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PubMed1990

Synaptic and intrinsic control of membrane excitability of neostriatal neurons. I. An in vivo analysis.

1. The relationship between membrane properties of neostriatal neurons and spontaneous and evoked synaptic potentials was studied with the use of intracellular recordings from anesthetized rats. Most of these neurons showed regular or irregular spontaneous depolarizing potentials that only in a few cases triggered action potentials at resting level. 2. The stimulation of the ipsilateral substantia nigra or of the sensorimotor cortex produced a relatively fast depolarizing post-synaptic potential (EPSP). In some cells this potential was followed by an inhibitory period that appeared as an hyperpolarization when the cell was depolarized from the resting level (inhibitory postsynaptic potential, IPSP). A late and long-lasting depolarization (LD) followed the EPSP or the EPSP-IPSP sequence. 3. Repetitive discharge with little adaptation was observed during direct depolarization. Most of the neurons tested for current-voltage (I-V) relationship showed nonlinearity of the input resistance in the hyperpolarizing direction. Spontaneous and evoked EPSPs were decreased in their amplitude and duration when the membrane potential was held at levels more hyperpolarized than -85 mV because of the strong rectification at these levels of hyperpolarization. 4. Local microiontophoretic application of bicuculline (BIC) or systemic administration of BIC and pentylenetetrazole (PTZ) produced a reduction of the IPSPs. The reduction of the inhibitory transmission caused a strong increase of the LD. The current-evoked firing pattern was not greatly altered. 5. The intracellular application of cesium increased the amplitude and the duration of the spontaneous depolarizations that triggered bursts of action potentials under this condition. Spikes were broadened and the rectification in the hyperpolarization direction was reduced. 6. Iontophoretically applied cadmium strongly depressed the amplitude of the spontaneous and evoked postsynaptic potentials. During cadmium application, nigral stimulation produced constant latency, all-or-none spikes in the absence of any synaptic potential. 7. Repetitive stimulation of the ipsilateral substantia nigra by electrical shocks (5 Hz, 25 s) produced a progressive and reversible decrease of the spontaneous depolarizing potentials (SDPs) and a decrease of the firing rate. In the same cells, when the train of stimulation was delivered in the ipsilateral cortex, a membrane depolarization coupled with an increase of the firing rate was observed. 8. We conclude that although synaptic circuits mediate a phasic inhibition in neostriatum, the low level of spontaneous firing of most neostriatal neurons is mainly because of the effects that membrane properties exert on the spontaneous and the evoked synaptic depolarizations in the striatum.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1982

Sensory transduction and neuronal transmission as related to ultrastructure and encoding of information in different labyrinthine receptor systems of vertebrates.

Mechano-electric transduction and neuronal transmission were studied in sensory systems ascending from and descending to single receptor cells of the labyrinth organs in submammalian vertebrates. The animals were young crocodiles (Caiman crocodilus), geckos (Gekko gecko, Tarentola mauritanica), and turtles (Pseudemys scripta elegans, Chinemys reevesii). Intracellular receptor potentials from the apical region of the hair cell (or from the ciliary surface) were recorded in the ampullar, macular, and papillar sensory cells. These single-cell responses are, within limits, proportional to stimulus amplitude, frequency, or phase and are bidirectional in that they show depolarization by kinociliopetal stereociliar displacement and hyperpolarization by kinociliofugal displacement. Synaptic potentials (presynaptic from the basal region of the hair cell, postsynaptic from the contacting nerve endings) were recorded in the utricular, saccular, and lagenar neuroepithelia with electron-optic localization of the in situ fixed microelectrode tip. As local excitatory or inhibitory processes, respectively, they follow the stimulus and receptor potential with latency and with nonlinear distortion. Action potentials (spikes), as synchronized by the excitatory synaptic potentials, were recorded from single nerve fibers or bipolar cells, related to ampullar, macular, or papillar receptor units. Unit responses and synaptic potentials were recorded from the first, second, and following centripetal and central neurons of the ascending systems, or from neurons of the descending systems in the brain stem or from centrifugal neurons. Such records were achieved during adequate mechanical or acoustical stimulation of the different receptor systems, with additional electrical stimulation, uni- or bilaterally. Thus, the influence of centripetal-centrifugal bilateral interaction on the receptor functions was measured, as inhibition or disinhibition, respectively. The input-output relations of these sequential stages of information transfer were plotted as histograms of different types, as characteristic curves, power spectra, or by correlation operations, with or without feedback, from the different systemic levels.U

Alligators and Crocodiles↗
PubMed1995

Intrinsic neuromodulation in the Tritonia swim CPG: the serotonergic dorsal swim interneurons act presynaptically to enhance transmitter release from interneuron C2.

Heterosynaptic enhancement of transmitter release is potentially very important for neuronal computation, yet, to our knowledge, no prior study has shown that stimulation of one neuron directly enhances release from an interneuron. Here, we demonstrate that in the marine mollusk Tritonia diomedea, the serotonergic dorsal swim interneurons (DSIs) heterosynaptically increase the amount of transmitter released from another interneuron, C2. Stimulation of a single DSI at physiological firing frequencies increases the size of synaptic potentials evoked by C2. This increase in synaptic efficacy is correlated with an increase in homosynaptic paired-pulse facilitation by C2. Thus, it is likely to be due to an enhancement of transmitter release from C2, rather than a postsynaptic action on the followers of C2. This is further supported by the fact that DSI stimulation enhances the strengths of all chemical synapses made by C2 within the swim network, regardless of their sign. Furthermore, DSI enhances the amplitude of C2 synaptic potentials recorded in neurons that DSI itself does not synapse with. Finally, DSI differentially modulates different synaptic inputs to the same postsynaptic target; while increasing C2-evoked EPSPs it simultaneously decreases the size of EPSPs evoked by other DSIs. The heterosynaptic facilitation of C2 synaptic potentials by DSI is not caused by a simple depolarization of C2, but may be a direct action on the transmitter release mechanism. This neuromodulatory effect, which is intrinsic to the circuitry of the central pattern generator for escape swimming in Tritonia, may be important for self-reconfiguration of the swim motor network.

Animals↗
PubMed2005

Analytical solution of the cable equation with synaptic reversal potentials for passive neurons with tip-to-tip dendrodendritic coupling.

A passive cable model is presented for a pair of electrotonically coupled neurons in order to investigate the effects of tip-to-tip dendrodendritic gap junctions on the interaction between excitation and either pre or postsynaptic inhibition. The model represents each dendritic tree by a tapered equivalent cylinder attached to an isopotential soma. Analytical solution of the cable equation with synaptic reversal potentials is considered for each neuron to yield a system of Volterra integral equations for the voltage. The solution to the system of linear integral equations (expressed as a Neumann series) is used to determine the current spread within the two coupled neurons, and to re-examine the sensitivity of the soma potentials (in particular) to the coupling resistance for various loci of synaptic inputs. The model is actually posed generally, so that active as well as passive properties could be considered. In the active case, a system of non-linear integral equations is derived for the voltage.

Dendrites↗
PubMed1990

Activation of a K-252b-Sensitive Protein Kinase is Necessary for a Post-Synaptic Phase of Long-Term Potentiation in Area CA1 of Rat Hippocampus.

K-252b, a potent inhibitor of protein kinases blocked a late phase of long-term potentiation (LTP) in area CA1 of rat hippocampal slices, resulting in decremental LTP. It also prevented the slowly developing increase in sensitivity of CA1 neurons to iontophoretically administered alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) which was seen in control slices that exhibit nondecremental LTP. However, K-252b applied 60 - 180 min after the induction of LTP had no effect on the potentiated synaptic and AMPA-induced responses. A K-252b-sensitive protein kinase may therefore be involved in a slowly developing postsynaptic component of LTP.

Journal Article↗
PubMed1968

Electrical activity observed in guinea-pig olfactory cortex maintained in vitro.

1. Electrical recordings were made from a preparation of guinea-pig olfactory cortex maintained in vitro.2. The response of the prepiriform area to a volley delivered to the lateral olfactory tract comprised a sharp negative deflexion upon which several positive notches were superimposed followed by a long-duration low-amplitude positive wave.3. Both the negative and positive waves were of maximal amplitude near the top surface of the preparation (the original cortical surface).4. Units recorded at depths of 250-350 mu showed facilitation and latency variation. The latency distribution of these spikes was very similar to that of the positive notches observed on the surface of the slice.5. The surface observed negative waves were rapidly abolished by oxygen lack.6. The negative and positive waves have been tentatively identified as the extracellular manifestations of the excitatory post-synaptic potentials (EPSPs) and inhibitory post-synaptic potentials (IPSPs) occurring in the apical dendrites.7. Some spontaneous activity was observed in a proportion of the preparations studied.8. The evidence presented here strongly supports the contention that portions of the mammalian brain may be maintained in a satisfactory functional condition when isolated from the body, provided that they are maintained in a suitable environment. We believe that such preparations will prove very useful for physiological studies of the mammalian brain.

Action Potentials↗
PubMed1983

Muscarinic inhibition of sympathetic C neurones in the bullfrog.

1. The muscarinic inhibitory post-synaptic potential (i.p.s.p.) in sympathetic C neurones has been characterized in an isolated preparation of bullfrog paravertebral chain ganglia. Interactions between the i.p.s.p. and two other synaptic potentials have also been examined. 2. A single presynaptic stimulus to a C cell produces a nicotinic excitatory post-synaptic potential (e.p.s.p.) followed by a muscarine i.p.s.p. The latency of the i.p.s.p. is 50 msec or longer and the response lasts for seconds. C cells receive multiple cholinergic innervation but the thresholds for activation of the e.p.s.p. and i.p.s.p. are inseparable. Trains of 50 or more presynaptic stimuli produce a non-cholinergic e.p.s.p. which follows the nicotinic e.p.s.p. and i.p.s.p. and which lasts for tens of seconds. 3. The i.p.s.p. produced by a single presynaptic stimulus can be 30 mV in amplitude. However, in most cells, a short train of stimuli applied at an optimal frequency of 10 Hz is required to produce a large i.p.s.p. 4. The i.p.s.p. is blocked by atropine but is not affected by catecholamine antagonists. 5. Ionophoretically applied acetylcholine (ACh) mimics the i.p.s.p. in its latency, time course and amplitude. In addition, the i.p.s.p. and the muscarinic response to ACh reverse polarity at the same membrane potential: -102 mV in normal Ringer solution. The i.p.s.p. reversal potential shifts by 55 mV/decade change in extracellular K+ concentration and is insensitive to the Cl- gradient. 300 microM-Ba2+ totally blocks the muscarinically activated conductance in a reversible manner. 6. Action potentials, when initiated by a supramaximal nicotinic e.p.s.p. or by an antidromic impulse, are not blocked by the i.p.s.p. 7. Near resting potential (-50 to -60 mV), C cells can fire repetitively. The non-cholinergic slow e.p.s.p. is often accompanied by oscillations in membrane potential and firing of action potentials. This repetitive firing of C cells, which appears to be enhanced by the non-cholinergic e.p.s.p., is strongly inhibited by the i.p.s.p. The inhibition can be mimicked by injection of very small hyperpolarizing currents (e.g. 25 pA). Interactions between the i.p.s.p. and the non-cholinergic e.p.s.p. can generate phasic bursting patterns in C cells. 8. The mechanism underlying the i.p.s.p. and the consequences of these findings for ganglionic integration are discussed.

Acetylcholine↗
PubMed1986

Action-potential duration and the modulation of transmitter release from the sensory neurons of Aplysia in presynaptic facilitation and behavioral sensitization.

Presynaptic facilitation of transmitter release from Aplysia sensory neurons is an important contributor to behavioral sensitization of the gill and siphon withdrawal reflex. The enhanced release is accompanied by reduction of the serotonin-sensitive S current in the sensory neurons and a consequent increase in duration of the presynaptic action potential (ranging from 10% to 30%). We find that changes of similar magnitude in the duration of depolarizing voltage-clamp steps in sensory neurons in intact abdominal ganglia yield increases in synaptic potentials of 45-120%. In dissociated cell culture, these changes lead to increases of 25-60% in the synaptic potential. Prolongation of presynaptic depolarization using voltage clamp or prolongation of the duration of the action potential by K(+)-channel blockers leads to prolongation of the time-to-peak of the synaptic potentials; similar changes in time-to-peak occur during presynaptic facilitation. The time-to-peak is not changed by homosynaptic depression or by changing the Ca(2+) concentration, procedures that alter release without changing the duration of the action potential. Preventing the spike from broadening by voltage clamping the presynaptic neuron substantially reduces or blocks the facilitation. These results suggest that broadening of the action potential during facilitation is a causal factor in the enhancement of transmitter release.

Journal Article↗
PubMed1997

Interleukin-6 inhibits long-term potentiation in rat hippocampal slices.

The effects of recombinant human interleukin-6 (rhIL-6) on long-term potentiation (LTP) induced in the Schaffer collateral/commissural-CA1 pathway were examined using rat hippocampal slices. Field excitatory postsynaptic potential was recorded in the stratum radiatum of the CA1 region. Ten-min applications of rhIL-6 (50-2000 U/ml), started 5 min before the tetanus, significantly inhibited the induction of LTP, and in high doses of rhIL-6 also inhibited short-term potentiation (over 200 U/ml) and post-tetanic potentiation (over 500 U/ml). The effects of rhIL-6 (500 U/ml) were completely abolished by the preincubation of the slices with monoclonal anti-IL-6 receptor antibody (16 microg/ml) for 2 h. Heat-inactivated rhIL-6 had no effect on the synaptic potentiation. RhIL-6 affected neither the previously established LTP nor the basal synaptic transmission. These findings indicated that rhIL-6 modulated synaptic potentiation through the IL-6 receptor-mediated process in the hippocampus, probably by affecting post- and presynaptic sites in the CA1 region. The possible mechanisms of the IL-6-induced suppression of the synaptic potentiation were discussed.

Action Potentials↗
PubMed1987

[Development of electrical activity of hypothalamic cells in culture].

The development of the electrical activity of hypothalamic cells was studied using intracellular and patch clamp recording technics on cultured hypothalamic neurones from 14 days mouse embryos. After 24 h of incubation, 15% of recorded cells were spontaneously active. During the first five days of culture this ratio increased exponentially to reach 95% at day 5. Between the 5th and the 9th day the spontaneous activity progressively decreased although the majority of cells remained excitable. Spontaneous activity reappeared after the 9th day and was underlain by a synaptic potential activity. During the first five days of culture, only a TTX sensitive inward current was observed in all cell tested. A calcium inward current appeared after the first week of incubation. It was recorded on 40% of cells at day 11th and in 80% of cells tested after a month of incubation. Our results show that electrical activity of cultured hypothalamic neurones develop in three stages. A first stage characterized by a spontaneous electrical activity without post synaptic potential, an intermediate stage during which a Calcium inward current appeared corresponding to synaptic contact development and a third stage during which post synaptic potential activity was observed, corresponding to synaptic contact maturation.

Animals↗
PubMed1995

Neurons derived from P19 embryonal carcinoma cells develop responses to excitatory and inhibitory neurotransmitters.

Cells of the P19 line of embryonal carcinoma cells differentiate into neurons, astrocytes and oligodendrocytes following treatment with retinoic acid. The neurons from these differentiating P19 cultures synthesize a pattern of neurotransmitters that resembles that of neurons of the forebrain. We treated P19 cells with retinoic acid and then implanted them into the striatum of adult rats. After times ranging from 1 to 15 weeks post-implantation, brain slices containing the implanted tissue were prepared and used for intracellular recording of electrical activity and responsiveness to application of neurotransmitters. Within 2 weeks of implantation, the P19-derived neurons had developed responsiveness to the excitatory neurotransmitter glutamate and the inhibitory transmitters gamma-aminobutyric acid and glycine. These neurons also exhibited spontaneous synaptic potentials. The responses to glutamate appear to be mediated by N-methyl-D-aspartic acid as well as non-N-methyl-D-aspartic acid receptor subtypes. Gamma-aminobutyric acid evoked bicuculline-sensitive depolarizing responses in the younger grafts and biphasic depolarizing/hyperpolarizing responses in older ones. Responses to glycine were strychnine sensitive and also showed age-related changes from depolarizing to biphasic character. Synaptic potentials in the younger grafts were exclusively depolarizing, but in older ones both depolarizing and hyperpolarizing events were observed. The synaptic potentials appear to arise from synaptic connections between P19-derived neurons within the grafts. Many of the features of P19-derived neurons are similar to those of neurons in the developing forebrain.

Animals↗
PubMed1988

Endogenous dopamine and dopaminergic agonists modulate synaptic excitation in neostriatum: intracellular studies from naive and catecholamine-depleted rats.

Intracellular recordings from slices of rat neostriatum were utilized to study the effects of endogenous dopamine and of exogenous dopaminergic agonists on the excitatory synaptic potentials evoked by the local stimulation of the slice. D-Amphetamine (0.1-5 microM), as well as dopamine, produced a dose-dependent decrease of the excitatory synaptic potentials. This effect was blocked by membrane hyperpolarization. The blockade of potassium channels by intracellular cesium or by extracellular 4-aminopyridine (0.5-1 mM) did not block the voltage-dependent effect of dopamine. The effects of D-amphetamine were antagonized by (R)-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepine-7 -ol (SCH 23390) (0.1-1 microM), an antagonist for D1 dopaminergic receptors, but not by sulpiride (0.1-1 microM), an antagonist for D2 receptors. Pretreatment of the animals with alpha-methyl-p-tyrosine (200 mg/kg) or with reserpine (5 mg/kg) blocked the amphetamine-induced effect on the synaptic potentials. In reserpinized animals, the hyperpolarization of the membrane potential did not block the dopamine-induced decrease of the synaptic excitation. After reserpine pretreatment bromocryptine and lysuride, D2 agonists which in control conditions were ineffective, also mimicked the effects of dopamine. In reserpinized rats, the inhibitory effects of the dopaminergic agonists were antagonized by sulpiride, but not by SCH 23390. We conclude that in naive animals endogenous dopamine mimics the voltage-dependent reduction of synaptic excitation produced by D1 activation, while in catecholamine-depleted rats dopamine lacks its voltage-dependent effect and interacts with "supersensitive" D2 receptors.

4-Aminopyridine↗
PubMed1993

Distribution of rubrospinal synaptic input to cat triceps surae motoneurons.

1. We evoked steady-state synaptic potentials in triceps surae motoneurons of the cat by stimulating the hindlimb projection area of the contralateral magnocellular red nucleus at 200 Hz. We measured the effective synaptic currents (IN) underlying the synaptic potentials using a modified voltage-clamp technique. We also determined the effect of the rubrospinal input on the discharge rate of some of the motoneurons by inducing repetitive discharge with long injected current pulses during which the red nucleus stimulation was repeated. 2. At motoneuron resting potential, the distribution of IN from the red nucleus within the triceps surae pools was qualitatively similar to the distribution of synaptic potentials: 86% of the putative type F motoneurons received a net depolarizing IN from the red nucleus stimulation, whereas only 38% of the putative type S units did so. The mean values of IN were significantly different in the two groups [+4.1 +/- 5.0 nA (SD) for putative type F and -1.6 +/- 3.1 nA for putative type S]. 3. However, when the values of IN at threshold for repetitive firing were estimated, the distribution of IN from the red nucleus was quite different. At threshold, all of the putative type S units received hyperpolarizing IN but so did nearly half of the putative type F units. 4. As would be expected from the wide range of IN at threshold (-20 to +12 nA), the red nucleus input produced dramatically different effects on the discharge of different motoneurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed2006

Kainate receptor activation potentiates GABAergic synaptic transmission in the nucleus accumbens core.

Inhibitory synaptic transmission plays an important role in regulating the activity of medium spiny neurons (MSNs) in the nucleus accumbens (NAcc). The kainate (KA) subtype of ionotropic glutamate receptor has been shown to potently modulate GABAergic synaptic transmission in several brain regions. Although KA receptor subunits are expressed in the NAcc, KA receptor modulation of GABAergic synaptic transmission in this brain region has not been previously examined. In the current study, we sought to determine if KA receptor activation could alter inhibitory synaptic transmission in the NAcc as it has been shown to do in other brain regions. Using the whole cell patch-clamp technique, we demonstrate that KA receptor activation potentiates evoked GABAergic synaptic transmission and increases the frequency of spontaneous, but not miniature, GABA(A)-receptor-mediated IPSCs in the NAcc. In contrast, KA has no effect on currents evoked by exogenous application of GABA onto MSNs. Taken together, these data suggest that activation of KA receptors in the NAcc core potently facilitates action-potential-dependent GABAergic synaptic transmission, likely via an excitation of presynaptic GABAergic interneurons.

Animals↗
PubMed1993

N-methyl-D-aspartate stimulates the dephosphorylation of the microtubule-associated protein 2 and potentiates excitatory synaptic pathways in the rat hippocampus.

We have studied the effect of brief (50-150 s) applications of N-methyl-D-aspartate (10-100 microM) on the phosphorylated state of the microtubule-associated protein 2 in slices of rat hippocampus. Following a similar experimental protocol we also studied the pattern of excitatory postsynaptic potentials intracellularly recorded in CA1 pyramidal cells elicited by stimulation of the Schaffer collateral-commissural pathway. N-Methyl-D-aspartate treatment produced a marked and specific dephosphorylation of the cytoskeletal microtubule-associated protein 2, which was not due to enhanced proteolytic activity. Dephosphorylation of the microtubule-associated protein 2 affects mainly the tubulin-binding domain of the molecule and seems to be a consequence of the activation of the Ca2+/calmodulin-dependent phosphatase calcineurin, as it is partially inhibited by calmidazolium but not by okadaic acid. A few minutes after N-methyl-D-aspartate treatment we observed a 23 +/- 17% increase in the amplitude of the monosynaptic excitatory postsynaptic potential recorded in the cells and the appearance of a large polysynaptic excitatory postsynaptic potential. Both effects lasted for several tens of minutes. The late polysynaptic potential was not observed when the CA3 and CA1 subfields were surgically separated. Our results indicate that the N-methyl-D-aspartate receptor activation leads to the dephosphorylation of the microtubule-associated protein 2 via a Ca2+/calmodulin phosphatase, probably calcineurine. This may, in turn, participate in the potentiation of synaptic efficacy.

Animals↗
PubMed1985

Properties of choroid and ciliary neurons in the avian ciliary ganglion and evidence for substance P as a neurotransmitter.

Intracellular recordings were made from identified choroid and ciliary neurons in the ciliary ganglion of the embryonic chick. Choroid neurons, which were innervated by multiple preganglionic fibers, frequently displayed noncholinergic slow excitatory postsynaptic potentials (EPSPs) following repetitive stimulation of the preganglionic nerve trunk. These slow potentials were blocked by high Mg2+/low Ca2+ buffer and were closely mimicked by bath application of substance P, which is known to be present within both populations of preganglionic nerve terminals. Substance P-induced depolarizations desensitized during prolonged exposure, at which time it was no longer possible to evoke slow synaptic potentials. Following manual voltage clamp to resting membrane potential, parallel increases in input resistance were seen during the slow EPSP and the response to substance P, suggesting that the two responses share common mechanisms. Ciliary neurons, which were innervated by a single preganglionic fiber and displayed dual electrical-chemical synapses, did not exhibit slow synaptic potentials and were unaffected by bath application of substance P. The magnitude and time course of fast nicotinic EPSPs elicited in ciliary neurons by 0.5 Hz presynaptic stimulation were also unchanged in the presence of 1 to 3 microM substance P. Although the ciliary and choroid neurons share a common embryological origin in the neural crest, they are specialized for quite different physiological roles. Integration of multiple presynaptic inputs occurs at choroid synapses, mediated by the presence of both subthreshold fast nicotinic EPSPs and the slow EPSP. In contrast, synapses on ciliary neurons have specializations which preclude any integrative function, including single innervation, a high quantal content, electrical coupling potentials, and a lack of slow synaptic potentials.

Animals↗
PubMed1989

Spontaneous epileptiform activity and alteration of GABA- and of NMDA-mediated neurotransmission in amygdala neurons kindled in vivo.

This study was designed to analyze in vitro the changes in synaptic potentials that occur in neurons of the basolateral amygdala 4-6 weeks after kindling in vivo. The following 3 phenomena were observed in basolateral neurons which were contralateral to the kindling site: (1) spontaneous epileptiform bursting; (2) evoked epileptiform bursting or 'extra' evoked synaptic potentials; and (3) the absence of GABAergic inhibitory postsynaptic potentials either spontaneous or evoked. Epileptiform bursting, spontaneous and evoked, and 'extra' evoked synaptic potentials were depressed by NMDA receptor antagonists and were recorded in normal physiological solution. These data suggest that the amygdala is an area of the brain particularly sensitive to epileptogenesis.

Animals↗
PubMed1973

Long-lasting potentiation of synaptic transmission in the dentate area of the unanaestetized rabbit following stimulation of the perforant path.

1. Potential changes evoked by stimulation of the perforant path have been recorded in the dentate area of the hippocampal formation in chronically prepared unanaesthetized rabbits.2. Components attributed to excitatory synaptic current flow and to action potentials in the granule cell population were distinguishable, with characteristics largely the same as in anaesthetized rabbits.3. Stimulation at 15/sec for several seconds usually led to the granule cells being more effectively activated by the individual stimuli of the train (;frequency potentiation'). Single stimuli then commonly produced multiple discharges in the granule cell population.4. After single periods of stimulation at 15/sec for 15-20 sec there was on 26% of the occasions (41% of those on which there was good frequency potentiation) a long-lasting potentiation of the responses to subsequent stimuli, lasting from 1 hr to 3 days.5. After a further 20% of the periods of repetitive stimulation there was a shorter lasting potentiation, and after 8% there was a short lasting depression.6. The potentiation, when present, was characterized by some or all of the following changes: increases in the amplitudes of the synaptic wave and population spike, reduction in the latency of the population spike, and reductions in the variability of the characteristics of the population spike.7. During the long-lasting potentiation there was an increase in the excitability of the post-synaptic cells and, on some but not all occasions, an increase in the extracellular current flow produced directly by synaptic action.

Action Potentials↗