A comparison of the post-synaptic potentials of Betz cells and alpha motor neurones of the cat.
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Synaptic inhibition of the M-current: slow excitatory post-synaptic potential mechanism in bullfrog sympathetic neurones.
1. Slow muscarinic excitatory post-synaptic currents (slow e.p.s.c.s) generated by preganglionic nerve stimuli were recorded in voltage-clamped bullfrog sympathetic neurones. 2. IM--an outward, voltage-dependent, K+-current--was inhibited during the slow e.p.s.c., and membrane conductance was reduced in a voltage-dependent manner. 3. The slow e.p.s.c. was associated with reduced outward rectification in the steady-state current--voltage (I/V) curve at membrane potentials more positive than--60 m V, with no change in the shape of the non-rectifying part of the I/V curve at more negative potential. 4. The amplitude of the slow e.p.s.c. was reduced by membrane hyperpolarization, to zero at membrane potentials equal to, or more negative than, -60 m V. The voltage sensitivity of the slow e.p.s.c. accorded with that of IM. 5. It is concluded that the slow e.p.s.c. results from a selective inhibition of IM.
Action Potentials↗
Frequency-dependent synaptic potentiation, depression and spike timing induced by Hebbian pairing in cortical pyramidal neurons.
Experiments by Markram and Tsodyks (Nature, 382 (1996) 807-810) have suggested that Hebbian pairing in cortical pyramidal neurons potentiates or depresses the transmission of a subsequent pre-synaptic spike train at steady-state depending on whether the spike train is of low frequency or high frequency, respectively. The frequency above which pairing induced a significant decrease in steady-state synaptic efficacy was as low as about 20 Hz and this value depends on such synaptic properties as probability of release and time constant of recovery from short-term synaptic depression. These characteristics of cortical synapses have not yet been fully explained by neural models, notably the decreased steady-state synaptic efficacy at high pre-synaptic firing rates. This article suggests that this decrease in synaptic efficacy in cortical synapses was not observed at steady-state, but rather during a transition period preceding it whose duration is frequency-dependent. It is shown that the time taken to reach steady-state may be frequency-dependent, and may take considerably longer to occur at high than low frequencies. As a result, the pairing-induced decrease in synaptic efficacy at high pre-synaptic firing rates helps to localize the firing of the post-synaptic neuron to a short time interval following the onset of high-frequency pre-synaptic spike trains. This effect may "speed up the time scale" in response to high-frequency bursts of spikes, and may contribute to rapid synchronization of spike firing across cortical cells that are bound together by associatively learned connections.
Action Potentials↗
Synaptic potentials evoked in spiny neurons in rat neostriatal grafts by cortical and thalamic stimulation.
1. Fetal rat striatal primordia were implanted into the neostriatum of adult rats 2 days after kainic acid lesion. Two to 6 mo after transplantation, in vivo intracellular recording and staining were performed to study the responses of spiny neurons in the grafts to the cortical and thalamic stimuli. The physiological characteristics and synaptic responses of 27 cells recorded in the grafts were compared with a sample of 23 neurons recorded from the surrounding host neostriatum in the same animals. Nineteen of the graft neurons and 19 of the host neurons were identified as spiny neurons by intracellular staining with biocytin. The responses of the remaining neurons were the same as those of identified spiny cells. 2. The spontaneous synaptically driven membrane potential shifts and long-lasting responses to afferent stimulation that are characteristic of neostriatal cells in normal animals were greatly reduced or absent in graft neurons. Presumably this reflects the reduction in synaptic input to the grafts and the lack of convergence of inputs from diverse sources. 3. Short-latency synaptic responses to cortical and thalamic stimulation were present and could consist of either excitatory postsynaptic potentials (EPSPs) or inhibitory postsynaptic potentials (IPSPs). The IPSPs were accompanied by a membrane conductance increase, and their reversal potentials could be altered by injection of chloride ions. Several minutes after impaling the cell, the IPSPs gradually disappeared, and the same stimuli could then evoke EPSPs. The disappearance of the IPSPs was independent of the presence of chloride in the electrodes. Most of the EPSP responses appeared to be monosynaptic but occurred at longer latencies than those seen in host neurons of the same type. 4. In cells not exhibiting IPSPs, or after the IPSP responses disappeared, cortical or thalamic stimulation could evoke slow depolarizing potentials and bursts of action potentials. These could not be evoked by current injection. They could be prevented or delayed by an exaggerated action potential after hyperpolarization that developed in neurons maintained in a depolarized state for several seconds, but could not be prevented by passage of hyperpolarizing current from the recording electrode. 5. The input resistance of graft spiny neurons was higher than that of the host cells, and time constants were longer. Both of these properties appeared to be due to the absence of the strong inward rectification that is usually present at resting membrane potentials in neostriatal neurons.
Animals↗
Synaptic potentials of primary afferent fibers and motoneurons evoked by single intermediate nucleus interneurons in the cat spinal cord.
Spike-triggered averaging of dorsal and ventral root potentials was used in anesthetized cats to disclose possible synaptic connections of spinal interneurons in the intermediate nucleus with afferent fibers and/or motoneurons. With this method we have been able to document the existence of a distinct group of interneurons whose activity was associated with the recording of inhibitory potentials in the ventral roots (iVRPs), but not with negative dorsal root potentials (nDRPs). The iVRPs had mean durations of 60.8 +/- 22.1 ms and latencies between 1.7 and 5.1 ms relative to the onset of the interneuronal spikes. Within this group of neurons it was possible to characterize two categories depending on their responses to segmental inputs. Most type A interneurons were mono- or disynaptically activated by group I muscle afferents and polysynaptically by low threshold (1.08-1.69 X T) cutaneous fibers. Type B interneurons were instead polysynaptically activated by group II muscle and by cutaneous fibers with thresholds ranging from 1.02 to 3.1 X T. Whenever tested, both type A and B interneurons could be antidromically activated from Clarke's columns. There was a second group of interneurons whose activity was associated with the generation of both iVRPs and nDRPs. These potentials had mean durations of 107.5 +/- 35.6 and 131.5 +/- 32 ms, respectively, and onset latencies between 1.7 and 6.1 ms. The interneurons belonging to this group, which appear not to send axonal projections to Clarke's column, could be classified in three categories depending on their responses to peripheral inputs. Type C interneurons responded mono- or disynaptically to group I muscle volleys and polysynaptically to intermediate threshold (1.22-2.7 X T) cutaneous afferents. Type D interneurons were polysynaptically activated by group II muscle afferents (2.3-8.5 X T) and by intermediate threshold (1.4-3 X T) cutaneous fibers and type E interneurons only by group I muscle afferents with mono- or disynaptic latencies. A third group of interneurons produced nDRPs without iVRPs. The nDRPs had onset latencies varying from 1.9 to 6.2 ms and mean durations of 130.0 +/- 34.6 ms. These neurons (type F) showed spontaneous and evoked bursts of activity and were not antidromically activated from Clarke's column. They responded to stimulation of low- and intermediate-threshold cutaneous fibers (1.04-2.9 X T) with mono- and polysynaptic latencies, but not by group I muscle fibers. Type F interneurons appear to be located in more superficial layers than all the other interneurons.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
D1-receptor dependent synaptic potentiation in the basal ganglia of quail chicks.
Properties of local synapses were analyzed in lobus parolfactorius (LPO; avian homologue of caudate-nucleus) of quail chicks by using slice preparations in vitro. Field-potential extracellular and whole-cell intracellular recordings revealed excitatory synaptic inputs converging from dorsal and ventral regions within LPO. With exogenous dopamine (100 microM) in the perfusate, synchronized conditioning stimulation induced biased changes in the dorsal and the ventral inputs; potentiation in the dorsal input and depression in the ventral input in average. On the other hand, de-synchronized conditioning failed to induce such biased changes, although the differences were not statistically significant. SCH-23390 (3 microM) blocked the dorsal potentiation, while AP-5 (100 microM) tended to block both of these changes. The plastic nature may underlie the memory formation in appetitive/aversive learning tasks.
Action Potentials↗
Membrane potential, synaptic activity, and excitability of hindlimb motoneurons during wakefulness and sleep.
1. The membrane potential and excitability of hindlimb motoneurons was recorded in chronically implanted, restrained cats during natural sleep and wakefulness. 2. The potential of all motoneurons varied in a systematic and predictable manner during the sleep-wake cycle, suggesting that all motoneurons contributed to variations in muscle tension across the cycle. 3. Motoneuron excitability and level of polarization did not change at sleep onset. 4. During REM sleep, motoneurons had a sustained hyperpolarization, a diminished probability of antidromic and monosynaptic activation, and a reduced responsiveness to depolarizing current pulses. Motoneuron excitability is thus reduced in this phase of sleep. 5. Synaptic activity, but not necessarily synaptic noise, was higher during REM sleep. Hindlimb motoneuron hyperpolarization in REM sleep in concluded to arise from augmented asynchronous inhibitory synaptic activity distributed on the soma.
Animals↗
Dehydroepiandrosterone sulfate alters synaptic potentials in area CA1 of the hippocampal slice.
The influences of the neurosteroid dehydroepiandrosterone sulfate (DHEAS) on neuronal properties and synaptic transmission in area CA1 of the hippocampus were examined using a slice preparation. DHEAS had no apparent effects upon cell membrane resistance or active cell responses to intracellular hyperpolarizing or depolarizing current pulses. However, DHEAS did increase the excitability of CA1 neurons in response to Schaffer collateral synaptic stimulation. This was apparent both in field potential recordings as well as intracellular recordings. Effects appeared within minutes following exposure to DHEAS and were reversible, suggesting a non-genomic mechanism of action. Intracellular recordings indicated that DHEAS increased the amplitudes of EPSPs associated with stimulation of Schaffer collateral fibers. The increased EPSP amplitudes resulted from DHEAS effecting an inhibition of fast IPSPs as well as a direct enhancement of excitatory synaptic transmission. No significant effects on slow IPSPs were noted. In summary, neurosteroids such as DHEAS may influence synaptic transmission through multiple mechanisms. Such influences result in increased excitability of postsynaptic neurons and indicate the profound influences neurosteroids may have to regulate neuronal activity in intact CNS structures.
Animals↗
Sustained enhancement of NMDA receptor-mediated synaptic potential by isoproterenol in rat amygdalar slices.
The effect of isoproterenol (Iso) on synaptic transmission mediated by the N-methyl-D-aspartate (NMDA) receptors (EPSPNMDA) was investigated in slices of rat amygdala using intracellular recording techniques. EPSPNMDA was isolated pharmacologically by application of a solution containing the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM) and GABAA receptor blocker bicuculline (20 microM). Superfusion of Iso (15 microM) produced a long-lasting enhancement of EPSPNMDA. Pretreatment the slices with propranolol (10 microM) completely prevented the effect of Iso confirming the mediation by beta-adrenergic receptors. These results provide the direct evidence for adrenergic modulation of excitatory amino acid neurotransmission in the vertebrate central nervous system.
6-Cyano-7-nitroquinoxaline-2,3-dione↗
Adenosine selectively blocks parallel-fiber-mediated synaptic potentials in rat cerebellar cortex.
Electrophysiological techniques were used to study the efficacy of adenosine in modulating synaptic transmission mediated from convergent parallel- and climbing-fiber inputs to Purkinje cells. Our results indicate that adenosine application leads to selective blocking of parallel fiber-mediated synaptic activity but not of climbing fiber activity. Adenosine does not alter the action-potential excitability properties of the parallel fibers. However, application of gamma-aminobutyric acid (GABA), which directly affects Purkinje cell dendritic membranes [Malenka, R. C. & Kocsis, J. D. (1982) J. Neurophysiol. 48, 608-621], leads to reduction of both parallel- and climbing-fiber synaptic activity. These results support the proposals that adenosine receptors in the cerebellar cortex are selectively localized on the nonmyelinated parallel fibers and that the blocking action of adenosine is the result of a mechanism other than direct alteration of axon excitability.
Adenosine↗
Voltage-clamp analysis of a self-inhibitory synaptic potential in the buccal ganglia of Aplysia.
1. In cholinergic neurones BL4, BL5, BR4, and BR5 of Aplysia buccal ganglia, each action potential is followed, in the same cell, by a curare- and high-Mg-sensitive hyperpolarizing after-potential which is enhanced by Ca. 2. In voltage-clamped neurons, substracting currents recorded in curare from currents recorded in sea water reveals that this potential is due to curare-sensitive currents which rise to a peak, then decay exponentially with an apparently voltage-independent time constant of 43 msec. Currents are produced by a voltage-independent, Ca-enhanced, conductance change with a 0-26 mumho peak and a -64 mV reversal potential. The curare-sensitive conductance is also sensitive to high Mg. 3. Both after-potential and curare- or Mg-sensitive current follow each action potential without failures, even in threshold-raising 80 mM-Ca-144-mM-Mg solutions. 4. Both after-potential and current decrease with repetitive firing or short inter-spike interval, possibly due to receptor desensitization. 5. The Mg- and curare-sensitive conductance is also blocked by 1 mM-ACh. 6. The data are consistent with the hypothesis that the hyperpolarization following action potentials in each of these four neurones is produced by a self-inhibitory synaptic mechanism.
Action Potentials↗
Substance P post-synaptically potentiates glutamate-induced currents in dorsal vagal neurons.
We examined the post-synaptic actions of glutamate, N-methyl-D-aspartate (NMDA) and substance P on dorsal vagal neurons, using the patch-clamp technique on brainstem slices of young rats. The vagal neurons were identified electrically and histologically. All vagal neurons responded to glutamate and NDMA and about 30% to substance P, with dose-dependent inward currents. The glutamate-induced currents were blocked partially by either CPP (3((R)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid) or CNQX (6-cyano-7-nitro-quinoxaline-2,3-dione), indicating that these currents resulted from the activation of at least two types of glutamate receptors: NMDA receptors and AMPA/kainate receptors. The NK1 receptor-selective antagonist, RP67580, blocked substance P-induced currents, suggesting that NK1 receptors do coexist with NMDA receptors and AMPA/Kainate receptors. Substance P potentiated the effects of glutamate. This potentiation lasted 10-20 min and was blocked by CPP and by RP67580, but not by CNQX, demonstrating that the increase in glutamate-induced currents resulted from the interaction between NK1 receptors and NMDA channels. These results provided the first evidence that the receptors for substance P and glutamate coexist on dorsal vagal neurons and interact with each other to modulate visceral efferent functions.
Animals↗
Intrinsic excitability, synaptic potentials, and short-term plasticity in human epileptic neocortex.
Although studies of epileptic human hippocampus suggest changes of synaptic and intrinsic excitability, few changes, save the appearance of spontaneous field/synaptic potentials, are known in epileptic neocortical tissue. However, invasive EEG and histological studies suggest that neocortical tissue, even in mesial temporal lobe epilepsy, can play an important role as an irritative zone or extrahippocampal focus. We hypothesized that intrinsic neuronal and synaptic excitability, as well as short-term plasticity, are altered in neocortical areas, particularly with elevated K+ levels as occur during seizures. We analyzed neuronal firing properties, synaptic responses, and paired-pulse plasticity in human neocortical slices from tissue resected during epilepsy surgery, both under normal and under pathological conditions, i.e., after elevating K+ (4/8 mM), with rat neocortical slices as controls. Neuronal firing properties were not different. We did find, however, alterations of synaptic responsiveness in epileptic tissue, i.e., an elevated network excitability with K+ elevations, and reduction of paired-pulse depression.
Adult↗
Synchronized high frequency synaptic potentials in medullary respiratory neurons.
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Animals↗
Ionic mechanism of GABAA biphasic synaptic potentials in gustatory nucleus of the solitary tract.
Gamma-aminobutyric acid (GABA) is the principal neurotransmitter of synaptic inhibition in the gustatory nucleus of the solitary tract (rNST). High-frequency activation of GABA neurons in the rNST results in biphasic inhibitory postsynaptic potentials (IPSPs) that are initially hyperpolarizing but then became depolarizing. Our results indicate that high-frequency stimulation evokes redistribution of Cl- and K+ ions that shifts IPSP reversal potential in a more positive direction, which produces a biphasic or depolarizing IPSP.
Animals↗
Excitatory synaptic potentials in spastic human motoneurons have a short rise-time.
This study assessed whether changes in size or time-course of excitatory postsynaptic potentials (EPSPs) in motoneurons innervating spastic muscle could induce a greater synaptic response, and thereby contribute to reflex hyperexcitability. We compared motor unit (MU) firing patterns elicited by tendon taps applied to both spastic and contralateral (nonspastic) biceps brachii muscle in hemiparetic stroke subjects. Based on recordings of 115 MUs, significantly shortened EPSP rise times were present on the spastic side, but with no significant differences in estimated EPSP amplitude. These changes may contribute to hyperexcitable reflex responses at short latency, but the EPSP amplitude changes appear insufficient to account for global differences in reflex excitability.
Excitatory Postsynaptic Potentials↗
[The learning dependent long-term synaptic potentiation in the rat hippocampal CA3 region].
The purpose of this study is to investigate the changes of synaptic efficacy in the rat hippocampal CA3 region during establishment, extinction and re-establishment of conditioned drink response by means of implanted electrodes and behavioral observation. The monosynaptic population excitatory postsynaptic potential (EPSPs) and population spike (PS) elicited by stimulating the perforant path were recorded. The results showed that the long-term potentiation (LTP) in the hippocampal CA3 region appeared with the establishment of conditioned response, the LTP extinguished with experimental extinction of conditioned response and reappeared during the re-establishment of conditioned response. Moreover, both maximal level of LTP and its complete extinction preceded those of conditioned behavior, suggesting that the LTP was learning-dependent. In addition, the enhanced PS was not presented immediately after behavioral training, and developed within subsequent 24 h, with a maximum at the 4th hour. The magnitude of conditioned response depended on the level of LTP. A cross-correlation analysis of the slopes of PS and EPSPs indicated that the changes of PS were caused by alterations of synaptic transmission. These results suggest that the learning-dependent LTP might be one of the neuronal substrates underlying behavioral learning and memory.
Action Potentials↗
Onset of optic nerve conduction and synaptic potentials in superior colliculus of fetal rats studied in vitro.
This article describes the onset of electrical excitability and synaptic transmission in the retinocollicular pathway of the fetal and early postnatal rat, utilizing a novel in vitro preparation. Although the optic nerve is visible in embryonic day (E) 14 brain, its stimulation produced no response in the superior colliculus (SC) until E16 when a low voltage simple negative wave was evoked. At E17 these potentials were blocked rapidly, completely, and reversibly when choline was substituted for sodium or with the addition of cobalt ions. In the course of establishing the block with either of the above agents the latency of response increased, indicating an action on axonal transmission. By E20 the collicular evoked potential showed a short followed by a longer latency wave. The latter was blocked by the glutamate antagonist kynurenic acid, with latency unaffected. Further examination of potentials with the addition of glutamatergic receptor subtype blockers aminophosphonopentanoic acid (APV) and 6-cyano-7-nitroquinoxaline-2,3-dione/6,7-dinitroquinoxaline- 2,3-dione (CNQX/DNQX) showed a clear abolition of the elicited potentials by E20 and older. Thus, fetal rat optic nerve fibers are capable of conduction in response to electrical stimulation as soon as they reach the SC at E16. Both sodium and calcium are involved. GABA-mediated modulation of axonal conduction is evident by E18. Glutaminergic synaptic transmission is established by E20. The timetable of fetal onset of capability to conduct and support synaptic transmission in the retinocollicular pathway is earlier than had previously been reported in vivo in the rat in which the superior colliculus neurones are said not to be driven by the optic nerve until 6 days post natal. This has relevance to the possible role of impulse activity in development of the pathway.
Animals↗