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 919 records · Page 51Linked to original sources

Time- and dose-dependent changes in neuronal activity produced by X radiation in brain slices.

A new method of exposing tissues to X rays in a lead Faraday cage has made it possible to examine directly radiation damage to isolated neuronal tissue. Thin slices of hippocampus from brains of euthanized guinea pigs were exposed to 17.4 ke V X radiation. Electrophysiological recordings were made before, during, and after exposure to doses between 5 and 65 Gy at a dose rate of 1.54 Gy/min. Following exposure to doses of 40 Gy and greater, the synaptic potential was enhanced, reaching a steady level soon after exposure. The ability of the synaptic potential to generate a spike was reduced and damage progressed after termination of the radiation exposure. Recovery was not observed following termination of exposure. These results demonstrate that an isolated neuronal network can show complex changes in electrophysiological properties following moderate doses of ionizing radiation. An investigation of radiation damage directly to neurons in vitro will contribute to the understanding of the underlying mechanisms of radiation-induced nervous system dysfunction.

Action Potentials↗

5-hydroxytryptamine is a fast excitatory transmitter at 5-HT3 receptors in rat amygdala.

A fast excitatory synaptic potential mediated by 5-hydroxytryptamine (5-HT) was recorded in rat lateral amygdala neurons in brain slices. The synaptic potential has brief duration (tens of milliseconds), is mimicked by 5-HT, is potentiated by a 5-HT uptake inhibitor, and is blocked by selective 5-HT3 receptor antagonists. The underlying synaptic current reversed polarity at about 0 mV. This is an example of fast neurotransmission in the mammalian brain mediated by an amine rather than an amino acid. The antiemetic, anxiolytic, and perhaps antipsychotic actions of 5-HT3 antagonists might result from blockade of such synapses.

2-Amino-5-phosphonovalerate↗

Effects of dopamine on the superior cervical ganglion of the rabbit.

1. The effects of dopamine on isolated rabbit superior cervical ganglion were investigated with intracellular recording techniques.2. Dopamine (10(-5)-10(-3)M) depressed the amplitude of the excitatory post-synaptic potential (e.p.s.p.) and blocked impulse transmission.3. Dopamine (10(-4)M) induced a slight (2-5 mV) post-synaptic hyperpolarization without altering membrane conductance.4. The post-synaptic membrane sensitivity to acetylcholine (ACh) applied iontophoretically was not affected by dopamine.5. Dopamine decreased the frequency of miniature excitatory post-synaptic potentials (m.e.p.s.p.s) in a high K(+) solution, with no change in the amplitude of m.e.p.s.p.s.6. Dopamine reduced the quantal content of the e.p.s.p. in a low Ca(2+) and high Mg(2+) solution, but had no effect on the quantal size.7. The ganglionic blocking effect of dopamine was antagonized by phenoxybenzamine, but not by propranolol.8. The results show that the ganglionic depressant effect of dopamine is exerted primarily through an alpha-adrenoceptive site at the presynaptic nerve terminal.

Acetylcholine↗

Over-expression of tau results in defective synaptic transmission in Drosophila neuromuscular junctions.

We have shown that over-expression of human tau (0N3R) in Drosophila larval motor neurons causes significant morphological and functional disruption to the neuromuscular junctions (NMJs). Tau-expressing NMJs are reduced in size with irregular and abnormal bouton structure. Immunocytochemical analysis shows that the abnormal NMJs still retain synaptotagmin expression and form active zones. Functionally, the NMJs exhibit abnormal endo/exocytosis as revealed by incorporation of the styryl dye FM1-43. Electrophysiological studies showed that with low frequency stimulation (1 Hz), evoked synaptic potentials produced from tau over-expressing motor neurons were indistinguishable from wild type, however, following high frequency stimulation (50 Hz), evoked synaptic potentials were significantly decreased. Analysis of the number and distribution of mitochondria showed that motor neurons over-expressing tau had a significant reduction in functional mitochondria in the presynaptic terminal. Collapsing the mitochondrial membrane potential in wild type larvae phenocopied the effects of tau over-expression on synaptic transmission. Our results demonstrate that tau over-expression in vivo cause a synaptic dysfunction, which may be caused by a reduced complement of functional mitochondria.

Animals↗

In vivo recording from identifiable neurons of the locomotor network in the developing zebrafish.

The zebrafish is a popular model for developmental studies due to its accessibility by cellular, molecular and genetic approaches. As a complement to these other methods, we have devised an exposed hindbrain/spinal cord preparation in the curarized zebrafish embryo and larva that permits intracellular labeling and patch clamp recording from individually identified sensory neurons, motoneurons and interneurons in vivo. Regular bursts of synaptic potentials and action potentials were observed under whole-cell current clamp in embryonic motoneurons and in some identified interneurons. Larval neurons showed prolonged depolarizations with synaptically driven bursts of action potentials. Frequent spontaneous synaptic potentials were observed and synaptic currents were effectively space clamped. It is thus feasible to study in vivo the properties of identifiable neurons of the developing locomotor network in the zebrafish, including their synaptic activity, firing patterns and interconnections.

Action Potentials↗

A barbiturate induced intensification of the inhibitory potential in slices of guinea-pig olfactory cortex.

1. A study has been made of the effect of barbiturates on membrane constants and synaptic potentials of neurones in the isolated guinea-pig olfactory cortex slice. 2. Normally, a long depolarizing i.p.s.p. follows the e.p.s.p. Pentobarbitone (0.1 mM) produced a tenfold increase in the duration of the high conductance phase of this i.p.s.p. 3. The i.p.s.p. was potentiated increasingly with higher barbiturate concentrations from 0.02 to 1.0 mM-pentobarbitone and 0.2 to 5 mM-phenobarbitone. 4. The resting membrane conductance, the initial phase of the e.p.s.p. and the threshold for the action potential were unaffected at lower concentrations. 5. The highest barbiturate doses increased the resting membrane conductance. This was associated with a depolarization of about 14 mV maximally and resulted in smaller synaptic potentials. The effect was probably generated by the same mechanism as the i.p.s.p. 6. This fortifies the idea that barbiturates have a primary action on prolonging inhibition rather than a depression in the excitatory potential.

Action Potentials↗

Persistent excitability changes in the piriform cortex of the isolated guinea-pig brain after transient exposure to bicuculline.

The development of long-lasting excitability changes after a single intracerebral injection of bicuculline (1 mM) in a restricted region of the anterior piriform cortex was studied by means of simultaneous intra- and extracellular recordings in the isolated guinea-pig brain preparation maintained in vitro by arterial perfusion. The transitory disinhibition induced by bicuculline revealed transient afterdischarges that were followed by the activation of a synaptic potential mediated by the recurrent propagation of the focal epileptiform activity along cortico-cortical associative fibres. The epileptiform associative potential persisted for the duration of the experiment. Both the induction and the long-term expression of the epileptiform associative potential were dependent on the activation of glutamatergic receptors of the NMDA type, as demonstrated by perfusion with the NMDA receptor antagonist 2-aminopentanoic acid (AP5) (100 microM). After bicuculline washout, piriform cortex neurons responded to afferent stimulation with a burst discharge superimposed on a paroxysmal depolarizing potential. The early component of the burst was mediated by a Ca(2+)-dependent, non-synaptic potential located at the proximal apical dendrites and soma of layer II-III cells, since (i) it was abolished by membrane hyperpolarization, (ii) it was not affected by AP5, (iii) it was correlated with a current sink in layer II, as demonstrated by current source density analysis of field potential laminar profiles, and (iv) it was abolished by cadmium (2-5 mM) applied locally in layer II. The late component of the burst response (i) coincided in time with the extracellular epileptiform associative potential, (ii) increased linearly in amplitude during membrane hyperpolarization, (iii) was blocked by AP5, and (iv) was correlated with an extracellular sink in layer Ib, where the associative fibres contact the distal apical dendrites of piriform cortex neurons. The results presented here indicate that a transient focal disinhibition promotes persistent intrinsic and synaptic excitability changes in piriform cortex neurons. These changes may be responsible for the propagation of epileptiform activity and for the induction of secondary epileptogenesis.

Animals↗

Synaptic and non-synaptic mechanisms underlying low calcium bursts in the in vitro hippocampal slice.

1. The epileptiform activity generated by lowering extracellular [Ca++] was studied in the CA1 subfield of rat hippocampal slices maintained "in vitro" at 32 degrees C. Extracellular and intracellular recordings were performed with NaCl and KCl filled microelectrodes. 2. Synaptic potentials evoked by stimulation of the stratum radiatum and alveus were blocked upon perfusion with artificial cerebrospinal fluid (ACSF) containing 0.2 mM Ca++, 4 mM Mg++. Blockade of synaptic potentials was accompanied by the appearance of synchronous field bursts which either occurred spontaneously or could be induced by stimulation of the alveus. 3. Both spontaneous and stimulus-induced low Ca++ bursts recorded extracellularly in stratum pyramidale consisted of a negative potential shift with superimposed population spikes. This extracellular event was closely associated with intracellularly recorded action potentials rising from a prolonged depolarization shift. Steady hyperpolarization of the cell membrane potential decreased the amplitude of the depolarizing shift suggesting that synaptic conductance were not involved in the genesis of the low Ca++ burst. 4. Spontaneous depolarizing inhibitory potentials recorded in normal ACSF with KCl filled microelectrodes were reduced in size in low Ca++ ACSF. However, small amplitude potentials could still be observed at a time when low CA++ bursts were generated by hippocampal CA1 pyramidal neurons. 5. Bicuculline methiodide, an antagonist of gamma-aminobutyric acid (GABA), was capable of modifying the frequency of occurrence and the shape of synchronous field bursts. The effects evoked by bicuculline methiodide were, however, not observed when 81-100% of NaCl was replaced with Na-Methylsulphate.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

Synaptic behaviour of myenteric neurones in the gastric corpus of the guinea-pig.

1. Synaptic behaviour of ganglion cells in the myenteric plexus of the corpus of the guinea-pig stomach was investigated using intracellular recording methods. Synaptic potentials were evoked by focal electrical stimulation of interganglionic fibre tracts or the surface of the ganglion containing the cell body from which the recording was obtained. 2. Fast excitatory postsynaptic potentials (EPSPs) mediated by nicotinic cholinergic receptors were the most common stimulus-evoked or spontaneously occurring synaptic events. 3. Fast EPSPs were evoked in every neurone and most neurones received multiple inputs from axons arriving in several different interganglionic fibre tracts. Several neurones received input from multiple axons in individual fibre tracts. 4. Fast EPSPs were evoked at stimulus frequencies up to 80 Hz without evidence of the 'run-down' phenomenon that characterizes fast EPSPs in the intestine. 5. Trains of EPSPs in the ganglion cell soma occurred with relatively long latencies following spike discharge evoked by intracellular current injection in the same neurone. This appeared to reflect return of excitatory synaptic input to the soma along recurrent connections within the synaptic network. 6. The safety factor for fast EPSPs to evoke spike discharge was highest for gastric I neurones. Probability of fast EPSPs triggering spikes was intermediate in neurones classified electrophysiologically as gastric II and was lowest in gastric III neurones, which never discharged spikes during a fast EPSP. 7. No slow excitatory or inhibitory synaptic potentials, like those found in intestinal ganglion cells, were evoked in gastric neurones by focal stimulation of the fibre tracts. 8. The results suggest that myenteric neurones in the gastric corpus of the guinea-pig have distinctive synaptic behaviour different from intestinal neurones in the same animal. This may be a reflection of adaptation for neural control of the specialized function of the effector systems in this region of the stomach.

Animals↗

Histamine as a neurotransmitter in the stomatogastric nervous system of the spiny lobster.

Histamine is a putative neurotransmitter in mammals and molluscs, but its role in the nervous systems of other animals is not known. This study examines the possibility that histamine is a neurotransmitter in an arthropod. Results show that first, 14 neurons in the stomatogastric ganglion of the spiny lobster respond to histamine. The response is inhibitory, is mediated by an increased conductance to chloride, and desensitizes with repeated applications of histamine. These same 14 neurons receive one type of synaptic potential from two extrinsic neurons, the "through-fibers" of the inferior ventricular nerve. This synaptic potential is also inhibitory, is mediated by an increased conductance to chloride, and is blocked when histamine receptors are desensitized. Second, assays of endogenous histamine indicate that histamine is distributed nonuniformly throughout the stomatogastric nervous system and that its distribution correlates with the axonal pathways and terminal arborizations of the inferior ventricular nerve through-fibers. Lastly, histamine is present in relatively high concentrations in the cell bodies of the through-fibers, whereas it is not detectable in other neurons in the stomatogastric system. These results suggest that histamine may be a transmitter in the lobster.

Action Potentials↗

Models of synchronized hippocampal bursts in the presence of inhibition. II. Ongoing spontaneous population events.

1. We extended our computer model of the CA3 region of the hippocampal slice in order to study spontaneous activity occurring in the presence and absence of synaptic inhibition. This was done by providing a steady inward current to the excitatory neurons, whose value was randomly chosen for each cell. With the parameters used, many of the excitatory cells would, if synaptically isolated, remain quiescent, whereas others would burst periodically with periods as brief as 750 ms. Simulations were run for as long as 10 s of neural activity. 2. In the presence of synaptic inhibition, neural activity became organized into recurring, partially synchronized events: clusters of neurons (6% to 12% of the population) would discharge together, with a period averaging 340 ms, shorter than the burst period of any individual neuron. A consequence of periodic clusters of cellular bursts was the widespread occurrence of periodic synchronized synaptic potentials, as have been observed in hippocampal slices and human temporal neocortical slices. The periods between these synaptic potentials are similar in the model to those observed experimentally. 3. The period could be slowed by either increasing the time constant of the slow inhibitory postsynaptic potential (IPSP), or by making the excitatory synapses more powerful. The period seems to be generated in part as follows. Consider those cells with rapid spontaneous discharge rates. An upper bound for the period corresponds to the interval between 1) such a cell's becoming responsive enough to an excitatory synaptic input to burst, and 2) such a cell's bursting spontaneously (i.e., in response to its own intrinsic inward current). For cells with rapid spontaneous discharge rates, the interval defined in this way is approximately 350 ms. 4. Different cells participated in each cluster. A given cluster was initiated by one cell or by two cells bursting together, and spread via excitatory synapses. Excitatory synaptic paths could be traced from the initiating cell(s), directly or through other participants, to all cells participating in a cluster. Spread of activity was limited by two mechanisms, so that not all cells synaptically excited by a participating cell would themselves participate. First, cells might be refractory from having participated in a recent cluster (since the intercluster period was less than the refractory time from a cellular burst to its responsiveness to a synaptic stimulus). Second, some cells might be synaptically inhibited. Synaptic inhibition in this model did not act rapidly enough to suppress the cluster totally.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

5-Hydroxytryptamine decreases the sensitivity of nicotinic acetylcholine receptor in bull-frog sympathetic ganglion cells.

The post-synaptic effects of 5-hydroxytryptamine (5-HT) were examined in neurones of bull-frog sympathetic ganglia with intracellular micro-electrode and voltage-clamp recording techniques. Atropine (1 microM) was used to block the muscarinic cholinoceptors. 5-HT reduced the amplitude of the fast excitatory post-synaptic potential (fast e.p.s.p.). 5-HT also reduced the mean amplitude of the miniature excitatory post-synaptic potentials (m.e.p.s.p.s) without affecting their frequency. Voltage-clamp studies showed that 5-HT decreased in a dose-dependent manner the amplitude of the acetylcholine (ACh) current produced by ionophoretic application of ACh to sympathetic neurones. The relationship between the log of the ACh dose, applied ionophoretically, and the peak ACh current (the dose-response curve) was examined in voltage-clamped neurones. 5-HT caused a parallel shift to the right of the dose-response curve for ACh. Analysis using a double reciprocal plot (Lineweaver-Burk plot) revealed that 5-HT increased the apparent dissociation constant (Km) of ACh for the receptor without changing the maximum ACh current (Vmax), suggesting a competitive antagonism. The relationship between the 5-HT dose and the magnitude of inhibition of the ACh current was obtained using two different amplitudes for the ACh response. The dose-response curve of 5-HT-induced inhibition using a relatively high amplitude ACh current, S1, was parallel with that for a relatively low amplitude ACh current, S2. The Dixon plot of these two curves yielded an apparent inhibition constant (Ki) of 42 microM. Both fast excitatory post-synaptic currents (fast e.p.s.c.s) and miniature excitatory post-synaptic currents (m.e.p.s.c.s) had single-exponential decay time courses. The time constants of fast e.p.s.c. decay (tau e) and m.e.p.s.c. decay (tau m) were not altered by 5-HT, suggesting that 5-HT does not change the kinetics of opening and closing of the ionic channel associated with the nicotinic receptor. 5-HT did not alter the reversal potential of the fast e.p.s.c. These results suggest that 5-HT decreases the sensitivity of the nicotinic receptor of sympathetic neurones, by interfering with ACh binding at the active site on the receptor-ionic-channel complex. 5-HT may physiologically inhibit cholinergic transmission as it is an endogenous substance which antagonizes the nicotinic receptor in post-ganglionic neurones of bull-frog sympathetic ganglia.

Acetylcholine↗

Transient and persistent consequences of acute stress on long-term potentiation (LTP), synaptic efficacy, theta rhythms and bursts in area CA1 of the hippocampus.

Previous studies reported that exposure to an acute stressor of restraint and intermittent tailshock impairs long-term potentiation (LTP) in area CA1 of the rat hippocampus. In the first experiment, the longevity of the stress-induced impairment of LTP was determined. LTP of the excitatory postsynaptic potential (EPSP) was impaired 2 but not 4 days after stressor cessation. Exposure to the stressor also persistently enhanced the synaptic response to the tetanic stimulation patterned after theta rhythm activity (10, 100 Hz bursts delivered at 5 Hz). In a second experiment, we tested the hypothesis that exposure to the stressor enhanced synaptic efficacy itself. EPSPs were recorded from freely moving rats before, during and after stressor exposure. The synaptic response was not enhanced during stressor exposure. Instead, cessation of the stressor (and perhaps movement associated with release from restraint) induced a transient (< 2 min) decrease in synaptic efficacy. To determine whether exposure to the stressor enhances endogenous theta rhythms in area CA1, electroencephalographic (EEG) recordings were obtained from freely moving rats before, during and after exposure to the stressor. The power of theta (4-8 Hz) and low frequency (0.1-3.9 Hz) activity was enhanced in response to the tailshock aspect of the stressor. Together, the results indicate that exposure to an acute stressful event increases theta activity and its cessation transiently decreases synaptic efficacy. These transient effects are succeeded by a persistently sensitized response to theta burst stimulation and impaired LTP.

Acute Disease↗

Modulating excitatory synaptic neurotransmission: potential treatment for neurological disease?

Excitatory neurotransmission at many CNS synapses depends upon AMPA-type glutamate receptors. Derangements in AMPA receptor-mediated synaptic transmission may be a contributing factor in neurological and neurodegenerative diseases and could be a target for therapeutic intervention. Drugs that positively modulate AMPA receptors by reducing AMPA receptor desensitization and/or slowing AMPA receptor deactivation, such as thiazide derivative (cyclothiazide, diazoxide, IDRA 21) and benzoylpiperidine derivatives (1-BCP, CX516, aniracetam), facilitate AMPA receptor-mediated processes and may have beneficial therapeutic effects. For example, AMPA modulators facilitate long-term potentiation, which may be important for memory storage, and facilitate memory encoding in behavioral experiments. Thus, AMPA modulators might ameliorate memory deficits that occur in dementia, such as Alzheimer's disease. However, AMPA receptor-mediated excitotoxicity may occur with excessive AMPA receptor activation such as in seizures or ischemia, and positive AMPA modulators would promote neuronal injury under those conditions. Regardless of the ultimate clinical utility of positive AMPA modulators, their discovery and study have already provided significant insight into the physiology and structural determinants of important AMPA receptor properties. This review attempts to synthesize a variety of studies that have utilized these AMPA modulators to gain insight into fundamental as well as clinically relevant AMPA receptor-mediated processes.

Animals↗

L-Glutamate effects on electrical potentials of synaptic plasma membrane vesicles.

The electrogenic nature of the L-glutamate-stimulated Na+ flux was examined by measuring the distribution of the lipophilic anion [35S]thiocyanate (SCN-) into synaptic membrane vesicles that were incubated in a NaCl medium. Concentrations of L-glutamate from 10(-7) to 10(-4) M added to the incubation medium caused an enhanced intravesicular accumulation of SCN-. Based on the SCN- distribution in synaptic membrane vesicles it was calculated that 10 microM L-glutamate induced an average change in the membrane potential of + 13 mV. L-Glutamate enhanced both the Na+ and K+ conductance of these membranes as determined by increases in SCN- influx. Other neuroexcitatory amino acids and amino acid analogs (D-glutamate, L-aspartate, L-cysteine sulfinate, kainate, ibotenate, quisqualate, N-methyl-D-aspartate, and DL-homocysteate) also increased SCN- accumulation in synaptic membrane vesicles. These observations are indicative of the activation by L-glutamate and some of its analogs of excitatory amino acid receptor ion channel complexes in synaptic membranes.

Animals↗

[Nootropic substances enhance the N-methyl-D-aspartate-induced short-term potentiation of synaptic transmission in rat hippocampal slices].

The nootropic agents pyracetam, ethymisole, N-5-oxynicotinoyl glutamate and beta-carboline derivative--ambocarb--enhance short-term potentiation of populational EPSP's amplitude of area CA1 pyramidal neurons in the slices of the rat hippocampus, which is evoked by NMDA. The inhibitors of protein kinases diminish the effect of pyracetam and ethymisole (tolbutamide), as well as all the studied nootropic drugs (polymyxin B and trifluoroperazine).

Animals↗