolarization with an action potential.

Action Potentials↗
PubMed2005

GABAergic signaling to newborn neurons in dentate gyrus.

Neurogenesis in the dentate gyrus begins before birth but then continues into adulthood. Consequently, many newborn granule cells must integrate into a preexisting hippocampal network. Little is known about the timing of this process or the characteristics of the first established synapses. We used mice that transiently express enhanced green fluorescent protein in newborn granule cells to examine their synaptic input. Although newborn granule cells had functional glutamate receptors, evoked and spontaneous synaptic currents were exclusively GABAergic with immature characteristics including slow rise and decay phases and depolarized reversal potentials. Synaptic currents in newborn granule cells were relatively insensitive to the GABA(A) receptor modulator zolpidem compared with neighboring mature granule cells. Consistent with the kinetics and pharmacology, newborn granule cells isolated by fluorescent cell sorting lacked the alpha1 GABA(A) receptor subunit. Our results indicate that newborn granule cells initially receive only GABAergic synapses even in the adult.

Age Factors↗
PubMed2002

A role for myotonic dystrophy protein kinase in synaptic plasticity.

Myotonic dystrophy (DM) is associated with an expanded triplet repeat in the 3'-untranslated region of the gene for myotonic dystrophy protein kinase (DMPK), which may reduce DMPK expression. It is unclear how reduced DMPK expression might contribute to the symptoms of DM because the normal function of DMPK is not yet understood. Thus we investigated the function of DMPK to gain insight into how reduced DMPK expression might lead to cognitive dysfunction in DM. We recently demonstrated a role for DMPK in modifying the cytoskeleton, and remodeling of the cytoskeleton is thought to be important for cognitive function. Therefore we hypothesized that DMPK might normally contribute to synaptic plasticity and cognitive function via an effect on actin cytoskeletal rearrangements. To test for involvement of DMPK in synaptic plasticity, we utilized the DMPK null mouse. This mouse showed no changes in baseline synaptic transmission in hippocampal area CA1, nor any changes in long-term synaptic potentiation (LTP) measured 3 h after induction. There was a significant decrease, however, in the decremental potentiation with a duration of 30-180 min that accompanies LTP. These results suggest a role for DMPK in synaptic plasticity that could be relevant to the cognitive dysfunction associated with DM.

Animals↗
PubMed1985

Control of swimming in the hydrozoan jellyfish Aequorea aequorea: direct activation of the subumbrella.

The epithelial cells that overlie the inner nerve ring of the hydrozoan jellyfish Aequorea aequorea were investigated ultrastructurally and electrophysiologically. The structurally unspecialized epithelial cells are interconnected by gap junctions and are electrically active during swimming as a single, long-duration action potential was recorded during each swim contraction. Intercellular electrical- and dye-coupling was demonstrated within the epithelial region extending into the velum and subumbrellar regions. Excitatory post-synaptic potentials were recorded from epithelial cells following swim motorneuron spikes with a short latency. Psps were up to 60 mV in amplitude and, when triggered in bursts, showed summation provided the interpulse interval was less than 25-35 ms. The initial gap in each of a series of bursts showed facilitation with the first few swim contractions following a period of inactivity. In actively swimming medusae, psp amplitude was relatively constant. The reversal potential for epithelial psp was estimated at between 0 and +20 mV. Spontaneous psps spread throughout the epithelial region electronically, but the amplitude decrease with conducting distance was less than that for current pulses injected into individual epithelial cells. This presumably represents the effect of widespread synaptic activation of epithelial cells via multiple input sites throughout the inner nerve ring as opposed to point-source input in current injection experiments. During a radial response, action potential amplitude was decreased and rise time increased due to decremental conduction through the inhibited region. It is postulated that conduction of a full action potential requires that electrotonic current spread from adjacent, active epithelial cells occur in synchrony with synaptic input from swim motoneurons.

Action Potentials↗
PubMed1985

Frequency-to-voltage conversion in the pyramidal tract neuron: an important role of the inhibitory postsynaptic potential.

Frequency-coded impulses are known to be converted into postsynaptic potentials (PSPs) at the synapse of a target neuron. This can be termed frequency-voltage (F-V) conversion. Studies on this problem in pyramidal tract neurons (PTNs) showed that not only the amplitude but also the duration of depolarizing PSPs was determined as a function of the input impulse frequency. Two opposite patterns of F-V conversion were observed following activation of two input systems to PTNs. Inhibitory postsynaptic potentials were found to play an important role in the regulation of the duration of PSPs by curtailing excitatory post-synaptic potentials.

Animals↗
PubMed1984

Compartmental models of electrotonic structure and synaptic integration in an identified neurone.

A three-compartment model of the electrotonic structure of an identified motoneurone, the median gastric (m.g.) neurone of the stomatogastric ganglion of the spiny lobster (Panulirus interruptus) was constructed, based on the passive response of the cell to a step of injected current. While its structure is only remotely related to that of the cell, the model is able to predict the passive response of the cell to any wave form of injected current. The shape of the m.g. neurone provided the basis for the development of a multicompartment model of the cell from the simple compartment model. Unlike the three-compartment model, the multicompartment model has a structure that corresponds closely to that of the cell while it retains the ability to predict the passive response of the cell to any wave form of injected current. The multicompartment model was used to analyse the electrotonic structure and synaptic integration of the cell. The axon acts as a current sink, causing steady-state voltage attenuation between the tips of different dendrites and the integrating segment to range between 26 and 89%. Steady-state voltage attenuation in the distal direction is 2% or less. Synaptic inhibition of m.g. by Interneurone 1 was simulated with simultaneously activated conductance-increase synapses located on all dendritic end-compartments of the model. Inhibitory post-synaptic potential (i.p.s.p.) wave forms recorded in the cell soma were duplicated in the soma compartment when the synaptic conductance change in each of the twenty-eight end-compartments was set equal to 5 nS for 8 ms. I.p.s.p. wave forms in dendritic end-compartments were 30% larger than the soma compartment i.p.s.p., while i.p.s.p.s in the integrating segment compartment were intermediate in size. Charge from a 92 mV, 1 ms action potential in the model axon was passively conducted from axonal compartments to the soma compartment of the model, where it reproduced the attenuated, broadened voltage wave forms of action potentials recorded in the cell soma. Passive spread of charge from an axonal action potentials to terminal dendritic compartments evoked potentials there that were 30% larger and faster than the corresponding soma compartment potential.

Action Potentials↗
PubMed1990

Depression and potentiation of the synaptic transmission between a granule cell and a Purkinje cell in rat cerebellar culture.

Both the depression and the potentiation of synaptic transmission between a cerebellar granule cell and a Purkinje cell, which are considered the cellular basis of motor learning, were established in a simple culture preparation. The repetitive stimulation of both a granule cell and an inferior-olivary neuron depressed the synaptic transmission, and the repetitive stimulation of only a granule cell potentiated the transmission. Thus, a simple model system, where detailed analysis of molecular and cellular mechanisms of synaptic plasticities can be performed, has been established.

Animals↗
PubMed1979

Morphine presynaptically inhibits a ganglionic cholinergic synapse.

The effects of morphine on synaptic transmission through the inferior mesenteric ganglion (IMG) were studied using intracellular recording techniques. Morphine produced a reversible, dose-dependent reduction in the quantal content of the synaptic potentials with little or no effect on quantal size or the properties of the ganglion cells. This effect of morphine was antagonized by naloxone suggesting the presence of specific preganglionic opiate receptors.

Animals↗
PubMed1984

Some functional consequences of GABA uptake by brain cells.

Recent electrophysiological studies on the rat hippocampus (in vivo and in vitro) provide further evidence that neuronal and glial uptake of the inhibitory transmitter gamma-aminobutyric acid (GABA) limits the intensity and the duration of effects not only of locally applied exogenous GABA but also of GABAergic inhibitory synaptic potentials (IPSPs). There is good reason to believe that such uptake is at least partly responsible for the 'fading' of GABA action. Moreover, because it is probably driven by the transmembrane Na+ electrochemical gradient and is accompanied by Na+ influx, GABA uptake is potentially electrogenic and therefore may have a depolarizing effect on both neurons and glia.

Animals↗