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PubMed1995

Enhancement of NMDA receptor mediated synaptic potentials of rat hippocampal neurones in vitro by thyrotropin releasing hormone.

The effects of thyrotropin releasing hormone (TRH) on excitatory postsynaptic potentials (EPSPs) evoked by electrical stimulation of Schaffer collaterals on CA1 neurones of the adult rat hippocampal slice preparation were investigated using intracellular recording under current clamp conditions. At resting membrane potential and in the presence of extracellular Mg2+, TRH (10-20 microM) largely potentiated NMDA receptor-mediated EPSPs while leaving those mediated by non-NMDA receptors unaffected. This phenomenon had a brief duration (approximately 2 min) and was not accompanied by changes in resting membrane potential or input conductance. It is suggested that TRH provided a transient upregulation of synaptic responses due to NMDA receptor activation.

Action Potentials↗
PubMedDate not supplied

[Relation between fast and slow elemental synaptic potentials in command neurons in Helix lucorum taurica L].

In experiments on a semi-intact snail preparation and a preparation of the snail isolated CNS, after spikes (Sp) evoked in presynaptic neurones by depolarizing current, not only rapid (R) EPSPs emerged in the command neurones of the defensive reaction of closing the pneumostome, but they were also followed by slow (S) EPSPs lasting over 2 min. For each single synaptic contact, the R and S EPSP amplitudes were in a good linear correspondence. In different synapses no direct connection was observed between R EPSP and S EPSP. It is suggested that R and S EPSPs may set in as a result of the action of different substances on the command neurones. Functional significance of S EPSPs with different amplitudes in different command neurones may consist in a prolonged specific preparation of the neurones for the action of stimuli.

Animals↗
PubMed2002

Localized synaptic potentiation by BDNF requires local protein synthesis in the developing axon.

Brain-derived neurotrophic factor (BDNF) is known to promote neuronal survival, guide axonal pathfinding, and participate in activity-dependent synaptic plasticity. In Xenopus nerve-muscle cultures, localized contact of a single BDNF-coated bead with the presynaptic axon resulted in potentiation of transmitter secretion at the developing synapses, but only when the bead was placed within 60 microm from the synapse. The localized potentiation induced by BDNF is accompanied by a persistent local elevation of [Ca(2+)](i) in the axon and requires constitutive presynaptic protein translation, even for axons severed from the cell body. Thus, presynaptic local TrkB signaling and protein synthesis allow a localized source of BDNF to potentiate transmitter secretion from nearby synapses, a property suited for spatially restricted synaptic modification by neurotrophins.

Acetylcholine↗
PubMed1993

Post-synaptic potentiation of vagal contractile responses by neurokinin A.

We have studied the effect of neurokinin A (NKA) on tracheal smooth muscle (TSM) contraction caused by administration of acetylcholine (ACh) intra-arterially (ia) into the tracheal circulation, or bilateral stimulation of the vagus nerves, in 26 mongrel dogs. The tracheal contractile response to 10(-7) mol NKA was 3.12 +/- 0.48 g/cm, 6.3 +/- 0.7%AChmax. Plasma histamine concentration was measured in the right atrium at the peak response following administration of NKA. Plasma histamine concentration was 3.33 +/- 2.05 ng/ml after 10(-7) mol NKA (vs. 1.82 +/- 0.54 ng/ml for control, P > 0.10). A frequency-response curve was generated by electrical stimulation of the caudal ends of cut cervical vagi over the range of frequencies 1-20 Hz (constant 30 V) at 15 s intervals 10 min before and 10 min after administration of 10(-8) mol NKA. Substantial augmentation of tracheal contractile responses to 10(-10)-10(-7) mol ia ACh was obtained 10 min after administration of NKA (P < 0.05). Significant potentiation of tracheal contraction to vagal stimulation for 10-20 Hz was also observed after administration of 10(-8) mol NKA (P < 0.05). We have demonstrated a substantial contractile effect of NKA on canine tracheal smooth muscle that is not related to histamine release from respiratory mast cells. We have also demonstrated that NKA causes augmentation of the parasympathetic tracheal contractile response induced by ia administration of ACh and efferent vagus nerve stimulation. These data suggest that potentiation of vagal contractile response by NKA is related to post-synaptic activation of the parasympathetic nerves.

Acetylcholine↗
PubMed1979

Ionic basis of different synaptic potentials mediated by an identified dopamine-containing neuron in Planorbis.

A specified dopamine neuron in Planorbis corneus produces dopamine-mediated e.p.s.ps, i.p.s.ps or biphasic, depolarizing-hyperpolarizing p.s.ps in different follower neurons. The excitatory potentials were of three types. Some follower neurons exhibited slow e.p.s.ps (ca 1 s), and a long-lasting, slowly desensitizing, depolarizing response to iontophoresed dopamine. Others showed rapid (ca. 150 ms) e.p.s.ps, often of variable amplitude, and a rapid, quickly desensitizing, response to iontophoresed dopamine. The rapid e.p.s.ps were sometimes followed by the inhibitory response (biphasic potential). The e.p.s.ps were potentiated by hyperpolarization and reduced by depolarization, though they could not be inverted. The slow e.p.s.p. was shown to be associated with an increase in membrane conductance, but it has proved difficult to elucidate the ions involved. A third type of e.p.s.p. was produced by electrical transmission. The inhibitory potentials were generally reduced in amplitude by artificial hyperpolarization but could rarely be inverted. This is probably due in part to the presence of of electrotonic coupling between these follower neurons. The i.p.s.ps were associated with an increase in conductance which appeared small when measured in the cell body. However, the i.p.s.ps produced considerable shunting of electrotonic transmission between coupled followers indicating a large increase in conductance at the synapse. I.p.s.ps were unaffected by Cl-free solution but they were greatly reduced, though rarely inverted, by increasing the external K concentration. They were blocked by intracellular tetraethylammonium, or cooling. The effects on corresponding responses to iontophoresed dopamine were in each case the same as on the i.p.s.ps. It is concluded that the i.p.s.ps mediated by the dopamine neuron are produced by an increase in permeability to K+. On a few occasions i.p.s.ps mediated by the dopamine neuron were potentiated by hyperpolarization. This appeared to be caused by a sharp increase in membrane resistance with hyperpolarization of these particular neurons. However, mediation by a mechanism of conductance decrease could not be completely excluded.

Animals↗
PubMed1986

[Effect of strontium, barium and manganese ions on non-adrenergic inhibitory synaptic potentials and the action of ATP in the smooth muscle of the human intestine].

The ionic mechanism of nonadrenergic inhibition in smooth muscles of human intestine was studied by the sucrose-gap method. The results obtained suggest that calcium-dependent potassium conductance which consists of apamin-sensitive and -insensitive components is involved in the action of nonadrenergic transmitter in smooth muscles of human intestine.

Adenosine Triphosphate↗
PubMed1983

Acetylcholine mediates a slow synaptic potential in hippocampal pyramidal cells.

The hippocampal slice preparation was used to study the role of acetylcholine as a synaptic transmitter. Bath-applied acetylcholine had three actions on pyramidal cells: (i) depolarization associated with increased input resistance, (ii) blockade of calcium-activated potassium responses, and (iii) blockade of accommodation of cell discharge. All these actions were reversed by the muscarinic antagonist atropine. Stimulation of sites in the slice known to contain cholinergic fibers mimicked all the actions. Furthermore, these evoked synaptic responses were enhanced by the cholinesterase inhibitor eserine and were blocked by atropine. These findings provide electrophysiological support for the role of acetylcholine as a synaptic transmitter in the brain and demonstrate that nonclassical synaptic responses involving the blockade of membrane conductances exist in the brain.

Acetylcholine↗
PubMed1999

Interleukin-1beta inhibits a tetraethylammonium-induced synaptic potentiation in the rat dentate gyrus in vitro.

The effect of the pro-inflammatory cytokine, interleukin-1beta on an NMDA receptor-independent form of synaptic plasticity brought about by the application of the K+ channel blocker tetraethylammonium, was examined in the rat dentate gyrus in vitro. Field excitatory postsynaptic potentials (EPSPs) were recorded from the medial perforant path of the dentate gyrus every 20 s. Perfusion of the K+ channel blocker, tetraethylammonium chloride (25 mM) for 10 min and subsequent washout gave rise to robust and long-term potentiation of the field EPSP slope (tetraethylammonium induced long-term potentiation; 125+/-5% of baseline 60 min following tetraethlylammonium-washout; n = 7, P < 0.05) Application of interleukin-1beta (1 ng/ml) for 30 min was found to inhibit the induction, but not the maintenance of the tetraethylammonium induced long-term potentiation (n = 8). Heat denatured interleukin-1beta had no effect on tetraethylammonium induced long-term potentiation (n = 6). The expression of tetraethylammonium induced long-term potentiation was found to be accompanied by an increase in the magnitude of paired pulse depression seen at interstimulus intervals of 20 and 100 ms (controls, 42+/-5% and 13+/-2%; tetraethylammonium, 62+/-5% and 22+/-2% respectively for both intervals; n = 6, P < 0.05). The increase in paired pulse depression at an interstimulus interval of 100 ms was significantly attenuated by pre-treatment of slices with interleukin-1beta. The inhibitory effect of interleukin-1beta on both tetraethylammonium induced long-term potentiation and the tetraethylammonium induced increase in paired pulse depression was antagonised by pre-incubation with the interleukin-1 receptor antagonist. Interleukin-1 receptor antagonist was found to have no effect on tetraethylammonium induced long-term potentiation when applied on its own (n = 5). The p38 mitogen activated protein kinase inhibitor SB203580 (4-(4-fluorophenyl)-2-(4 methylesulfinylphenyl)-5-(4-pyridyl)1H-imidazole) was also found to inhibit the induction of tetraethylammonium induced long-term potentiation (n = 6). These findings suggest a possible role for interleukin-1beta in the modulation of NMDA receptor-independent synaptic plasticity in the rat dentate gyrus.

Animals↗
PubMed1991

Synaptic potentials evoked by convergent somatosensory and corticocortical inputs in raccoon somatosensory cortex: substrates for plasticity.

1. "Unmasking" of weak synaptic connections has been suggested as a mechanism for the early changes in cortical topographic maps that follow alterations of sensory activity. For such a mechanism to operate, convergent sensory inputs must already exist in the normal cortex. 2. We tested for topographic and cross-modality convergence in primary somatosensory cortex of raccoon. The representation of glabrous skin of forepaw digits was chosen because, even though it is dominated by inputs from the glabrous skin of a single digit, it nevertheless comes to respond to stimulation of other digits when, e.g., a digit is removed. 3. Intracellular recordings were made from 109 neurons in the representation of glabrous skin of digit 4. Neurons were tested for somatosensory inputs with electrical and natural stimulation of digits. 4. Excitatory postsynaptic potentials (EPSPs) were evoked in 100% of the neurons (109/109) by electrical stimulation of glabrous skin of digit 4, and in 79% (31 of 39) by vibrotactile stimulation. 5. Glabrous skin of digit 4 was not the sole source of somatosensory inputs. A minority of neurons generated EPSPs after electrical stimulation of hairy skin of digit 4 (10 of 98 neurons, 10%). Electrical stimulation of digits 3 or 5 evoked EPSPs in 22 of 103 neurons (21%). Natural stimulation (vibrotactile or hair bending) was also effective in most of these latter cases (digit 3, 6/7; digit 5, 9/10). 6. Intracortical microstimulation of the "heterogeneous zone" was used to test for corticocortical connections to neurons in the glabrous zone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

The effects of Ca2+, Mg2+ and kynurenate on primary afferent synaptic potentials evoked in cat spinal cord neurones in vivo.

1. A technique was developed for perfusing the central canal of the cat spinal cord over a defined region to alter the extracellular environment and examine the effects of various ions and pharmacological agents on synaptic transmission in vivo. 2. Monosynaptic excitatory postsynaptic potentials (EPSPs) evoked by hindlimb muscle nerve stimulation were recorded intracellularly from dorsal spinocerebellar tract (DSCT) neurones in Clarke's column, in close proximity to the central canal. 3. The effects of central canal perfusion of solutions containing Ca2+, Mg2+ and kynurenate on the monosynaptic afferent EPSP were examined. 4. Perfusion of the central canal with solutions containing a high Mg2+ concentration completely and reversibly blocked the monosynaptic EPSP, while perfusion with solutions containing a high Ca2+ concentration produced up to a fourfold increase in the peak amplitude of the EPSP. This large increase in the EPSP indicates that the pool of quanta available for release is considerably greater than estimated from previous quantal analysis studies at this synaptic connection. 5. Perfusion of the central canal with kynurenate, an antagonist at excitatory amino acid receptors, resulted in a complete block of the monosynaptic EPSP in DSCT neurones. This provides direct evidence that an excitatory amino acid, such as glutamate, is released from primary muscle afferent terminals in Clarke's column of the cat spinal cord in vivo.

Animals↗
PubMed1991

Quantal components of the synaptic potential induced in hippocampal neurons by activation of granule cells, and the effect of 2-amino-4-phosphonobutyric acid.

The probabilistic nature of excitatory postsynaptic potentials (EPSPs) induced monosynaptically in CA3 neurons by impulses of granule cells was studied in thin transverse sections of the guinea pig hippocampus. More than 600 EPSPs were recorded under several conditions, their amplitudes were measured, and histograms representing the EPSP amplitude distribution were constructed. Quantal parameters were estimated by the method of maximum likelihood. Of 9 neurons examined in the control solution, one neuron showed an exceptionally large number of transmission failures. The amplitude distribution of EPSPs recorded from this neuron could be described by Pascal statistics, but not by binomial or Poisson statistics. The EPSP amplitude distribution from the other neurons could be described by either binomial, Poisson, or Pascal predictions with a minor preference for the last statistic. When an apparently homogeneous group of data was divided into two subgroups and parameters were estimated separately, inconsistent values were obtained in some neurons with no failures. 2-Amino-4-phosphonobutyric acid (APB) suppressed the EPSPs reversibly at relatively low concentrations. Theoretical curves calculated according to the Pascal statistics fit quite well to the entire amplitude distribution of EPSPs recorded under the action of APB. The suppression of EPSPs by APB was accompanied by a marked decrease in mean quantal content (m) with no significant reduction in mean quantal amplitude (q). A quantum induced an increase in membrane conductance of about 150 pS. These results suggest that the release probability of the mossy fiber terminal fluctuates temporally according to a gamma distribution, and that APB reduces the liberation of the transmitter from mossy fiber terminals, thereby suppressing transmission between mossy fibers and CA3 neurons.

Aminobutyrates↗
PubMed1978

Durations of unitary synaptic potentials help time a behavioral sequence.

Recordings in identified neurons and muscles that mediate crayfish tailflips reveal inhibitory postsynaptic potentials of two distinct durations. Those of long duration are recorded in five classes of cells in the flexion circuit, while those of short duration are recorded in three classes of cells in the extension circuit. The durations of the inhibitory postsynaptic potentials are matched to the durations of inhibition required by the different phases of the behavior.

Animals↗
PubMed2001

Spread of synaptic potentials through electrical synapses in Retzius neurones of the leech.

We studied the spread of excitatory postsynaptic potentials (EPSPs) through electrical synapses in Retzius neurones of the leech Haementeria officinalis. The pair of Retzius neurones in each ganglion is coupled by a non-rectifying electrical synapse. Both neurones displayed synchronous EPSPs of varying amplitudes and rise times. The kinetics of synchronous EPSPs was similar in 79 % of the EPSP pairs. In the remaining 21 %, one EPSP was smaller and slower than the other, suggesting its passive spread from the other neurone. The proportion of these events increased to 75 % in the presence of Mg(2+) in the bathing fluid. This spread of EPSPs from one neurone to another was tested by producing artificial EPSPs by current injection into the soma of one Retzius neurone. The artificial EPSPs were smaller and arrived more slowly at the soma of the coupled neurone. The coupling ratios for the EPSPs were proportional to the coupling ratio for long steady-state pulses in different neuronal pairs. Our results showed that EPSPs spread from one Retzius neurone to the other and support the idea that EPSP spread between electrically coupled neurones may contribute to the integration processes of neurones.

Animals↗