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PubMed1991

Variable initial depolarization in Stein's neuronal model with synaptic reversal potentials.

The effect of a variable initial value is examined in Stein's stochastic neuronal model with synaptic reversal potentials under the conditions of a constant threshold and a constant input. The moments of the interspike interval distribution are presented as the functions of the initial depolarization which ranges from inhibitory reversal potential to the threshold potential. Normal, exponential and transformed Gamma distributions are tested for the initial value of depolarization. The coefficient of variation is shown to be greater than one when the initial depolarization is sufficiently above the resting level. An interpretation of this result in the terms of spatial facilitation is offered. The effect of a random initial value is found to be most pronounced for the neurons depolarized to a near threshold level.

Animals↗
PubMed1997

Gammahydroxybutyrate (GHB) receptor ligand effects on evoked synaptic field potentials in CA1 of the rat hippocampal slice.

GHB produced a concentration-dependent depression of evoked synaptic field potentials (EFPs) recorded extracellularly in the CA1 region of the in vitro rat hippocampal slice. The concentration/response function revealed a threshold near 1 mM, with IC50 of 10.85 mM and a Hill coefficient of 1.29. The gamma-aminobutyric acid B-receptor (GABA-B) agonist baclofen also depressed the EFP, but even maximally effective concentrations of the GABA-B antagonist 2-hydroxy-saclofen (800 microM) could not completely block the GHB-induced EFP depression. Nor was GHB-induced EFP depression blocked by the GHB receptor "antagonist" NCS-382, which does not displace GABA-B receptor ligands. However, NCS-382 produced a concentration-dependent increase in EFP slope. The threshold concentration was about 100 microM but the maximally effective concentration, and thus the IC50, could not be determined in the perfusion slice system. NCS-382 may be an inverse agonist at hippocampal GHB receptors, or else endogenous hippocampal GHB receptor ligands medicate a tonic inhibition in CA1. At concentrations sufficient to induce EFP depression GHB did not alter pH. Although isosmotic sucrose did depress CA1 EFPs it was essentially ineffective at the IC50 for GHB. Gamma-butyrolactone, a prodrug of GHB, was only 1/20th as effective as GHB. This is consistent with previous data suggesting that GBL is freely permeable (does not substantially disturb tonicity) and that brain has very little capacity to either enzymatically convert the lactone to GHB or respond to the lactone itself.

Animals↗
PubMed1986

Presynaptic inhibition produced by an identified presynaptic inhibitory neuron. I. Physiological mechanisms.

We have examined the synaptic conductance mechanisms underlying presynaptic inhibition in Aplysia californica in a circuit in which all the neural elements are identified cells (Fig. 1). L10 makes connections to identified follower cells (RB and left upper quadrant cells, L2-L6). These connections are presynaptically inhibited by stimulating cells of the L32 cluster (4). L32 cells produce a slow inhibitory synaptic potential on L10. This inhibitory synaptic potential is associated with an apparent increased membrane conductance in L10. Both the inhibitory postsynaptic potential (IPSP) and the conductance increase are voltage dependent; the IPSP could not be reversed by hyperpolarizing the membrane potentials to - 120 mV. The hyperpolarization of L10 induced by L32 reduces the transmitter output of L10 and thereby contributes to presynaptic inhibition. However, this hyperpolarization accounts for about 30% of the effect because presynaptic inhibition can still be observed even when the hyperpolarization of L10 by L32 is prevented by voltage clamping. When L10 is voltage clamped, stimulation of L32 produces a slow outward synaptic current associated with an apparent increased conductance. Both the synaptic current and conductance change measured under clamp are voltage dependent, and the outward current could not be reversed. This synaptic current is not mediated by an increase in C1- conductance. It is sensitive to external K+ concentration, especially at hyperpolarized membrane potentials. With L10 under voltage clamp, stimulation of L32 also reduces a slow inward current in L10. This current has time and voltage characteristics similar to those of the Ca2+ current. Presynaptic inhibition is still produced by L32 when L10 is voltage clamped, and transmitter release is elicited by depolarizing voltage-clamp pulses. This component of presynaptic inhibition, which accounts for approximately 70% of the inhibition, appears to be due to a decrease in the Ca2+ current in the presynaptic neuron.

Abdomen↗
PubMed1985

An intracellular study of the synaptic input to sympathetic preganglionic neurones of the third thoracic segment of the cat.

In chloralose anaesthetized, paralyzed and artificially ventilated cats intracellular recordings were obtained from sympathetic preganglionic neurones (SPN) of the third thoracic segment of the spinal cord identified by antidromic stimulation of the white ramus T3. The synaptic input to SPNs was assessed, in cats with intact neuraxis or spinalized at C3, by electrical stimulation of segmental afferent fibres in intercostal nerves and white rami of adjacent thoracic segments and by stimulation of the ipsi- and contralateral dorsolateral funiculus and of the dorsal root entry zone of the cervical spinal cord. In both preparations SPNs showed on-going synaptic activity which predominantly consisted of excitatory post-synaptic potentials (EPSPs). Inhibitory post-synaptic potentials (IPSPs) were rarely observed. EPSPs were single step (5 mV) or, less frequently, large (up to 20 mV) summation EPSPs. The proportion of SPNs showing very low levels of on-going activity was markedly higher in spinal than in intact cats. Stimulation of somatic and sympathetic afferent fibres evoked early EPSPs (amplitude 3 mV, latency 5-22.3 ms), and late, summation EPSPs (amplitude up to 20 mV, latency 27-55 ms). Early and late EPSPs were evoked in nearly all SPNs in which this synaptic input was tested in the intact preparation (from 79-93% of the SPNs). In spinal cats, early EPSPs were evoked in 88% of the SPNs, whereas late EPSPs were recorded only in half of the neurones. No evidence for a monosynaptic pathway from these segmental afferent fibres to SPNs was obtained. In both intact and spinal cats, stimulation of the dorsolateral funiculus evoked early and late EPSPs in SPNs. Late EPSPs were recorded in 70% and 37% of the SPNs in intact and spinal cats, respectively. Early EPSPs, however, were evoked in all neurones. The early EPSPs evoked by stimulation of the dorsolateral funiculus had several components which are suggested to arise from stimulation of descending excitatory pathways with different conduction velocities. The following conduction velocities were calculated in intact (spinal) cats: 9.5-25 m/s (7.8-13.2 m/s), 5.7-9.5 m/s (5.5-7.8 m/s), 3.8-5.7 m/s (3.2-5.5 m/s), and 2.6-3.8 m/s (2.1-3.2 m/s). EPSPs of these various groups were elicited in a varying percentage in SPNs. EPSPs of the most rapidly conducting pathway were subthreshold for the generation of action potentials; some EPSPs of this group had a constant latency suggesting a monosynaptic pathway to SPNs. Stimulation of the dorsal root entry zone at the cervical level yielded essentially the same results as stimulation of the dorsolateral funiculus.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMedDate not supplied

Potentiation of synaptic transmission in the hippocampus by phorbol esters.

Protein kinase C (PKC), a calcium-dependent phospholipid-sensitive kinase which is selectively activated by phorbol esters, is thought to play an important role in several cellular processes. In mammalian brain PKC is present in high concentrations and has been shown to phosphorylate several substrate phosphoproteins, one of which may be involved in the generation of long-term potentiation (LTP), a long-lasting increase in synaptic efficacy evoked by brief, high-frequency stimulation. Since the hippocampus contains one of the brain's highest levels of binding sites for phorbol esters and is the site where LTP has been most thoroughly characterized, we examined the effects of phorbol esters on hippocampal synaptic transmission and LTP. We found that phorbol esters profoundly potentiate excitatory synaptic transmission in the hippocampus in a manner that appears indistinguishable from LTP. Furthermore, after maximal synaptic enhancement by phorbol esters, LTP can no longer be elicited. Although the site of synaptic enhancement during LTP is not clearly established, phorbol esters appear to potentiate synaptic transmission by acting primarily at a presynaptic locus since changes in the postsynaptic responses to the putative transmitter, glutamate, cannot account for the increased synaptic responses induced by phorbol esters. These findings, in conjunction with previous biochemical studies, raise the possibility that, in mammalian brain, PKC plays a role in controlling the release of neurotransmitter and may be involved in the generation of LTP.

Animals↗
PubMed1976

A comment on Martin's relation.

In the limit of slowly varying synaptic conductance changes, a quantity proportional to the quantal content of a synaptic potential is provided by Martin's formula: 1/(VO/Vp-1), where Vp is the peak amplitude of the synaptic potential and Vo is the synaptic equilibrium potential. If the synaptic conductance change is not slowly varying on the time scale of the postsynaptic cell's membrane time constant, Martin's formula overestimates the effects of nonlinear summation and provides an upper limit for the actual quantal content. In the limit of rapidly varying synaptic conductance changes the quantity ln(1/[1-Vp/Vo]) is proportional to the quantal content. This formula underestimates the effects of nonlinear summation and gives a lower limit for the quantal content for cases in which the synaptic conductance is not rapidly varying. These two formulas used together provide upper and lower bounds to the correction for nonlinear summation of postsynaptic potentials.

Electric Conductivity↗
PubMed2006

Fibrillar beta-amyloid impairs the late phase of long term potentiation.

Synaptic dysfunction is involved in early stages of Alzheimer's disease (AD). Amyloid-beta peptides (Abeta), a neuropathologic hallmark of the disease, have been shown to alter synaptic function. Given that Abeta is present in different forms including monomeric, oligomeric and fibrillar species, we have investigated whether fibrillar Abeta impairs synaptic function. Here we report that a synthetic fibrillar form of Abeta impairs the late protein-synthesis dependent phase of LTP without affecting the early protein-synthesis independent phase. These findings add to previous reports that Abeta oligomers are highly toxic to cells and might cause synaptic dysfunction, and suggest that a therapeutic intervention in AD should include the use of drugs inhibiting and disassembling fibril formation in addition to drugs inhibiting oligomers formation.

Alzheimer Disease↗
PubMed2002

Cerebellar input to magnocellular neurons in the red nucleus of the mouse: synaptic analysis in horizontal brain slices incorporating cerebello-rubral pathways.

We studied the synaptic input from the nucleus interpositus of the cerebellum to the magnocellular division of the red nucleus (RNm) in the mouse using combined electrophysiological and neuroanatomical methods. Whole-cell patch-clamp recordings were made from brain slices (125-150 microm) cut in a horizontal plane oriented to pass through both red nucleus and nucleus interpositus. Large cells that were visually selected and patched were injected with Lucifer Yellow and identified as RNm neurons. Using anterograde tracing from nucleus interpositus in vitro, we examined the course of interposito-rubral axons which are dispersed in the superior cerebellar peduncle. In vitro monosynaptic responses in RNm were elicited by an electrode array placed contralaterally in this pathway but near the midline. Mixed excitatory post-synaptic potentials (EPSPs)/inhibitory post-synaptic potentials (IPSPs) were observed in 48 RNm neurons. Excitatory components of the evoked potentials were studied after blocking inhibitory components with picrotoxin (100 microM) and strychnine (5 microM). All RNm neurons examined continued to show monosynaptic EPSPs after non-N-methyl-D-aspartate (NMDA) glutamate receptor components were blocked with 10 microM 6,7-dinitroquinoxaline-2,3-dione or 5 microM 2,3-dihydro-6-nitro-7-sulfamoyl-benzo(f)-quinoxaline (NBQX; n=12). The residual potentials were identified as NMDA receptor components since they (i) were blocked by the addition of the NMDA receptor antagonist, D,L-2-amino-5-phosphonovaleric acid (APV), (ii) were voltage-dependent, and (iii) were enhanced by Mg(2+) removal. Inhibitory components of the evoked potentials were studied after blocking excitatory components with NBQX and APV. Under these conditions, all RNm neurons studied continued to show IPSPs. Blockade of GABA(A) receptors reduced but did not eliminate the IPSPs. These were eliminated when GABA(A) receptor blockade was combined with strychnine to eliminate glycine components of the IPSPs. Thus, IPSPs evoked by midline stimulation of the superior cerebellar peduncle, while blocking alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and NMDA receptors, raise the possibility of direct inhibitory inputs to RNm from the cerebellum. In summary we propose that the special properties of the NMDA receptor components are considered important for the generation of RNm motor commands: their slow time course will contribute a steady driving force for sustained discharge and their voltage dependency will facilitate abrupt transitions from a resting state of quiescence to an active state of intense motor command generation.

Animals↗
PubMed1992

Redox modulation of NMDA receptor-mediated synaptic activity in the hippocampus.

The sulfhydryl reducing agent dithiothreitol (DTT) and the oxidizing agent 5,5-dithio-bis-2-nitrobenzoic acid (DTNB) reversibly modulate the component of synaptic potentials mediated by N-methyl-D-aspartate (NMDA) receptors in slices of hippocampal area CA1. DTT (1 mM) reversibly potentiates NMDA receptor-mediated synaptic potentials while DTNB (1 mM) has the opposite effect. However, treatment of the slices with the irreversible sulfhydryl alkylating agent N-ethylmaleimide (300 microM) prevents DTNB from reversing the potentiation induced by DTT. These results further implicate the redox modulatory site as a regulator of the NMDA receptor-channel complex in vivo.

Animals↗
PubMed1991

Fatty acids modulate excitability in guinea-pig hippocampal slices.

A variety of fatty acids produced sustained changes in excitability in the guinea-pig hippocampal slice. Although each fatty acid was unique, a general pattern was evident. During a 30-min exposure, the synaptic potential was minimally affected, although population spike amplitude showed significant increases. With wash, synaptic efficacy increased. The increase in the synaptic potential was significant with arachidonic acid (100 microM), oleic acid (100 microM), myristic acid (250 microM) and capric acid (250 microM). Also with wash, the coupling between the synaptic potential and the population spike was reduced significantly for most of the fatty acids tested: arachidonic acid (50 microM, 100 microM), linoleic acid (100 microM) oleic acid (100 microM), stearic acid (100 microM), myristic acid (250 microM) and capric acid (250 microM, 500 microM). The fatty acids may influence neuronal excitability, in part, through a direct membrane action. The observed synaptic enhancement is consistent with a role for a fatty acid in long-term potentiation. In addition, fatty acid exposure mimics the effects of X-radiation. We suggest that free radical-induced release of fatty acids contributes to electrophysiological damage in a number of pathological states.

Action Potentials↗
PubMed1997

Role of mast cell- and non-mast cell-derived inflammatory mediators in immunologic induction of synaptic plasticity.

We have previously discovered a long-lasting enhancement of synaptic transmission in mammal autonomic ganglia caused by immunological activation of ganglionic mast cells. Subsequent to mast cell activation, lipid and peptide mediators are released which may modulate synaptic function. In this study we determined whether some mast cell-derived mediators, prostaglandin D2 (PGD2; 1.0 microM), platelet aggregating factor (PAF; 0.3 microM) and U44619 (a thromboxane analogue; 1.0 microM), and also endothelin-1 (ET-1; 0.5 microM) induce synaptic potentiation in the guinea pig superior cervical ganglion (SCG), and compared their effects on synaptic transmission with those induced by a sensitizing antigen, ovalbumin (OVA; 10 micrograms/ml). The experiments were carried out on SCGs isolated from adult male guinea pigs (200-250 g) actively sensitized to OVA, maintained in oxygenated Locke solution at 37 degrees C. Synaptic potentiation was measured through alterations of the integral of the post-ganglionic compound action potential (CAP). All agents tested caused long-term (LTP; duration > or = 30 min) or short-term (STP; < 30 min) potentiation of synaptic efficacy, as measured by the increase in the integral of the post-ganglionic CAP. The magnitude of mediator-induced potentiation was never the same as the antigen-induced long-term potentiation (A-LTP). The agent that best mimicked the antigen was PGD2, which induced a 75% increase in CAP integral for LTP (antigen: 94%) and a 34% increase for STP (antigen: 91%). PAF-, U44619-, and ET-1-induced increases in CAP integral ranged for LTP from 34 to 47%, and for STP from 0 to 26%. These results suggest that the agents investigated may participate in the induction of A-LTP.

Animals↗
PubMed1985

An intracellular study of dentate, CA1 and CA3 neurones in the mouse hippocampal slice.

Intracellular recordings were made from CA1 and CA3 pyramidal cells and from dentate granule cells of the mouse hippocampal slice preparation. The passive electrical properties of the cells and their responses to electrical stimulation of the major antidromic and orthodromic pathways were explored. The majority of cells were impaled between 60 and 100 micron from the surface of the slice. Mean resting potentials were about -66 mV for dentate and CA1 cells and -61 mV for CA3 cells. Mean input resistances were 87, 78 and 73 M omega respectively, with a range of 30-160 M omega for all three populations. Action potential amplitudes ranged from 70 to 110 mV and were typically about 90 mV. Current-voltage (I-V) plots for all three populations were ohmic within a range 10-20 mV negative to the resting potentials. The chord resistance of the I-V relation was lower at more negative potentials and higher at more positive potentials than at the resting potential. Antidromic stimulation at intensities subthreshold for action potential invasion of the impaled cell gave rise to inhibitory post-synaptic potentials (i.p.s.p.s) in CA1 and CA3 cells. The reversal potential of the i.p.s.p.s lay between -65 and -75 mV. They were chloride dependent and could be attenuated by application of bicuculline methiodide. No recurrent i.p.s.p. was seen in dentate cells when using potassium-acetate-filled electrodes. If potassium-chloride-filled intracellular electrodes were used, thus raising the intracellular chloride ion concentration, an antidromically evoked, bicuculline-sensitive depolarizing post-synaptic potential (p.s.p.) could be evoked. Thus, a gamma-aminobutyric acid (GABA)-mediated recurrent inhibitory pathway was present in the slice in all three cell populations but appeared to be difficult to evoke reliably in the dentate gyrus. Orthodromic excitation of CA1 and CA3 cells evoked an excitatory post-synaptic potential (e.p.s.p.) followed by a biphasic hyperpolarization. The early hyperpolarization, lasting about 50 ms, reversed at about -65 mV and was chloride dependent. The later hyperpolarization lasted up to 400 ms, reversed at about -85 mV, and was chloride independent. The e.p.s.p. evoked in dentate cells by stimulation of the perforant path was biphasic and was followed by a hyperpolarization lasting 300-600 ms. The hyperpolarization resembled the late hyperpolarization described above. The two components of the e.p.s.p. may have been produced by the combined activation of the medial and lateral components of the perforant path. Small-amplitude regenerative potentials have been seen in all three cell types.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1980

Lobster neuromuscular junctions treated with black widow spider venom: correlation between ultrastructure and physiology.

Black widow spider venom (BWSV) causes marked physiological and morphological alterations at the lobster neuromuscular junction. BWSV is also active at vertebrate neuromuscular junctions but the component which acts on the lobster preparation is different from the one which affects vertebrates. Following exposure to BWSV, lobster neuromuscular junctions showed elevated frequencies of spontaneous miniature synaptic potentials for 15-30 min. Nerve-evoked synaptic potentials became blocked during this period. Subsequently, spontaneous miniature potentials disappeared and less frequent 'giant' spontaneous potentials appeared. Ultrastructural examination of excitatory and inhibitory nerve terminals showed that both types were affected by venom treatment. In untreated terminals, synaptic vesicles were grouped near the dense specialized membranes of the synapses. Soon after venom treatment, the synaptic vesicles were dispersed throughout the terminals and many larger and elongated vesicular structures were apparent. At the time of appearance of 'giant' spontaneous potentials, few synaptic vesicles were seen in the terminals, but large irregular vacuoles were present. Many mitochondria within the nerve terminals were swollen or disrupted, while nearby muscle mitochondria remained normal in size and appearance. Very few presynaptic dense bodies ('active zones') were seen at synapses of affected terminals. The observations are consistent with the hypothesis that BWSV allows an abnormal amount of Ca2+ to enter the nerve terminals, causing the various physiological and morphological changes.

Animals↗
PubMed2003

Correlation of electrophysiology, shape and synaptic properties of myenteric AH neurons of the guinea pig distal colon.

Well-defined correlations between morphology, electrophysiological properties and the types of synaptic inputs received are established for myenteric neurons in the guinea pig ileum. However, in the distal colon, the correlations between AH electrophysiological properties, presence of fast excitatory post-synaptic potentials (EPSPs) and neuronal shape have been inadequately resolved and it is unknown whether any colon neurons receive synaptic inputs that generate sustained excitation. In this work, we have used intracellular recording, dye filling via the recording electrode, and immunohistochemistry to classify distal colon neurons. Neurons (24 of 168) had Dogiel type II morphology and 42% of these were dendritic type II neurons, compared to about 10% in the ileum. All Dogiel type II neurons had AH electrophysiological properties, including a prolonged post-spike after-hyperpolarization (AHP). None of these received fast excitatory post-synaptic potentials, 11 of 22 tested exhibited sustained slow post-synaptic excitation (SSPE) in response to 1 Hz pre-synaptic stimulation and 13 of 15 tested were immunoreactive for calbindin. Neurons (127) had Dogiel type I, filamentous or other uniaxonal cell shape and S type electrophysiology. Neurons of this group had fast excitatory post-synaptic responses to stimulation of synaptic inputs, but did not exhibit a prolonged post-spike after-hyperpolarization or sustained slow post-synaptic excitation. Another group of neurons (17) had both AH electrophysiological characteristics and fast excitatory post-synaptic potentials. These neurons had Dogiel type I, filamentous or other uniaxonal shapes, but none had Dogiel type II morphology and none showed sustained slow post-synaptic excitation. It is concluded that Dogiel type II neurons are all AH neurons and are probably intrinsic sensory neurons that could be involved in long-term changes in excitability in the colon. All other neurons are monoaxonal; these are motor neurons and interneurons, and most are S neurons, electrophysiologically. A small number of monoaxonal neurons display AH electrophysiology and also receive fast excitatory synaptic inputs. These include motor and interneurons, but not sensory neurons.

Action Potentials↗
PubMed1986

Enkephalin and substance P modulate synaptic properties of chick ciliary ganglion neurons in cell culture.

Since enkephalin- and substance P-like immunoreactive materials have been identified in preganglionic terminals of the avian ciliary ganglion, we tested the effects of enkephalin and substance P directly on chick ciliary ganglion neurons in dissociated cell culture. Under these conditions the neurons form cholinergic synapses with each other that are spontaneously active. Both peptides modulate properties of membrane components associated with synaptic transmission between the neurons. Enkephalin causes a 60% reduction in the mean amplitude of the excitatory synaptic potentials, and the effect appears to be presynaptic in origin: enkephalin does not alter acetylcholine sensitivity on the neurons, but does inhibit Ca2+ influx as reflected by a 38% shortening of the Ca2+ component of the action potential. Both the reduction in synaptic potential amplitude and the shortening of the Ca2+ action potential produced by enkephalin are blocked by naloxone. Substance P, on the other hand, has no effect on Ca2+ action potentials but does reduce the time course of acetylcholine responses in the neurons by a mechanism consistent with enhanced receptor desensitization. Decay of the acetylcholine voltage response in the absence of substance P is described by a single exponential process with a time constant of 4-5 s. Coapplication of acetylcholine and substance P results in a second exponential decay process with a time constant of about 1 s that appears after a 200-400 ms lag period. Preincubation with substance P alone does not decrease the peak voltage response or shorten the lag, suggesting that either agonist or activated receptor is necessary for the substance P effect. These findings suggest modulatory roles for the peptides in ganglionic transmission.

Acetylcholine↗
PubMed1997

In vivo intracellular characteristics of inferior colliculus neurons in guinea pigs.

Intracellular in vivo recordings of physiologically identified inferior colliculus central nucleus (ICc) auditory neurons (n = 71) were carried out in anesthetized guinea pigs. The neuronal membrane characteristics are described showing mainly quantitative differences with a previous report [Nelson, P.G. and Erulkar, S.D., J. Neurophysiol., 26 (1963) 908-923]. The spontaneous spike activity was consistent with the discharge pattern of most extracellularly recorded units. The action potentials showed different spike durations, short and long, and some of them exhibited hyperpolarizing post-potentials. There were also differences in firing rate. The ICc neurons exhibited irregular activity producing spike trains as well as long silent periods (without spikes). Intracellular current injection revealed membrane potential adaptation and shifts that outlasted the electrical stimuli by 20-30 ms. Both evoked synaptic potentials and the spike activity in response to click and tone-burst stimulation were analyzed. Depolarizing-hyperpolarizing synaptic potentials were found in response to contralateral and binaural sound stimulation that far outlasted the stimulus (up to 90 ms). When ipsilaterally stimulated, inhibitory responses and no-responses were also recorded. Although few cells were studied, a similar phenomenon was observed using tone-burst stimulation; moreover, a good correlation was obtained between membrane potential shifts and the triggered spikes (input-output relationship). These in vivo results demonstrate the synaptic activity underlying many of the extracellularly recorded discharge patterns. The data are consistent with the known multi-synaptic ascending pathway by which signals arrive at the ICc as well as the descending corticofugal input that may contribute to the generation of long duration post-synaptic potentials.

Acoustic Stimulation↗
PubMed1992

Ca2+ entry via postsynaptic voltage-sensitive Ca2+ channels can transiently potentiate excitatory synaptic transmission in the hippocampus.

We have studied the role of Ca2+ entry via voltage-sensitive Ca2+ channels in long-term potentiation (LTP) in the CA1 region of the hippocampus. Repeated depolarizing pulses, in the presence of the NMDA receptor antagonist D-APV and without synaptic stimulation, resulted in a potentiation of excitatory postsynaptic potentials (EPSPs) or currents (EPSCs). This depolarization-induced potentiation was augmented in raised extracellular Ca2+ and was blocked by intracellular BAPTA, a Ca2+ chelator, or by nifedipine, a Ca2+ channel antagonist, indicating that the effect was mediated by Ca2+ entry via voltage-sensitive Ca2+ channels. Although the peak potentiation could be as large as 3-fold, the EPSP(C)s decayed back to baseline values within approximately 30 min. However, synaptic activation paired with depolarizing pulses in the presence of D-APV converted the transient potentiation into a sustained form. These results indicate that a rise in postsynaptic Ca2+ via voltage-sensitive Ca2+ channels can transiently potentiate synaptic transmission, but that another factor associated with synaptic transmission may be required for LTP.

2-Amino-5-phosphonovalerate↗
PubMed2003

Group II and III metabotropic glutamate receptors and the control of the nucleus reticularis thalami input to rat thalamocortical neurones in vitro.

Intracellular recordings were made from neurones in the thalamic reticular nucleus (TRN) and ventro-basal (VB) thalamus in slices of rat midbrain in vitro. Electrical stimulation of the medial lemniscus or TRN resulted in the generation of complex synaptic potentials containing disynaptic inhibitory post-synaptic potentials (IPSPs) in VB thalamocortical neurones. Analysis of the excitatory synaptic responses in TRN neurones indicates they can produce burst output response irrespective of the level of sub-threshold membrane potential. This suggests that network-evoked IPSPs in VB thalamocortical neurones occur following a burst of TRN action potentials. Using ionotropic glutamate receptor antagonists, the activation of these disynaptic events was blocked, and the monosynaptic IPSPs that resulted from the direct activation of the TRN could be isolated. The selective Group II agonists LY354740 (1-10 microM) and N-acetyl-aspartyl-glutamate (NAAG; 100-500 microM) both caused a reversible depression of these monosynaptic TRN IPSPs without any effect on membrane potential or input resistance. Likewise, the specific Group III agonist L-2-amino-4-phosphonobutanoate (10-500 microM), but not (RS)-4-phosphonophenylglycine (1 and 30 microM) also caused a reversible depression of these IPSPs, again without any effect on membrane potential or input resistance.Thus, the IPSPs recorded in VB thalamocortical neurones, evoked by TRN activation, can be depressed by the activation of either Group II or III metabotropic glutamate receptors. This is consistent with the location of these receptor types on the presynaptic terminals of TRN axons in the VB thalamus. This raises the possibility that, during periods of intense excitatory activity, glutamate release could influence the release of GABA from TRN axon terminals in the thalamus. In addition, as NAAG is located in the axons and terminals arising from the TRN, there is the possibility that this dipeptide is also released by these terminals to control the release of GABA during periods of high activity in the TRN.

Animals↗