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PubMed1977

Physiological and kinetic properties of cholinergic receptors activated by multiaction interneurons in buccal ganglia of Aplysia.

1. Neurons of Aplysia buccal ganglia contain three types of acetylcholine (ACh) receptors, each of which has been characterized by its sensitivity to inhibitors and kinetics of desensitization and by the properties of the conductance change it controls, including reversal potential, major ion, and functional consequence. The receptors are classified as depolarizing, slowly decrementing hyperpolarizing, and rapidly decrementing hyperpolarizing. Identified neurons are innervated by identified cholinergic multiaction interneurons; the form of the postsynaptic potential produced depends on the number and class of receptor found on each cell. 2. Interneuronal action potentials produce monosynaptic IPSPs by activating slowly decrementing hyperpolarizing receptors on seven cells in each ganglion. The IPSP reversal potential of 75 mV is shifted 42 mV in a depolarizing direction in Cl = free seawater. The ACh response has a reversal potential identical to that of the PSP; the PSP is blocked by 10(-4) g/ml curare but unaffected by hexamethonium. Interneuronal action potentials also produce monosynaptic EPSPs with a -14 mV extrapolated reversal potential by activating depolarizing receptors on one cell in each ganglion. This PSP is blocked by 10(-4) g/ml hexamethonium and mimicked by a Na-dependent ACh response. 3. Each interneuronal action potential also produces a diphasic depolarizing-hyperpolarizing synaptic potential in one cell in each ganglion as a result of released ACh acting on two classes of postsynaptic receptor on the same cell. One of these receptors is depolarizing; the other is a rapidly decrementing hyperpolarizing receptor. The two differ in their sensitivity to inhibitors, and the conductance changes they produce differ in their reversal potential, duration, and functional consequences. Both components can be mimicked by iontophoretic application of ACh. 4. Although the hyperpolarizing receptors on the inhibitory and diphasic follower cells have similar sensitivity to inhibitors and control similar conductance changes, they differ in their kinetics of desensitization. The hyperpolarizing receptor on the diphasic cell shows marked decrement to repeated presynaptic action potentials and to repeated iontophoretic application of ACh. This decrement is greater than that seen in either the hyperpolarizing receptor on the inhibitory follower cell or the depolarizing receptor on the dual follower cell. The shape of the PSP in the diphasic follower and its effect on firing of the cell are thus functions of both membrane potential and the degree of desensitization of the receptor. 5. Rate of desensitization is, therefore, an additional criterion for characterizing otherwise similar receptors for neurotransmitters.

Acetylcholine↗
PubMed1980

Influence of raphe nuclei on neuronal transmission from perforant pathway through dentate gyrus.

1. In chronically prepared, freely moving rats, electrical stimulation was applied to the perforant pathway and monosynaptic responses were recorded extracellularly in the ipsilateral dentate gyrus. In some tests a stimulus was also applied to the median raphe nucleus (mr) prior to activating the perforant pathway. Experiments were performed during two behavioral conditions: slow-wave sleep (SWS) and the still, alert state (SAL). Two varieties of evoked responses were recorded: those due to synchronous firing of neuronal action potentials (evoked action potentials or EAPs) and those produced by excitatory synaptic activity (evoked synaptic potentials or ESPs). 2. As reported previously (38), perforant path stimulation elicited EAPs of greater magnitude during SWS than during SAL. The application of a prior stimulus to mr (prestimulation) markedly increased the already elevated EAPs observed during SWS. The EAPs during SAL were unaffected by prestimulation. 3. The minimum delay time (time between mr and perforant path stimuli) at which the augmentation of the EAPs appeared during SWS was approximately 5 ms. The augmentation reached a maximum at delay times of 25-40 ms and was present up to a delay time of 150 ms. 4. As in former experiments (38), ESPs recorded in the molecular layer of the dentate gyrus after perforant path stimulation were found to be greater during SAL than during SWS. Prestimulation of mr had no significant effect on the ESPs at any level of the molecular layer during either SWS or SAL. 5. The perforant path afferent volley was recorded at high gain in the dentate gyrus. Its amplitude was found to be solely dependent on perforant path stimulus intensity and not on behavioral state or the prestimulation of mr. 6. In preparations anesthetized with Chloropent (82% chloral hydrate, 18% pentobarbital; Fort Dodge Laboratories, Fort Dodge, IA), prestimulation was applied at each of a number of loci within the pons and medulla, including mr, As in SWS, prestimulating mr resulted in augmented EAPs with a minimum delay time of 5 ms. Similar augmented responses were observed when stimulation was applied at other raphe nuclei (dorsal raphe, pontis, magnus, and pallidus), but there was no augmentation when stimulation was applied at other brain stem sites. Threshold stimulus intensities for producing augmented EAPs in the raphe nuclei were less than 30 microA. 7. In freely moving animals it was first established that the EAP responses during SWS were markedly greater than during SAL. Midline lesions were then made at the rostrocaudal level of mr. Following the lesions, there was no longer any significant difference in the magnitude of the EAPs recorded during the two behaviors. 8. These findings suggest that tonic influences arising from raphe nuclei during SWS may be involved in the facilitation of neuronal transmission through the dentate gyrus observed during this behavioral state.

Animals↗
PubMed1992

Characterization of the integration time for the stabilization of long-term potentiation in area CA1 of the hippocampus.

In area CA1 of the hippocampus, synaptic activation of NMDA receptors during postsynaptic depolarization can generate either a decremental synaptic potentiation termed short-term potentiation (STP) or stable, long-term potentiation (LTP). Examining the relationship between these two forms of synaptic enhancement should provide information about the intracellular processes responsible for the stabilization of LTP. Using the hippocampal slice preparation, initial experiments confirmed that STP can be generated either by a weak tetanus or by pairing a single EPSP with postsynaptic depolarization. Following the generation of submaximal LTP, application of a weak, STP-inducing tetanus resulted in STP (not LTP), suggesting that the processes responsible for stabilizing LTP must be activated during induction and cannot be accessed at later times. To determine the interval over which processes activated during STP can be integrated and result in stable LTP (the "integration time" for the stabilization of LTP), a fixed number of afferent stimuli were given at varying intervals (5-60 sec) during postsynaptic depolarization. Using either extracellular or whole-cell recording, LTP was rarely (11% of experiments) elicited at 1 min intervals and frequently (76% of experiments) elicited at 10 sec intervals. These results indicate that following a single EPSP during postsynaptic depolarization, the processes responsible for the stabilization of LTP decay significantly within approximately 1 min, although this value may depend on the level of activation of the requisite intracellular processes.

Animals↗
PubMed2002

Tetanus toxin induces long-term changes in excitation and inhibition in the rat hippocampal CA1 area.

Intrahippocampal tetanus toxin induces a period of chronic recurrent limbic seizures in adult rats, associated with a failure of inhibition in the hippocampus. The rats normally gain remission from their seizures after 6-8 weeks, but show persistent cognitive impairment. In this study we assessed which changes in cellular and network properties could account for the enduring changes in this model, using intracellular and extracellular field recordings in hippocampal slices from rats injected with tetanus toxin or vehicle, 5 months previously. In CA1 pyramidal neurones from toxin-injected rats, the slope of the action potential upstroke was reduced by 32%, the fast afterhyperpolarisation by 32% and the slow afterhyperpolarisation by 54%, suggesting changes in voltage-dependent conductances. The excitatory postsynaptic potential slope was reduced by 60% and the population synaptic potential slope was reduced at all stimulus intensities, suggesting a reduced afferent input in CA1. Paired-pulse stimulation showed an increase of the excitability ratio and an increase of cellular excitability only for the second pulse, suggesting a reduced inhibition. The polysynaptic inhibitory postsynaptic potential was reduced by 34%, whereas neither the inhibitory postsynaptic potential at subthreshold stimulus intensities,nor the pharmacologically isolated monosynaptic inhibitory postsynaptic potential were different in toxin-injected rats, suggesting a reduced synaptic excitation of interneurones. Stratum radiatum stimuli in toxin-injected rats, and not in controls, evoked antidromic activation of CA1 neurones, demonstrating axonal sprouting into areas normally devoid of CA1 pyramidal cell axons.We conclude that this combination of enduring changes in cellular and network properties, both pro-epileptic (increased recurrent excitatory connectivity, reduced recurrent inhibition and reduced afterhyperpolarisations) and anti-epileptic (impaired firing and reduced excitation), reaches a balance that allows remission of seizures, perhaps at the price of persistent cognitive impairment.

Action Potentials↗
PubMed2006

Arm immobilization causes cortical plastic changes and locally decreases sleep slow wave activity.

Sleep slow wave activity (SWA) is thought to reflect sleep need, increasing after wakefulness and decreasing after sleep. We showed recently that a learning task involving a circumscribed brain region produces a local increase in sleep SWA. We hypothesized that increases in cortical SWA reflect synaptic potentiation triggered by learning. To further investigate the link between synaptic plasticity and sleep, we asked whether a procedure leading to synaptic depression would cause instead a decrease in sleep SWA. We show here that if a subject's arm is immobilized during the day, motor performance deteriorates and both somatosensory and motor evoked potentials decrease over contralateral sensorimotor cortex, indicative of local synaptic depression. Notably, during subsequent sleep, SWA over the same cortical area is markedly reduced. Thus, cortical plasticity is linked to local sleep regulation without learning in the classical sense. Moreover, when synaptic strength is reduced, local sleep need is also reduced.

Adult↗
PubMed1994

NK1 and NK2 receptors contribute to C-fibre evoked slow potentials in the spinal cord.

Small diameter primary afferents produce slow synaptic potentials in spinal neurones. These can be recorded as prolonged ventral root potentials (VRPs) in the isolated neonatal rat spinal cord preparation. The VRP elicited by stimulating C-fibres consists of two phases: an early phase comprising a monosynaptic and a short polysynaptic response identical to that elicited by low threshold A beta fibres and a late phase which has an initial component (0.1-1 s) which is sensitive to N-methyl-D-aspartic acid receptor antagonism and a very long lasting second component (1-20 s) which is resistant to these antagonists. We now demonstrate that the slowest component of the VRP is significantly reduced by both NK1 and NK2 tachykinin receptor antagonists and as a consequence, tachykinins have a particular contribution to the cumulative depolarization produced by low frequency (1 Hz) C-fibre stimulation.

Amino Acid Sequence↗
PubMed1977

The effects of strontium and barium ions at synapses in sympathetic ganglia.

1. A study has been made of the effects of Sr2+ and Ba2+ ions at synapses in isolated superior cervical ganglia of guinea-pigs. Intracellular recordings of membrane potential were made from ganglion cells in the presence of different concentrations of Ca2+, Sr2+ and Ba2+ ions. 2. The addition of Sr2+ (2-5 mM) caused little change in resting membrane potential; in contrast, Ba2+ (1-6 mM) always depolarized the cells and prolonged the duration of action potentials. 3. The resting frequency of spontaneous miniature excitatory post-synaptic potentials (min. e.p.s.p.s) was briefly accelerated by the addition of either Sr2+ or Ba2+, but subsequently returned to about control levels. 4. Following replacement of Ca2+ by Sr2+, e.p.s.p.s could always be evoked during repetitive stimulation of preganglionic axons at a fixed latency after the nerve impulses ('phasic' transmitter release). Replacement of Ca2+ by Ba2+ produced many asynchronous e.p.s.p.s during trains of impulses ('residual' transmitter release). 5. By analysis of the interaction between Sr2+ and Ca2+, Sr2+ was shown to have a partial agonist action on 'phasic' transmitter release. The same analysis applied to Ba2+ failed to demonstrate either a partial agonist or antagonist action. 6. Both Sr2+ and Ba2+ prolonged e.p.s.p.s. Changes in Sr2+ could mainly be attributed to its effect on cell input resistance; Ba2+ may also prolong the time course of transmitter release. 7. The increased frequency of min. e.p.s.p.s which occurs during repetitive stimulation was potentiated by both Sr2+ and Ba2+, Ba2+ being about twice as potent as Sr2+. This activation of 'residual' transmitter release is independent of the action of these ions on 'phasic' release. 8. It is concluded that the reported maintenance by Ba2+ of acetyl-choline output from perfused ganglia results from the asynchronous release of large numbers of quanta during trains of impulses.

Acetylcholine↗
PubMed1992

Direct measurement of quantal changes underlying long-term potentiation in CA1 hippocampus.

The modification responsible for the long-term synaptic potentiation (LTP) that follows a brief conditioning period is not known. To elucidate this change, we have resolved quantal levels of transmission before and after induction of LTP. We find an increase both in the number of quanta released and in quantal amplitude, consistent with combined pre- and postsynaptic modifications. On average, about 60% of LTP can be accounted for by presynaptic enhancement. The increase in either quantal amplitude or quantal content varies significantly among different experiments, but is inversely correlated with its initial value. These results may help to reconcile the different views concerning the site of LTP expression.

Animals↗
PubMed1983

An intracellular analysis of geniculo-cortical connectivity in area 17 of the cat.

The latencies of excitatory and inhibitory post-synaptic potentials (e.p.s.p.s and i.p.s.p.s) evoked by electrical stimulation of afferents from the lateral geniculate nucleus were recorded in neurones of area 17 of the cat visual cortex. After application of an extrapolation procedure to compensate for the conduction time of the afferent axons, a histogram of latencies formed three distinct peaks. Potentials in each of these were interpreted as being mediated by mono-, di- and trisynaptic pathways. Characteristic laminar differences in the extracellular field potentials evoked from the lateral geniculate nucleus (l.g.n.) and in the antidromic activation of neurones from the l.g.n. and superior colliculus were used to determine the laminar position of recorded neurones. It was found that within a given layer, all cells maintained similar connexions with relay cells in the l.g.n. Cells in layers 3, 4, upper 5 and 6 were monosynaptically excited by geniculate afferents, while cells in layers 2 and lower 5 received only indirect excitation via other cortical neurones. Layer 3 cells were unique in receiving a prominent disynaptic e.p.s.p. in addition to the direct excitation from the l.g.n. Late, trisynaptic e.p.s.p. components were seen in many layer 5 and 6 cells. The orderly laminar arrangement of the connexions had the consequence that identified cortico-geniculate neurones were monosynaptically excited and cortico-collicular neurones di- and trisynaptically excited by geniculate afferents. Cortico-cortical neurones in layers 2 and 3 received di- or mono- plus disynaptic excitation, depending on laminar position. Post-synaptic inhibitory potentials were evoked in all impaled cells, following stimulation of the geniculo-cortical pathway. Except for a few layer 2 cells, this inhibition was mediated through disynaptic pathways of the feed-forward type. There was a good positive correlation between conduction times for monosynaptic e.p.s.p.s and disynaptic i.p.s.p.s in the same cells, suggesting that cortical neurones receive excitation and inhibition from the same type of geniculate afferents. The stimulating electrodes activated not only geniculo-cortical afferents, but antidromically activated cortical efferent neurones from their extracortical axons. These neurones possess intracortical collaterals, and care must be taken to distinguish the resulting potentials from those mediated by orthodromic activation of geniculate afferents. In doing so, evidence was obtained for excitatory connexions from layers 2 and 3 to layer 5, from layer 5 to layer 6, and from layer 6 to layer 4. Typical recurrent inhibition was not observed.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1984

Relation between structural and release parameters at the frog sensory-motor synapse.

The sensory-motor synaptic connexions in the frog lumbar cord have been used to examine the relationship between the statistical characteristics of the unitary excitatory post-synaptic potential (e.p.s.p.) and the number and organization of synaptic contacts determined when the primary afferent fibre used in evoking the e.p.s.p., and a motoneurone in which it was recorded, were both labelled with horseradish peroxidase (HRP). A significant correlation is found between the number of contacting boutons and the amplitude of the chemical component of the unitary e.p.s.p.s generated at the same connexions. The amplitude fluctuation patterns of the single-fibre e.p.s.p.s could be fitted by both Poisson and binomial distribution. The number of presumed Poisson release sites as estimated from the ratio Vmax/v (where Vmax is the maximal amplitude of the chemical component of e.p.s.p. and v is quantal size) is always less than or equal to the total number of boutons observed histologically. In three connexions there was a close correspondence between the number of binomial release units, n, and the number of contact regions formed by the tight clusters of contacting boutons. The unit potential amplitude estimated from the Poisson distribution is found to be two to three times smaller than the quantal size calculated from binomial distribution. A similar numerical relationship was found between the number of contacting boutons and the number of contact regions. It is suggested that at a single bouton, transmission results in release of a single quantum of transmitter, whereas the binomial quantum probably reflects the multi-quantal release occurring simultaneously at boutons comprising a contact region. A significant correlation is found between the mean quantum content estimated either from Poisson or binomial distribution and the number of contacting boutons and contact regions respectively, indicating the dependence of quantal release on the magnitude of synaptic surface. No correlation is found between the motoneuronal soma diameter and the quantal size, although the former is significantly correlated with the number of contacting boutons.

Action Potentials↗
PubMed1988

Postsynaptic calcium is sufficient for potentiation of hippocampal synaptic transmission.

Brief repetitive activation of excitatory synapses in the hippocampus leads to an increase in synaptic strength that lasts for many hours. This long-term potentiation (LTP) of synaptic transmission is the most compelling cellular model in the vertebrate brain for learning and memory. The critical role of postsynaptic calcium in triggering LTP has been directly examined using three types of experiment. First, nitr-5, a photolabile nitrobenzhydrol tetracarboxylate calcium chelator, which releases calcium in response to ultraviolet light, was used. Photolysis of nitr-5 injected into hippocampal CA1 pyramidal cells resulted in a large enhancement of synaptic transmission. Second, in agreement with previous results, buffering intracellular calcium at low concentrations blocked LTP. Third, depolarization of the postsynaptic membrane so that calcium entry is suppressed prevented LTP. Taken together, these results demonstrate that an increase in postsynaptic calcium is necessary to induce LTP and sufficient to potentiate synaptic transmission.

Animals↗
PubMed1987

Field potential evidence for long-term potentiation of feed-forward inhibition in the rat dentate gyrus.

Trains of high-frequency stimulation to the perforant path cause (i) long-term potentiation (LTP) of the population excitatory post-synaptic potential (EPSP), (ii) a lasting increase in the population spike, and (iii) a lasting alteration of the relationship between the EPSP and population spike (E-S relationship), consisting of a decreased x-intercept and decreased slope of the linear regression. To compare the thresholds of these changes, we applied a series of trains, increasing in duration from below LTP threshold. The EPSP potentiated with about the same low threshold as the reduction in E-S slope, whereas the reduction in E-S x-intercept required longer trains. In the second experiment, LTP of the EPSP was reduced by concurrent high-frequency stimulation of the commissural input and a lasting reduction of the population spike height was observed. In a third experiment, picrotoxin, an antagonist of gamma-aminobutyric acid (GABA)-mediated inhibition, blocked the decrease in slope of the E-S relationship which normally accompanies LTP. These results imply that perforant path/granule cell LTP is normally accompanied by long-term potentiation of a feed-forward inhibitory pathway which may involve interneurones.

Animals↗
PubMed1989

Selective depression of GABA-mediated IPSPs by somatostatin in area CA1 of rabbit hippocampal slices.

In area CA1 of hippocampus, a subpopulation of gamma-aminobutyric acid (GABA)-containing interneurons that make synaptic contacts on pyramidal cells also contains the neuropeptide, somatostatin. The effects of GABA and somatostatin on hippocampal pyramidal cells have been investigated separately, but it is not known whether an interaction occurs between these co-localized substances. We demonstrate that somatostatin has a potent inhibitory effect on GABA-mediated synaptic potentials which hyperpolarize pyramidal cells. This effect may be relevant to the well-documented epileptogenicity of the hippocampus, as well as the phenomenon of long-term potentiation, which is a well-studied example of synaptic plasticity.

Action Potentials↗
PubMed2006

Experience-dependent formation and recruitment of large vesicles from reserve pool.

The sizes and contents of transmitter-filled vesicles have been shown to vary depending on experimental manipulations resulting in altered quantal sizes. However, whether such a presynaptic regulation of quantal size can be induced under physiological conditions as a potential alternative mechanism to alter the strength of synaptic transmission is unknown. Here we show that presynaptic vesicles of glutamatergic synapses of Drosophila neuromuscular junctions increase in size as a result of high natural crawling activities of larvae, leading to larger quantal sizes and enhanced evoked synaptic transmission. We further show that these larger vesicles are formed during a period of enhanced replenishment of the reserve pool of vesicles, from which they are recruited via a PKA- and actin-dependent mechanism. Our results demonstrate that natural behavior can induce the formation, recruitment, and release of larger vesicles in an experience-dependent manner and hence provide evidence for an additional mechanism of synaptic potentiation.

Animals↗
PubMed1993

Nicotinic and muscarinic synaptic transmission in canine intracardiac ganglion cells innervating the sinoatrial node.

Nicotinic and muscarinic mediated synaptic mechanisms were investigated in isolated, canine intracardiac ganglia taken from the right atrial fat pad. Using conventional intracellular microelectrode recording techniques on 216 neurons, fast and slow synaptic potentials were evoked by single or trains of stimulation of presynaptic fibers in interganglionic nerves. By varying the stimulus intensity, single or multiple fast excitatory postsynaptic potentials (f-EPSPs) were evoked, indicating the convergence of synaptic inputs on these cells. These f-EPSPs often reached the action potential threshold, were enhanced by the acetylcholinesterase inhibitor physostigmine and were blocked by the nicotinic antagonist hexamethonium. The f-EPSPs were accompanied by a decreased input resistance and had an extrapolated reversal potential of -7.1 mV, suggesting increased conductances to more than one cation. Repetitive presynaptic stimulation evoked slow excitatory postsynaptic potentials (s-EPSPs) in 41% of the cells while slow inhibitory postsynaptic potentials (s-IPSPs) or s-IPSPs followed by s-EPSPs were evoked in 19% of the cells. All slow potentials were abolished by atropine and low Ca2+/high Mg2+ solutions and enhanced by physostigmine. Hexamethonium and adrenergic receptor antagonists had no effects on s-EPSP and s-IPSP. The M1 receptor antagonist pirenzepine reversibly blocked the s-EPSP but not the s-IPSP. On the other hand, the M2 receptor blocker 4-diphenyl-acetoxy-N-methyl piperidine methiodide (4-DAMP) had no effects on the s-EPSP. These observations suggest that s-EPSPs and s-EPSPs are mediated by distinct muscarinic receptors. The amplitude of the s-EPSP and the depolarization evoked by the muscarinic agonist, bethanechol were accompanied by increased input resistance. These responses were decreased in amplitude by membrane hyperpolarization and either reversed polarity or declined to zero amplitude at about -80 mV, suggesting the inhibition of a potassium conductance.

Acetylcholine↗
PubMed1987

Morphological and physiological studies of development of the monosynaptic reflex pathway in the rat lumbar spinal cord.

1. The developmental process of the monosynaptic reflex pathway was investigated morphologically and electrophysiologically in isolated lumbar spinal cords of new-born and fetal rats. 2. Dorsal root fibres were stained with horseradish peroxidase in the fourth lumbar (L4) segment at different ages ranging from embryonic day (E) 15.5 to post-natal day (P) 0. At E15.5, several collaterals issued from axons in the dorsal funiculus and reached the dorsal part of the dorsal horn. At E16.5, the number of collaterals entering the grey matter increased. Also, a group of collaterals extended ventralwards forming a bundle, and reached the intermediate region. At E17.5, a small number of collaterals reached the motor nuclei. The number of collaterals entering the motor nuclei increased almost linearly with age: 0 at E15.5 and at E16.5, 27 at E17.5, 184 at E18.5, 432 at E19.5 and 746 at P0. 3. The tips of collaterals and their branches had growth cones, boutons (round or oval varicosities) or other varicosities. The mean number of branches with these structures per collateral in the motor nuclei was 1.2 at E17.5, 2.5 at E18.5, 3.6 at E19.5 and 5.8 at E20.5. 4. The percentage of collaterals having growth cones in the motor nuclei was 75% at E17.5, 70% at E18.5, 38% at E19.5 and 15% at E20.5. 5. The mean number of boutons per collateral in the motor nuclei was 0.6 at E17.5, 3.2 at E18.5, 4.9 at E19.5 and 10.7 at E20.5. This increase with age was caused by both branching of collaterals and the increase in the number of boutons of the en passant type. The estimated total number of boutons in the motor nuclei of the L4 segment steeply increased after E17.5: 16 at E17.5, ca. 600 at E18.5, ca. 2000 at E19.5 and ca. 8000 at E20.5-P0. 6. Stimulation of the L4 dorsal root evoked a reflex response in the L4 ventral root, recorded as the ventral root potential, in two out of nine preparations at E15.5 and in all preparations at and after E16.5. The onset of the ventral root potential indicated the onset of excitatory post-synaptic potentials in motoneurones. The segmental latency of the ventral root potentials was markedly shortened between E17.5 and E18.5 (from 12.5 to 7.2 ms) and essentially unchanged at the later stages. 7. The magnitude of monosynaptic reflex responses in the L4 segment gradually increased with age during prenatal stages, becoming maximal at P2-3 and then decreased at the following stages (P4-P8).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Synaptic excitation in cultures of mouse spinal cord neurones: receptor pharmacology and behaviour of synaptic currents.

Fast monosynaptic excitatory post-synaptic potentials between spinal cord neurones in cell culture (s.c.-s.c. e.p.s.p.s) were studied with current-clamp and two-electrode voltage-clamp methods. The reversal potential, response to acidic amino acid antagonists, and behaviour of the synaptic current were examined. The amplitude of the e.p.s.p. increased with membrane potential hyperpolarization and decreased with depolarization. The reversal potential of the e.p.s.p. was +3.8 +/- 2.5 mV (mean +/- S.E. of mean). The reversal potential for responses to ionophoretically applied L-glutamate and L-aspartate was also near 0 mV. The acidic amino acid antagonist, cis-2,3-piperidine dicarboxylic acid (PDA, 0.25-1.0 mM) reversibly antagonized the monosynaptic e.p.s.p.s as well as responses to kainate (KA) or quisqualate (QA). The selective N-methyl-D-aspartate antagonist, (+/-) 2-amino-5-phosphonovaleric acid (APV), had little effect on either the monosynaptic e.p.s.p.s or responses to QA or KA at concentrations that abolished responses to L-aspartate. Under voltage clamp, the peak synaptic current (e.p.s.c.) was linearly related to the membrane potential, increasing in amplitude with hyperpolarization and decreasing with depolarization from the resting potential. The decay of a somatic e.p.s.c. was well fitted by a single exponential function with a time constant of 0.6 ms at 25 degrees C. E.p.s.c.s which had proximal dendritic locations had decay time constants of 1-2 ms. The decay time constant was voltage-insensitive between -80 and +10 mV. We suggest that an acidic amino acid receptor other than that for NMDA mediates excitatory transmission at the s.c.-s.c. synapse; and that the underlying conductance mechanism is voltage insensitive with an estimated mean channel lifetime of less than 1 ms.

2-Amino-5-phosphonovalerate↗
PubMed1994

Effects of an N-methyl-D-aspartate antagonist and a GABAergic antagonist on entorhinal tetanic responses during the early stages of amygdala kindling in rats.

Changes in synaptic potentials during each train stimulation (tetanic responses) have been suggested to intimately relate to the development of kindling. We examined the effects of an NMDA antagonist, carboxypiperazinephosphonate (CPP), and a GABAergic antagonist, picrotoxin, on entorhinal tetanic responses evoked by train stimuli (10 Hz, 100 pulses) at the developmental stage (seizure stage; 0-2) of amygdala kindling in conscious rats, to clarify the significance of facilitation in tetanic responses and the roles of NMDA and GABA receptors in the development of kindling. Facilitation of tetanic responses was noted as a progressive increase in both amplitude and duration of negative potentials in the tetanic responses, especially during the later half of train pulses (51-100). The negative potential area (mV x ms) of the averaged tetanic responses was used as an estimate of the magnitudes of excitatory synaptic activity in the tetanic responses, and correlated significantly (P < 0.001) with the duration of afterdischarges (AD). CPP (10 mg/kg) reversibly blocked AD in association with a significant decrease (P < 0.05) in the negative potential area. The CPP-sensitive component consisted of a slow negative potential with a duration longer than 60 ms and was greater in the later tetanic responses (51-100) than the earlier ones (1-50). Picrotoxin (2-3 mg/kg), which did not produce convulsions, significantly (P < 0.005) increased the negative potential area in the tetanic responses in association with a reversible decrease in the AD threshold. Although positive potentials ascribable to inhibitory synaptic activity were often negligible in the tetanic responses in controls, picrotoxin further decreased the positive potentials of tetanic responses, if any.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗