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Linear relationship between the maintenance of hippocampal long-term potentiation and retention of an associative memory.

The hypothesis that the maintenance or decay of an associative memory trace after an extended retention interval is a function of the residual strength of the synapses originally strengthened during learning was examined in a classical conditioning paradigm in which high-frequency stimulation of a hippocampal input--the medial perforant path--served as a conditioned stimulus. Rats received perforant path stimulus-foot shock pairings while engaged in a previously acquired food-motivated lever-pressing task. Conditioned suppression of lever pressing was the behavioral measure of learning and retention of the association. Stimulus trains to the perforant path at an intensity above the threshold for eliciting a population spike induced long-term potentiation of synaptic transmission in the dentate gyrus. Synaptic potentials recorded extracellularly in the dentate gyrus were subsequently monitored for 31 days to examine quantitatively the decay of synaptic potentiation, a period after which retention of the learned association was assessed. All rats learned the association to a similar extent and displayed equivalent amounts of long-term potentiation by the end of conditioning. A slowly decaying function of synaptic potentiation was observed in remembering rats, i.e., rats with high retention performance after the 31-day learning-to-retention interval, while forgetting was associated with a rapid decay of long-term potentiation. Behavioral performance at the long-term memory test was linearly correlated with the amplitude of long-term potentiation maintained just prior to the retention test. The results favor the hypothesis that long-term associative memory depends, at least in part, on the maintenance of elevated synaptic strengths in the pathway activated during learning and suggest a role for the lasting component of long-term potentiation in the maintenance of memory.

Animals↗

Non-synaptic depolarizing potentials in rat supraoptic neurones recorded in vitro.

Intracellular recordings obtained from eighty-two supraoptic nucleus neurones in perfused explants of rat hypothalamus revealed a mean resting membrane potential of -66 +/- 5 mV (S.D.) and spike amplitudes of 70-106 mV. When recorded with K acetate-filled micropipettes, non-spike membrane voltage fluctuations included spontaneous depolarizing and hyperpolarizing potentials. Spontaneous hyperpolarizing potentials peaked in 3-5 ms and decayed exponentially with a mean time constant of 20.2 +/- 0.1 ms, 1.6 times the membrane time constant of 13.8 +/- 0.1 ms. These potentials were identified as spontaneous inhibitory post-synaptic potentials, and all demonstrated a common reversal potential near -80 mV, a depolarizing shift of this reversal potential during intracellular Cl- accumulation, and reversible blockade by raising [Mg2+] to 15 mM in the perfusate. Depolarizing potentials with features typical of spontaneous excitatory post-synaptic potentials i.e. brief (8-20 ms) depolarizing transients, were rarely recorded with K acetate-filled micropipettes. Instead, most neurones demonstrated what are termed non-synaptic depolarizing potentials (n.s.d.p.s) lasting 20-125 ms (mean 86.4 +/- 8.6 ms (S.E. of mean)) with a rise time 21.1 +/- 2.8 ms and a decay time of 16.3 +/- 2.8 ms (n = 28 measured). Unlike typical spontaneous post-synaptic potentials, these events could sustain a constant peak amplitude for most of their duration. These n.s.d.p.s displayed a strong voltage-dependent behaviour and were detected only at membrane potentials within 5-7 mV of the threshold for spike initiation. Spontaneous slow depolarizing membrane shifts preceding or following phasic bursts, or any manipulation (e.g. current step, sinusoid, depolarizing after-potential) causing the membrane potential to enter this range of activation, prompted their appearance. N.s.d.p.s were completely insensitive to the presence of 15 mM-Mg2+ but they were reduced in size and frequency when Ca2+ were replaced with Co2+ or Mn2+. They were detected at a more positive membrane potential when Na+-dependent action potentials were blocked with tetrodotoxin. The size, voltage-dependent and non-synaptic nature of these depolarizing potentials raises the possibility that they reflect the activity of individual (or small clusters of) ionic channels carrying inward current. Their ability to serve as prepotentials to trigger spikes is deemed to be particularly important for promoting the onset of phasic bursts in supraoptic neurosecretory neurones.

Acetates↗

Opiates and opioid peptides modify sensory evoked potentials and synaptic excitability in the rat dentate gyrus.

The effects of morphine and the synthetic opioid peptide D-Ala2-MePhe4-Met-O-ol-enkephalin (FK 33-824) on averaged (AEPS) potentials evoked by a tone and extracellular synaptic potentials (EPSs) in the perforant path, recorded from the outer molecular layer (OM) of the dentate gyrus, were examined in rats trained to respond in an auditory discrimination task. Potentials evoked by a tone were systematically altered by both peripheral (intraperitoneal) and central (intracerebroventricular) administration of opioids. The short-latency negative (N1) component of the average evoked potential was increased in amplitude and the longer-latency negative (N2) component was decreased in amplitude by administration of opioids. At the same time, perforant path extracellular synaptic potentials were enhanced after administration of opioids. The changes in the average evoked potential and extracellular synaptic potentials in the perforant path were reversed by subsequent administration of naloxone. The significance of these results is discussed in terms of a possible role of endogenous opioid peptides in modulating the synaptic efficacy of the perforant path during the transmission of sensory information to the hippocampus from the entorhinal cortex.

Animals↗

Mitochondrial involvement in post-tetanic potentiation of synaptic transmission.

Posttetanic potentiation (PTP) is an essential aspect of synaptic transmission that arises from a persistent presynaptic [Ca2+]i following tetanic stimulation. At crayfish neuromuscular junctions, several inhibitors of mitochondrial Ca2+ uptake and release (tetraphenylphosphonium or TPP+, carbonyl cyanide m-chlorophenylhydrazone or CCCP, and ruthenium red) blocked PTP and the persistence of presynaptic residual [Ca2+]i, while endoplasmic reticulum (ER) Ca2+ pump inhibitors and release channel activators (thapsigargin, 2,5-di-(tert-butyl)-1,4-benzohydroquinone or BHQ, and caffeine) had no effects. PTP apparently results from the slow efflux of tetanically accumulated mitochondrial Ca2+.

Animals↗

Electrophysiology and Pharmacology of the Corticothalamic Input to Lateral Thalamic Nuclei: an Intracellular Study in the Cat.

Though most experimental evidence indicates that the corticothalamic (CT) pathway would exert a direct excitatory action on thalamic relay neurons, the electrophysiological features of this excitation have never been clearly described. A methodological problem in previous electrophysiological studies was that direct corticofugal effects on relay cells could not be separated from those mediated by collateral activation of reticular thalamic neurons. In the present study, the reticular complex was lesioned by kainic acid and the CT response of relay neurons of the ventral lateral nucleus was recorded intracellularly in cats under pentobarbital or urethane anaesthesia. Following reticular thalamic lesions, a prominent depolarization was triggered in thalamic relay cells by stimulation of the CT pathway. This depolarization strongly drove spike discharges, and its amplitude augmented when the stimulation rate exceeded 2 Hz. Tetanizing the CT input with short trains (100 - 200 Hz for 200 - 300 ms) produced a similar augmentation to test volleys for 15 - 30 s after the tetanos. The CT excitation and its frequency-dependent augmentation were depressed by ketamine injection or by local application of N-methyl-D-aspartate (NMDA) antagonists. The augmenting phenomenon appeared strictly homosynaptic. For instance, it did not appear during repetitive stimulation of the cerebellar input, nor did the CT input potentiate subthreshold synaptic potentials of cerebellar origin during a conditioning procedure. Conversely, the cerebellar excitation was depressed when it occurred during the CT depolarization. It is concluded that the direct synaptic responses induced by CT fibres in relay neurons are mediated at least partly by the activation of NMDA receptors. Moreover, the marked non-linear additivity of cerebellar and CT synaptic potentials raises questions concerning the presumed improvement of thalamic transmission of peripheral informations ensured by the CT input. Instead, both inputs could compete for control of the firing of thalamic neurons. The numerical importance of CT fibres and the strong augmenting mechanism operating at synaptic sites in the thalamus suggest that the role of the thalamus is not only to transfer peripheral informations toward the cortex, but also and mainly to feed back to the cortex a modified copy of its own neuronal constructs.

Journal Article↗

Succinate increases neuronal post-synaptic excitatory potentials in vitro and induces convulsive behavior through N-methyl-d-aspartate-mediated mechanisms.

Succinate is a dicarboxylic acid that accumulates due to succinate dehydrogenase inhibition by malonate and methylmalonate exposure. These neurotoxins cause increased excitability and excitotoxic damage, which can be prevented by administering high amounts of succinate. In the present study we investigated whether succinate alters hippocampal field excitatory post-synaptic potentials. Bath application of succinate at intermediate concentrations (0.3-1 mM) increased the slope of field excitatory post-synaptic potentials in hippocampal slices, and at high concentrations (above 1 mM) did not alter or decrease field excitatory post-synaptic potentials slope. Succinate-induced enhancement of field excitatory post-synaptic potentials slope was abolished by the addition of d-2-amino-5-phosphonovaleric acid (50 microM) to the perfusate, supporting the involvement of N-methyl-d-aspartate receptors in the excitatory effect of this organic acid. Accordingly, succinate (0.8-7.5 micromol) i.c.v. administration caused dose-dependent convulsive behavior in mice. The i.c.v. co-administration of MK-801 (7 nmol) fully prevented succinate-induced convulsions, further suggesting the involvement of N-methyl-d-aspartate receptors in the convulsant action of succinate. Our data indicate that accumulation of moderate amounts of succinate may contribute to the excitotoxicity induced by succinate dehydrogenase inhibitors, through the activation of N-methyl-d-aspartate receptors.

Animals↗

Differential localization of 5-HT1 receptors on myenteric and submucosal neurons.

Intracellular recordings were made from guinea pig enteric neurons, and the effects of 5-hydroxytryptamine (5-HT) and the 5-HT1 selective agonists 5-carboxyamidotryptamine (5-CT) and 8-hydroxy-2-(n-dipropylamino)tetralin (DPAT) were studied on membrane potential and synaptic potentials. Most myenteric AH neurons were hyperpolarized when these agonists were applied by superfusion; this hyperpolarization was due to an increase in potassium conductance. Membrane hyperpolarizations to 5-HT, 5-CT, or DPAT were never observed in submucous neurons. Fast nicotinic excitatory postsynaptic potentials (EPSPs) and slow EPSPs recorded from S neurons in the myenteric plexus were suppressed by 5-HT, 5-CT, and DPAT; slow EPSPs in myenteric AH neurons were also inhibited by these agonists. Fast and slow EPSPs recorded from submucous S neurons were not affected by 5-CT or DPAT. However, slow EPSPs recorded from submucous AH neurons were readily blocked by 5-CT and DPAT. The results indicate that 5-HT1 receptors are located on the cell bodies of myenteric but not submucosal neurons. The nerve terminals that release the mediator or mediators of fast and slow synaptic potentials in myenteric neurons also have 5-HT1 receptors and presumably arise from other myenteric neurons; the nerve terminals responsible for the slow EPSP to AH neurons seem to be the only elements of the submucous plexus that express 5-HT1 receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

Neurons dissociated from rat myenteric plexus retain differentiated properties when grown in cell culture. III. Synaptic interactions and modulatory effects of neurotransmitter candidates.

We have used intracellular recordings to study synaptic interactions between myenteric neurons grown in dissociated cell culture. Intracellular stimulation of individual myenteric neurons caused several types of synaptic effects in nearby neurons: fast excitatory synaptic potentials mediated by nicotinic acetylcholine receptors; slow, non-cholinergic synaptic potentials; dual transmission having both fast cholinergic and slow non-cholinergic components and inhibition of spontaneously occurring fast nicotinic synaptic potentials. Fast nicotinic synaptic potentials were elicited by about 40% of neurons tested and often occurred spontaneously. The fast synaptic potentials were similar to those that have been studied in other autonomic neurons with respect to their estimated reversal potential and their sensitivity to cholinergic antagonists. The amplitudes of the fast synaptic potentials declined if evoked at frequencies greater than 0.5 Hz. Potentiation of the fast synaptic potentials was observed following high-frequency stimulation of presynaptic neurons. Several transmitter candidates modulated fast cholinergic transmission. Substance P and vasoactive intestinal peptide promoted nicotinic transmission by causing increased amplitudes of evoked and spontaneous fast synaptic potentials and an increased frequency of spontaneous synaptic potentials. gamma-Aminobutyrate and [Met]enkephalin both caused decreased amplitudes and frequency of nicotinic synaptic potentials. Serotonin depressed synaptic potentials in some neurons while enhancing them or having no effect in others. Slow, non-cholinergic, synaptic potentials were elicited by about 10% of neurons tested. These synaptic effects lasted 15-300s, caused depolarizations of 3-15 mv and were accompanied by increased neuronal input resistance. The transmitter(s) causing these slow synaptic potentials has not yet been identified.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Physiological correlates of responses to gamma-aminobutyric acid (GABA) recorded from rat visual cortical neurons in vitro.

Responses to focal application of gamma-aminobutyric acid (GABA) were compared to synaptic potentials elicited by afferent stimulation of rat visual cortical neurons, using a slice preparation and conventional intracellular recording techniques. GABA produced three types of responses: a brief hyperpolarization (mean reversal potential, -72 mV), brief depolarization (mean reversal potential, -50 mV), or a prolonged hyperpolarization (mean reversal potential, -80 mV). Synaptic potentials included simple or complex EPSPs and EPSPs followed by mono- or biphasic IPSPs. A comparison of the characteristics of the GABA responses and synaptic potentials indicated that GABA may mediate both phases of the IPSP in these cells. Our results suggest that despite differences in the circuitry of the visual cortex as opposed to other neocortical and allocortical (hippocampal) areas (Mountcastle and Poggio, 1968; Colonnier and Rossignol, 1969; Creutzfeldt, 1978; Kuhlenbeck, 1978), the inhibitory control of cortical pyramidal and nonpyramidal neurons by GABA is quite similar.

Action Potentials↗

Compartmentalized PKA signaling events are required for synaptic tagging and capture during hippocampal late-phase long-term potentiation.

Synaptic plasticity, the activity-dependent change in the strength of neuronal connections, is a proposed cellular mechanism of memory storage that is critically regulated by protein kinases such as cAMP-dependent protein kinase (PKA). Despite the fact that a neuron contains thousands of synapses, the expression of synaptic plasticity can be specific to subsets of synapses. This is surprising because signal transduction pathways underlying synaptic plasticity involve diffusible second messenger molecules such as cAMP and diffusible proteins such as the catalytic subunit of PKA. One way in which this specificity can be achieved is by the localization of signal transduction molecules to specific subcellular domains. Spatial compartmentalization of PKA signaling is achieved via binding to A kinase-anchoring proteins (AKAPs). We report here that pharmacological inhibition of PKA anchoring impairs synaptically activated late-phase long-term potentiation (L-LTP) in hippocampal slices. In contrast, potentiation that is induced by the pharmacological activation of the cAMP/PKA pathway, which can potentially affect all synapses within the neuron, is not impaired by inhibition of PKA anchoring. These results suggest that PKA anchoring may be particularly important for events that occur at the synapse during the induction of L-LTP, such as synaptic tagging and capture. Indeed, our results demonstrate that blocking PKA anchoring impairs synaptic tagging and capture. Thus our data highlight the idea that PKA anchoring may allow for specific populations of synapses to change in synaptic strength in the face of plasticity-related transcription that is cell-wide.

Adaptor Proteins, Signal Transducing↗

An electrophysiological analysis of the effects of morphine on the calcium dependence of neuromuscular transmission in the mouse vas deferens.

1 The effects of morphine on the Ca-dependence of the synaptic potential amplitude in the mouse vas deferens have been determined. 2 The synaptic potential increased with a power factor of 2.4 for [Ca]o between 0.7 mM and 1.8 mM. Morphine (40 nM) decreased the synaptic potential, without altering the second power relationship between the synaptic potential and [Ca]o. 3 Morphine reversed the depression in the synaptic potential which develops during a short high-frequency (10 Hz) train of impulses to facilitation. Consequently the synaptic potential beyond the tenth impulse was unaffected by morphine. 4 Morphine did not alter the facilitation of the synaptic potential which develops during a short low-frequency (less than or equal to 2 Hz) train of impulses in normal [Ca]o. Consequently morphine decreased the synaptic potential for each impulse by about the same percentage amount. 5 Morphine increased the small facilitation in the synaptic potential which occurs during a short low-frequency (less than or equal to 2 Hz) train of impulses in high [Ca]o. This facilitation approximated the predictions based on the assumption that each impulse leaves residual Ca ions bound to receptors involved in transmitter release from the nerve terminal.

Action Potentials↗

Synaptic mechanisms that generate network oscillations in the absence of discrete postsynaptic potentials.

Synaptic mechanisms were examined in the pyloric network of the lobster stomatogastric which generate network oscillations in the absence of discrete postsynaptic potentials (PSPs). In normal saline, the unstimulated pyloric network underwent weak bursting in only a few cells. Stimulation of the input nerve, or bath application of the input neurotransmitter dopamine, produced similar vigorous bursting in many pyloric neurons. In saline-containing tetrodotoxin (TTX) plus dopamine, action potentials and corresponding discrete PSPs were blocked, but the underlying slow wave oscillations in network neurons continued. No oscillations occurred in TTX-saline without dopamine. The generation of these nonspiking network oscillations can be explained by the interaction between two synaptic mechanisms which do not produce discrete PSPs: neurotransmitter activation of bursting pacemaker oscillations in a single network neuron, and graded inhibition between network neurons.

Action Potentials↗

Chemical transmission between individual Retzius and sensory neurones of the leech in culture.

1. Chemical synaptic transmission develops between individual identified neurones dissected from leech ganglia and maintained in culture. Impulses in Retzius cells give rise to hyperpolarizing synaptic potentials in pressure (P) sensory cells. In suitable medium the potentials develop by 3 days and can be observed for more than 3 weeks. 2. The synaptic potentials occur after a synaptic delay, exhibit facilitation and depression and are reversed by hyperpolarization. The blocking effects of reduced calcium and raised magnesium concentrations in the bathing fluid provide additional evidence for the chemical nature of transmission. 3. An increase in chloride conductance is involved in the generation of the synaptic potential in the P cell. With high intracellular Cl in the post-synaptic cell, the synaptic potentials become reversed and amplified. The amplitudes of these reversed responses range from 1 to 20 mV with a falling phase lasting for seconds. 4. Changes in the membrane potential of the presynaptic cell that modify the amplitude and duration of the action potential influence the efficacy of transmission. In addition, impulses in Retzius cells initiated from hyperpolarized values of membrane potential evoke smaller synaptic potentials in the P cells than impulses arising from a depolarized level. 5. With neurones placed directly next to one another in the dish, maintained depolarization of the presynaptic Retzius cell in the absence of conducted action potentials gives rise to slow synaptic potentials in the P cells. In some pairs, the response in the P cell consists of a marked increase in 'noise'. 6. Injection of horseradish peroxidase into the Retzius cell reveals neurites with distinctive varicosities growing over the P cell.

Animals↗

Ionic basis of presynaptic inhibitory potentials at crayfish claw opener.

1. Intracellular recordings from the claw opener excitor axon of the crayfish, Procambarus clarkii, were obtained near the terminal arborizations of the axon on the surface of the opener muscle. Rest potential in the excitor axon averaged --80 mV over 20 cells. Action-potential amplitude and duration averaged 100 mV and 2 ms, respectively. 2. A single action potential in the opener inhibitor axon produces a hyperpolarizing synaptic potential (average amplitude 0.3 mV) in the excitor axon. The apparent reversal potential of this inhibitory synaptic potential is approximately 5 mV more negative than rest in control saline. No excitor axons were observed to have depolarizing synaptic potentials at rest. 3. A decrease in external chloride concentration from 240 to 24 mM causes the apparent reversal potential to depolarize an average of 12 mV, with no change in rest potential. In low-chloride saline, the synaptic potential evoked by stimulation of the inhibitor axon becomes depolarizing. 4. An increase in external potassium concentration from 5 to 10 mM causes the apparent reversal potential to depolarize by 16 mV; however, rest potential depolarizes by 10 mV. Low external potassium has the opposite effects, causing both rest potential and the apparent reversal potential to hyperpolarize. 5. Presynaptic inhibition at the Procambarus claw opener neuromuscular junction appears to be mediated by a hyperpolarizing synaptic potential. The results of these experiments suggest that chloride serves as the charge for the presynaptic potential. The evidence for a direct involvement of potassium as a charge carrier is equivocal due to Donnan equilibrium effects involving Cl.

Animals↗

Modulation of GABA-mediated synaptic transmission by endogenous zinc in the immature rat hippocampus in vitro.

1. Intracellular recordings from postnatal 2- to 12-day-old (P2-12) rat hippocampal CA3 pyramidal neurones exhibited spontaneous synaptic potentials mediated by GABAA receptors. These potentials can be separated on the basis of amplitude into two classes which are referred to as small and large. 2. The large depolarizing potentials were reversibly inhibited by the Zn2+ chelator 1,2-diethyl-3-hydroxypyridin-4-one (CP94). The small inhibitory postsynaptic potentials. (IPSPs) were apparently unaffected. 3. Stimulation of the mossy fibre pathway evoked composite excitatory postsynaptic potentials (EPSPs) and IPSPs. Threshold stimulus-evoked synaptic potentials were mediated by GABAA receptors and were reversibly blocked by CP94. The responses evoked by suprathreshold stimulation and persisting in the presence of bicuculline or CP94 were partially inhibited by 2-amino-5-phosphonopropionic acid (AP5) and were completely blocked with 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). 4. L-Histidine, which preferentially forms complexes with Cu2+ > Zn2+ > Fe2+ > Mn2+, inhibited both naturally occurring spontaneous and evoked GABAA-mediated large synaptic potentials without affecting the neuronal resting membrane properties. Exogenously applied Zn2+ induced large spontaneous synaptic potentials and prolonged the duration of the evoked potentials. These effects were reversibly blocked by histidine. 5. The metal chelating agent diethyldithiocarbamate had little effect on the large amplitude synaptic potentials. 6. The transition metal divalent cations Fe2+ and Mn2+ did not initiate large synaptic potentials in CA3 neurones; however, Cu2+ depolarized the membrane and enhanced both excitatory and inhibitory synaptic transmission, resulting in a transient increase in the frequency of the large amplitude events. In comparison, zinc increased the frequency of the large potentials and also induced such events in neurons (P4-21) where innate potentials were absent. The postsynaptic response to ionophoretically applied GABA was either unaffected or slightly enhanced by Zn2+. 7. Under conditions favouring the activation of non-NMDA receptors, excitatory synaptic transmission was unaffected by CP94 but was depressed by Zn2+. Responses to ionophoretically applied glutamate were not inhibited by Zn2+, indicating that Zn2+ affects excitatory synaptic transmission via a presynaptic mechanism. 8. We conclude that the naturally occurring large synaptic potentials in young CA3 neurones are apparently induced by endogenous Zn2+ which can promote or synchronize the release of GABA in the immature hippocampus.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

Embryonic development of synapses on spiking local interneurones in locust.

The development of synapses on an identified population of spiking local interneurones in the thoracic ganglia of embryonic locusts was examined by means of intracellular horseradish peroxidase injection and electron microscopy. In adult locusts, spiking local interneurones of the midline group receive direct inputs onto a ventral field of branches from leg mechanosensory afferents and in turn make output synapses, mainly from a dorsal field of branches, directly upon leg motor neurones, nonspiking local interneurones, and intersegmental interneurones. The aim of this study is to examine the development of these connections. These interneurones are born relatively late in embryogenesis and are not identifiable until approximately 55% of development. At this time (55-60%) only simple filopodial contacts or punctate contacts are evident between the stained interneurones and other neurones. By 65-70% embryogenesis, vesicles are found adjacent to regions where apposed membranes are symmetrically thickened with amorphous electron-dense material. These symmetrical contacts lack distinct presynaptic bar-shaped densities and therefore, are not considered to be synapses. At this stage, the interneurones do not produce action potentials upon intracellular injection of depolarising current. Morphologically identifiable synapses, with vesicles, a presynaptic bar, and relatively little postsynaptic density, are first evident at 70-75%, coincident with the time of arrival of the majority of leg mechanosensory afferents into the central nervous system. At this stage, action potentials and synaptic potentials are also recorded for the first time. The midline spiking interneurones thus become electrically excitable when synapses are first recognisable, at approximately 70% embryogenesis. Most of the synapses found on the interneurones are outputs. The ratio of outputs to inputs on ventral branches is 7.5:1 which contrasts markedly to the adult ratio of 1:2. By 85-90%, output synapses still predominate on the ventral branches, but the ratio of outputs to inputs is reduced to almost 2:1. Dorsal branches have predominantly output synapses throughout embryogenesis. The ratio of dorsal outputs to inputs at 85-90% is 8.5:1 which compares with the adult ratio of 6.5:1. At this stage, action potentials and synaptic activity are always recorded.

Action Potentials↗

Time course of changes in long-term potentiation of synaptic transmission following subcortical deafferentation on the rat hippocampus.

Brief tetanic stimulation potentiates synaptic transmission both in the CA1 and dentate area of slices cut from normal rats. This long-term potentiation (LTP) was assayed in slices made at various times from rats subjected to complete bilateral sectioning of all subcortical afferents which enter the hippocampus. Over about one week survival time, LTP is present in the CA1 region of all and also in the fascia dentata of about 50% of slices. We found no signs of LTP in the dentate area of slices cut over 8 weeks after deafferentation, while the responses were clearly potentiated in the CA1 area of the same slices. Four week was the longest period when a somewhat modified version of LTP could be produced in the subcortically deafferented dentate area. The results confirm previous reports that subcortical afferents mediate some unknown factors essential for maintenance of long-term plasticity of intrinsic synapses in the fascia dentata. This unidentified, perhaps trophic influence diminishes in about 4 weeks after severing the subcortical fibers. In contrast, maintenance of subcortical inputs are apparently not required for the LTP in the intrinsic CA1 synapses.

Afferent Pathways↗

Felbamate decreases synaptic transmission in the CA1 region of rat hippocampal slices.

The antiepileptic drug felbamate (FBM) is known to block N-methyl-D-aspartate receptor-mediated responses and to decrease voltage-sensitive Na+ and Ca+2 channels. The present work was aimed at investigating the actions of FBM on synaptic potentials in the hippocampus, a region frequently involved in epileptic discharges. In rat hippocampal slices, application of FBM (100-1300 microM, 10 min) elicited a concentration-dependent, fully reversible decrease in amplitude of electrically evoked population spikes recorded extracellularly from the CA1 pyramidal cell layer. In intracellular recordings, FBM (50-300 microM) decreased the amplitude of excitatory postsynaptic potentials and reduced the probability of firing action potentials upon synaptic activation. Action potential frequency adaptation (accommodation), which typically limits repetitive firing in CA1 pyramidal cells, was increased. By using a paired-pulse protocol, FBM (300 microM) depressed the amplitude of paired excitatory postsynaptic potentials, without affecting the facilitation of the second response. In nominally Mg(+2)-free solution, FBM (100 microM) blocked N-methyl-D-aspartate receptor-mediated synaptic excitatory postsynaptic potentials isolated by the presence of 10 microM 6-nitro-7-sulfamoylbenzo(f)quinoxaline hydrochloride, a selective alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor antagonist, and 10 microM bicuculline or 25 microM picrotoxin. This effect was not reversed by the addition of 300 microM Gly. All these effects contribute to decrease excitatory synaptic transmission and are likely to limit neuron recruitment and propagation of epileptic discharges.

Animals↗