Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Synaptic Potentials”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,675 records · Page 93Linked to original sources
PubMed1988

Mechanism of synaptic inhibition by noradrenaline acting at alpha 2-adrenoceptors.

The actions of agonists at alpha 2-adrenoceptors were investigated on single cells of the submucous plexus of the guinea pig small intestine. Intracellular recordings were made from neurons in vitro, and noradrenaline and other agonists were applied by adding them to the superfusion solution. The actions of noradrenaline released from terminals of sympathetic nerves was also studied by stimulating the nerves and recording the inhibitory postsynaptic current; this current can be mimicked by brief applications of noradrenaline from a pipette tip positioned within 50 micron of the neuron. The alpha 2-adrenoceptor-bound noradrenaline with an apparent dissociation constant of 15 microM, determined by the method of partial irreversible receptor inactivation: clonidine and 5-bromo-6-(2-imidazolin-2-ylamino)-quinoxaline (UK 14304) had dissociation constants of 36 nM and 2.5 microM respectively. Noradrenaline and UK 14304 caused maximal hyperpolarizations, or outward currents; clonidine was a full agonist in only 4 of 35 cells, a partial agonist in 25 cells, and without effect in 4 cells. Clonidine acted as a competitive antagonist of noradrenaline in those cells in which it lacked agonist action; its dissociation equilibrium constant determined by Schild analysis was about 20 nM. The potassium conductance increased by the alpha 2-adrenoceptor agonists, whether they were applied exogenously or released by stimulation of presynaptic nerves, showed marked inward rectification. The neurons showed inward rectification also in the absence of agonist; both types of rectification were eliminated by rubidium (2 mM), barium (3-30 microM) and caesium (2 mM). When the recording electrodes contained the nonhydrolysable derivative of guanosine 5'-triphosphate (GTP), guanosine 5'-O-(3-thiotriphosphate, GTP-gamma-S), the effects of applied alpha 2-adrenoceptor agonists did not reverse when they were washed from the tissue, implying that GTP hydrolysis is necessary for the termination of agonist action. Pretreatment with pertussis toxin abolished the inhibitory synaptic potential (IPSP) and agonist-induced hyperpolarizations. Phorbol 12,13-dibutyrate, forskolin, cholera toxin and sodium fluoride did not affect the responses to alpha 2-adrenoceptor agonists. The synaptic hyperpolarization resulting from sympathetic nerve stimulation, or the hyperpolarization evoked by a brief (3-5 ms) application of noradrenaline, began after a latency of about 30 and 60 ms respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Algorithms↗
PubMed1993

Algorithms for detection and measurement of spontaneous events.

The development of the personal computer and its mass storage capabilities has enabled long-term digitization of voltage records at high sampling rates. This paper presents a program that employs algorithms to analyze a sampled record for spontaneously occurring events. A detection algorithm employs amplitude and temporal parameters to identify the onsets of these events. Other algorithms then characterize size and shape features of these events. Examples of the results of these algorithms are given for intracellularly recorded excitatory postsynaptic potentials (EPSPs). These algorithms permit rapid and accurate quantitation of tens of thousands of events that may occur over many minutes. It is suggested that this set of algorithms may be applied to biological events other than synaptic potentials.

Algorithms↗
PubMed1977

[Mechanism of disorders of inhibition of electrogenesis in spinal alpha-motor neurons in experimental local botulin poisoning].

Disorders of postsynaptic inhibition and of the spinal cord alpha-motoneurons were studied in cats with experimental local botulinum intoxication. A significant decrease of the reciprocal, and, to a lesser extent, of polysynaptic inhibitory postsynaptic potential (IPSP) was noted. With the appearance of total paralysis of the muscles in the poisoned extremity there proved to be an even greater depression of the reciprocal and polysynaptic IPSP; however, they never disappeared or turned into depolarization potentials. Synaptic permeability of motor neurons as a rule decreased during the IPSP development, this indirectly indicating a reduction of ion transport.

Animals↗
PubMed1983

Statistical study on reverberation between two mutually excitatory neuron groups.

The reverberation that occurs between two neuron groups, which have excitatory mono-synaptic random connections with each other can be studied theoretically by employing a model neuron, which expresses well the characters of a real neuron. In this model we consider three effects, which are; the effect of the summation of the excitatory post-synaptic potential (EPSP) of neurons; the effect of the spontaneous firing of neurons as a noise in groups and the effect of the relative refractory period of neurons. As a result, it is shown that under the effect of the summation of the EPSP of neurons and the effect of the noise, the systematic threshold p theta takes the same value as is observed in practice. The effect of the relative refractory period has been considered in order to explain the low speed of the increase in firing activity, as observed in the reverberating system. It suppresses slightly the speed of the increase in firing activity (pi) in the system. Moreover, the speed can be suppressed by making the refractory effect strong according to the increase of pi. However, the initial increase of pi at a high speed that was observed in the experiment cannot be explained simply by the effect of the refractoriness, even if it were the absolute refractoriness.

Action Potentials↗
PubMed2004

Somatosensory evoked potentials (SEPs) recorded from deep brain stimulation (DBS) electrodes in the thalamus and subthalamic nucleus (STN).

OBJECTIVE: To examine the location of deep brain stimulation (DBS) electrode somatosensory evoked potentials (SEPs) and determine the generators of the median nerve SEPs recorded in thalamus and subthalamic nucleus (STN). METHODS: SEPs were recorded from contacts of DBS electrodes and microelectrodes in thalamus and STN to establish the latencies of N13, N18 and N20 in 24 patients (8 tremor, 4 chronic pain, 12 Parkinson disease) undergoing chronic DBS. RESULTS: A large SEP with a mean latency of 17.9+/-1.7 ms was recorded from thalamic contacts. Phase reversal occurred at the horizontal level of the anterior commissure-posterior commissure line. Smaller potentials with similar latency but no reversal could be recorded from STN electrodes. CONCLUSIONS: We propose that the thalamic SEP is generated by excitatory post-synaptic potentials in sensory relay neurons in nucleus ventrocaudalis. A small potential in STN at a similar latency, may be due to volume conduction from thalamus. Intraoperative and postoperative SEP recordings from DBS electrodes could be used to determine the optimal position of the contacts relative to the sensory pathways and the choice of contacts for chronic stimulation.

Adult↗
PubMed2006

Contrasting effects of the persistent Na+ current on neuronal excitability and spike timing.

The persistent Na+ current, INaP, is known to amplify subthreshold oscillations and synaptic potentials, but its impact on action potential generation remains enigmatic. Using computational modeling, whole-cell recording, and dynamic clamp of CA1 hippocampal pyramidal cells in brain slices, we examined how INaP changes the transduction of excitatory current into action potentials. Model simulations predicted that INaP increases afterhyperpolarizations, and, although it increases excitability by reducing rheobase, INaP also reduces the gain in discharge frequency in response to depolarizing current (f/I gain). These predictions were experimentally confirmed by using dynamic clamp, thus circumventing the longstanding problem that INaP cannot be selectively blocked. Furthermore, we found that INaP increased firing regularity in response to sustained depolarization, although it decreased spike time precision in response to single evoked EPSPs. Finally, model simulations demonstrated that I(NaP) increased the relative refractory period and decreased interspike-interval variability under conditions resembling an active network in vivo.

Action Potentials↗
PubMed1997

Structural-functional differences of a crab motoneuron to four stomach muscles.

A motor unit in the stomach of the blue crab, Callinectes sapidus, consists of four separate muscles involved in different aspects of the trituration and filtering of food. Motor nerve terminals to two of the muscles (CPV7a and GM5) release small amounts of transmitter (low-output) while those to the other two muscles (CV2 and CV3) release between three and five-fold greater amounts (high-output). Structural features underlying the disparity in synaptic strength were analysed with thin serial-section electron microscopy. Nerve terminals were similar in their volume percent of mitochondria, clear vesicles and dense core vesicles among the four muscles. This was also the case for the number and size of synaptic contacts. However, presynaptic dense bars representing active zones were longer and occurred more frequently at high-output synapses than at low-output ones. High-output synapses were also characterized by the close spacing of adjacent dense bars. The longer and more closely spaced dense bars at high-output synapses would be factors in the generation of larger synaptic potentials in these terminals compared to their low-output counterparts. Other factors, however, need to be considered to fully account for the physiological differences in synaptic strength among the four muscles.

Animals↗
PubMedDate not supplied

A neglected 'accessory' vasomotor pathway: implications for blood pressure control.

1. Distinct from 'regular' sympathetic preganglionic neurons, there exists a population of 'accessory' preganglionic neurons. The latter are distinguishable by their unmyelinated axons and their different functional properties. They synapse on the same ganglion cells. 2. Ongoing sympathetic activity is driven by 'regular' preganglionic neurons. 3. 'Accessory' preganglionic neurons drive hexamethonium-resistant ganglionic transmission: part of this is muscarinic and part not (possibly peptidergic or nitrergic). 4. 'Accessory' preganglionic neurons supply cardiovascular (vasomotor, cardiac, adrenal), but apparently not other, sympathetic pathways. 5. 'Accessory' preganglionic neurons are activated by arterial chemoreceptors. 6. Brief activation of 'accessory' preganglionic neurons potentiates ongoing post-ganglionic activity for tens of minutes by an action at the ganglion. This is probably by enabling previously subthreshold excitatory post-synaptic potentials to trigger action potentials. 7. Evidence is presented that microinjections of GABA into the rostral ventrolateral medulla activate the 'accessory' pathway while inhibiting the 'regular' pathway. 8. A role for this 'accessory' pathway in the long-term control of blood pressure in health and disease is predicted, but still untested.

Animals↗
PubMed1982

Quantal analysis of a decremental response at hair cell-afferent fibre synapses in the goldfish sacculus.

1. On application of a step decrement in the sound intensity, the amplitude of excitatory post-synaptic potentials (e.p.s.p.s) recorded intracellularly from large afferent auditory fibres in goldfish's sacculus showed a decremental response in which the amplitude of the e.p.s.p.s was temporarily reduced to a very low level, but soon returned to a new steady level appropriate to the decreased sound intensity. This response seems to underlie the temporary reduction in the rate of afferent discharge observed in the mammalian cochlea upon cessation of sound or upon reduction of its intensity 2. A statistical analysis revealed that reduction in the size of the mean quantal content (m) during the decremental response was associated with reduction in the size of binomial population (n), but not that of the probability (p) of any one of the available quanta actually being used. 3. The temporary reduction in the size of n during the decremental responses can be explained if it is assumed that replenishment to vacant release sites was channelled to high threshold sites and that the low threshold sites were bypassed. The mechanism underlying this special type of replenishment is discussed in relation to the ultrastructural features of presynaptic sites in the hair cell.

Animals↗
PubMed2006

Requirement of TORC1 for late-phase long-term potentiation in the hippocampus.

Late-phase long-term potentiation (L-LTP) and long-term memory depend on the transcription of mRNA of CRE-driven genes and synthesis of proteins. However, how synaptic signals propagate to the nucleus is unclear. Here we report that the CREB coactivator TORC1 (transducer of regulated CREB activity 1) undergoes neuronal activity-induced translocation from the cytoplasm to the nucleus, a process required for CRE-dependent gene expression and L-LTP. Overexpressing a dominant-negative form of TORC1 or down-regulating TORC1 expression prevented activity-dependent transcription of CREB target genes in cultured hippocampal neurons, while overexpressing a wild-type form of TORC1 facilitated basal and activity-induced transcription of CREB target genes. Furthermore, overexpressing the dominant-negative form of TORC1 suppressed the maintenance of L-LTP without affecting early-phase LTP, while overexpressing the wild-type form of TORC1 facilitated the induction of L-LTP in hippocampal slices. Our results indicate that TORC1 is essential for CRE-driven gene expression and maintenance of long-term synaptic potentiation.

Active Transport, Cell Nucleus↗
PubMed1992

An intracellular study of the effects of GABA on frog tectal neurones in vitro.

The effects of gamma-aminobutyric acid (GABA) on neurones of the amphibian optic tectum were studied with current- and voltage-clamp recording from an isolated preparation of the midbrain of the frog Rana temporaria. Bath-applied GABA (1 mM) enhanced depolarizing synaptic potentials evoked in layer 6 tectal neurones by orthodromic stimulation of the optic tract. GABA also facilitated Na(+)- and Ca(2+)-dependent action potentials elicited by intracellular injection of depolarizing current. These actions of GABA were associated with comparatively small changes in membrane potential and their reversal potential was dependent on the Cl- equilibrium potential. Changes in input resistance observed during application of GABA were small and in part accountable for by the rectifying properties of the cell membrane. Tetrodotoxin (TTX; 1 microM) did not block the action of GABA on these neurones. These results show that externally applied GABA was able to raise directly the intrinsic excitability of frog tectal neurones and to enhance excitatory synaptic transmission elicited by stimulation of optic nerve fibres.

Action Potentials↗
PubMed1976

Physiological and morphological effects of post-ganglionic axotomy on presynaptic nerve terminals.

1. Electrophysiological and electron microscope studies were done on cells in the ciliary ganglion of chickens which had been axotomized on the day of hatching. 2. By the third day after post-ganglionic axotomy both electrical and chemical transmission through the ganglion were severely depressed; by the fifth day ganglionic transmission had disappeared. 3. Action potential initiation and conduction in axotomized cells and in their associated presynaptic nerve terminals were unimpaired 3-4 days after axotomy. 4. Depression of ganglionic transmission in 3-4 day axotomized preparations was due to a reduction in amplitude of both the excitatory post-synaptic potential (e.p.s.p.) and the electrical coupling potential in individual ganglion cells. 5. In addition to being reduced in amplitude, e.p.s.p.s in axotomized cells were more subject to fatigue during low frequency (1/sec) stimulation. 6. The reduction in e.p.s.p. amplitude was due to a reduction in both the mean quantal content of the e.p.s.p.s and the calculated depolarization produced by an individual quantum of transmitter. On the average the e.p.s.p. was reduced by a factor of about 4, the mean quantum content to about two thirds normal and the quantal size to about a third normal, compared with responses in unaxotomized cells of the same age. 7. Ultrastructural studies revealed a progressive maturation of pre-synaptic terminals in normal ganglia between 0 and 9 days after hatching. Over this period the content of synaptic vesicles and mitochondria in the terminals increased and the background matrix became more dense. 8. After axotomy these signs of maturation was abolished or reversed, particularly from the third day onward. In addition there was an increase in the number of cell sections in which no synaptic terminals were observed. 9. It was concluded that loss of synaptic transmission was due to at least three factors: a reduction in release of transmitter from presynaptic terminals, a reduction in quantal size, probably due to a loss of post-synaptic sensitivity, and a partial loss of presynaptic contact.

Action Potentials↗
PubMed1993

Lateral olfactory tract input to dentate gyrus is depressed by prior noradrenergic activation using nucleus paragigantocellularis stimulation.

Nucleus paragigantocellularis stimulation potentiates the medial perforant path population spike in the dentate gyrus via beta-receptor activation. In this study, the same paragigantocellularis stimulation preceding lateral olfactory tract pulses depressed the lateral perforant path mediated synaptic potential in dentate gyrus. Depression of the lateral olfactory tract input was blocked by a beta-antagonist. These in vivo results confirm in vitro reports that norepinephrine induces potentiation of medial perforant path input and depression of lateral perforant path input to dentate gyrus.

Animals↗
PubMed1991

Activation of NMDA receptors is necessary for fast information transfer at brainstem vagal motoneurons.

The involvement of N-methyl-D-aspartate (NMDA) excitatory amino acid subtype receptors in synaptically driven excitatory responses of ambigual motoneurons was investigated in vivo and in vitro. In urethane-anaesthetized rats, fictive oesophageal peristalsis evoked by topical application of muscarine (0.05-0.5 nmol) to the dorsal surface of the solitarial complex (NTS) was reversibly blocked by ipsilateral intraambigual injection of DL-2-amino-7-phosphonoheptanoic acid (AP-7, 0.5-1.5 nM) and (+-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP; 0.5-1.5 nM). In brainstem sagittal slices, post-synaptic potentials were recorded from neurons of the compact formation of the nucleus ambiguus (AMBc). Stimulation of presumptive NTS afferents elicited a complex excitatory postsynaptic potential (EPSP) which usually consisted of both a high-threshold fast (HTF) and a low-threshold slow (LTS) component. Bath perfusion with AP-7 (30-50 microM) and CPP (50 microM) selectively blocked the HTF without affecting the LTS component, while kynurenate (1 mM) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 5-10 microM) nonselectively suppressed both components. With sufficient stimulus strength, the EPSP generated a single spike arising from the HTF component. AP-7 (50 microM) either blocked the spike or increased the firing threshold. Furthermore, at the resting membrane potential, bath-applied NMDA induced a net inward current (269 +/- 189 pA) which had a negative slope in the range of -95 to -35 mV. In conclusion, NMDA receptors participate in solitario-ambigual synaptic transmission under physiological conditions and activation of these receptors is necessary for functional information transfer in this pathway.

2-Amino-5-phosphonovalerate↗
PubMed1994

Actions of 5-hydroxytryptamine on ventral tegmental area neurons of the rat in vitro.

Intracellular recordings were made with conventional microelectrodes and with whole-cell patch-clamp electrodes from neurons of the rat ventral tegmental area and substantia nigra zona compacta in vitro. Neurons were distinguished as principal cells and secondary cells; it is known from previous work that most principal cells contain dopamine whereas secondary cells do not. 5-Hydroxytryptamine (5-HT; 3-100 microM) depolarized (or evoked an inward current at -60 mV) 46% of 153 principal cells; a small proportion (11%) of cells were hyperpolarized (or showed outward current at -60 mV). Secondary cells were equally likely to be depolarized (or inward current at -60 mV, 30% of 80 cells) or hyperpolarized (or outward current at -60 mV, 28%). approximately 40% of each type of cell were unaffected by 5-HT. Depolarizing responses of 5-HT were mimicked by (+/-)-1-(2,5-dimethoxy-4-iodophenyl)- 2-aminopropane (DOI) and blocked by ketanserin. Hyperpolarizing responses were mimicked by dipropyl-5-carboxamidotryptamine and reversed polarity at the K+ equilibrium potential. Inhibitory postsynaptic potentials (or currents) mediated at GABAA receptors occurred spontaneously in some principal cells; they were reversibly blocked by tetrodotoxin and bicuculline. 5-HT either increased or decreased the frequency of these synaptic potentials but did not change their mean amplitude or decay time.(ABSTRACT TRUNCATED AT 250 WORDS)

Amphetamines↗
PubMed1980

Inhibition of transmitter release in bullfrog sympathetic ganglia induced by gamma-aminobutyric acid.

1. Effects of gamma-aminobutyric acid (GABA) on the nicotinic synapses in bullfrog sympathetic ganglia were studied. 2. When GABA (100 microM--1 mM) was applied to the ganglion, the post-synaptic membrane depolarized slightly and transiently with a slight decrease in the membrane resistance. 3. GABA (5 microM--1 mM) decreased the amplitude of the fast excitatory post-synaptic potentials (fast e.p.s.p.) and its quantal content without a significant change in the quantal size, and these effects were seen even after the subsidence of the membrane depolarization. Picrotoxin (10 microM) did not antagonize the GABA action. 4. The sensitivity of the subsynaptic membrane to ACh was unaffected by GABA. On the other hand, the synaptic current underlying the fast e.p.s.p. was significantly depressed in the presence of GABA. 5. Neither the frequency nor the amplitude of the miniature e.p.s.p.s which occurred spontaneously were altered by GABA, in either normal or high K+ solutions. 6. The depressant action of GABA on the fast e.p.s.p. was not changed in a high K+ solution, while it was markedly decreased in a Cl- -deficient solution. 7. A small, but significant reduction in the amplitude of the presynaptic terminal spike recorded with a focal extracellular electrode was observed under the effect of GABA. 8. It was concluded that GABA inhibits synaptic transmission of bullfrog sympathetic ganglion mainly by decreasing the evoked release of transmitter and only partly by post-synpatic action. Possible mechanisms of the presynaptic action of GABA were discussed.

Acetylcholine↗
PubMed1992

The integrative role of synaptic cotransmission in the bullfrog vasomotor C system: evidence for a synaptic gain hypothesis.

Understanding the integrative significance of synaptic cotransmission is a central problem in autonomic physiology. What are the functional roles of slow synaptic potentials in autonomic ganglia? This paper reviews the problem and its historical roots by focusing on work in the amphibian paravertebral sympathetic system. The phenotypic properties that distinguish the sympathetic B and C cell systems are summarized. Then, a synaptic gain hypothesis is proposed for the integrative function of muscarinic and peptidergic synapses in the vasomotor C system. The model states that the peripheral output of the vasomotor system is subject to synaptic amplification by two gain stages in series. The first gain stage is postulated to arise in ganglia from interactions between two slow postsynaptic potentials; the excitatory response mediated by luteinizing hormone releasing hormone, and the inhibitory response mediated by the muscarinic action of acetylcholine. The second gain stage is postulated to arise in arteries from interactions between two postganglionic cotransmitters: epinephrine and neuropeptide Y. A circuit with these properties would enable preganglionic patterns of electrical activity to regulate the system's output over a wider dynamic range than possible without cotransmitters.

Animals↗
PubMed1993

Depression of glutamatergic and GABAergic synaptic responses in striatal spiny neurons by stimulation of presynaptic GABAB receptors.

The influence of gamma-aminobutyric acidB (GABAB) receptor stimulation on the excitatory and inhibitory synaptic potentials and membrane properties of identified striatal spiny neurons was examined in a corticostriatal slice preparation. Stimulation of the subcortical white matter evoked a monosynaptic, excitatory postsynaptic potential (EPSP) and a polysynaptic, inhibitory postsynaptic potential (IPSP) in spiny neurons. The EPSP had two components: a large amplitude response which could be blocked by the kainate/quisqualate receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM), and a small amplitude, long-duration depolarization which could be blocked by the N-methyl-D-aspartate receptor antagonist, d-(-)-2-amino-5-phosphonovaleric acid (APV, 100 microM). The IPSP was observed as a membrane depolarization when recorded from neurons at resting membrane potential. However, when neurons were injected with the Na(+)-channel blocker, QX-314, allowing cells to be depolarized above their spike thresholds, a prominent hyperpolarizing IPSP was readily observed which could be blocked by the GABAA antagonist, bicuculline (10-50 microM). This bicuculline-sensitive IPSP was responsible for the inhibition of EPSP amplitude and probability of spike discharge revealed using paired stimulation of the subcortical white matter. The amplitude of both the EPSP and the IPSP were depressed by the GABAB receptor agonist, p-chlophenyl-GABA (baclofen, 0.5-100 microM) in a concentration-dependent manner. Baclofen also blocked paired stimulus inhibition of spike discharge. These effects of baclofen persisted in slices in which the cortex was removed and were reversed by the GABAB receptor antagonist, 3-amino-3-hydroxy-2-(4-chlorophenyl)-propanesulphonic acid (saclofen, 100-500 microM). In contrast to its profound influence on synaptic input, baclofen did not alter resting membrane potential, input resistance, membrane current-voltage relationship, or spike threshold of the cells recorded, and therefore did not appear to exert direct postsynaptic effects on the striatal spiny neurons. Taken together, these data indicate that the depressant effects of baclofen on EPSPs are mediated through GABAB receptors located on the terminals of glutamatergic afferents within the striatum. Moreover, the results suggest that the actions of baclofen on IPSPs and paired stimulus inhibition are produced by activation of GABAB receptors within the striatum at a site presynaptic to spiny neurons, either on the terminals of GABAergic afferents or on an interposed non-spiny GABAergic cell. Thus, GABAB hetero- and auto-receptors have the capacity to provide a negative feedback mechanism through which the major excitatory and inhibitory inputs to striatal spiny neurons are regulated.

2-Amino-5-phosphonovalerate↗