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PubMed2003

Enhanced long-term potentiation in the hippocampus of rats expressing mutant presenillin-1 is age related.

Electrophysiological recordings were made from Fischer rats engineered to express the human presenilin 1 gene carrying the M146V mutation. Extracellular recordings of field excitatory post-synaptic potential (EPSPs) were made to investigate EPSP properties, paired pulse responses, posttetanic potentiation, and long-term potentiation in the stratum radiatum and dentate gyrus of hippocampal slices maintained in vitro. Transgenic rats aged approximately 6 months showed no differences from their wild-type littermates in any of these properties. However, at 18 months, long-term potentiation in the CA1 was facilitated in the transgenic rats with a different pattern of synaptic enhancement. No changes were observed in paired pulse facilitation (PPF) or post-tetanic potentiation (PPT) and no changes were seen in the dentate gyrus. Field potential amplitudes were significantly greater and PPF was enhanced in the CA1 of all older rats. Intracellular recordings from CA1 pyramidal cells of the older group of rats revealed no differences in the passive or active membrane properties of cells in the two groups, but intracellularly recorded EPSPs were significantly longer.

Aging↗
PubMed1984

Electrophysiological mechanisms of kainic acid-induced epileptiform activity in the rat hippocampal slice.

Depression of GABA-mediated IPSPs has been proposed to be a crucial factor in the onset of epileptiform activity in most models of epilepsy. To test this idea, we studied epileptiform activity induced by bath application of the excitatory neurotoxin kainic acid (KA) in the rat hippocampal slice. Repetitive field potential firing, spontaneous or evoked, occurred during exposure to KA. Intracellular records from 52 CA1 pyramidal cells during changes from control saline to saline containing 1 microM KA indicated that KA depolarized cells an average of about 5 mV and caused a 15% decrease in input resistance. Action potentials and current-induced burst afterhyperpolarizations did not change significantly. In several cells the tonic effects of KA were preceded by a transient phase of sporadic, spontaneous depolarizations of 2 to 10 mV and 50 to 200 msec duration. These phasic depolarizations were blocked by hyperpolarization. The major effect of 1 microM KA was a depression of synaptic potentials. Initially, KA depressed fast GABA-mediated IPSPs and slow, non-GABA-mediated late hyperpolarizing potentials to 23% and 40% of control values, respectively. IPSP depression correlated closely with onset of burst potential firing in response to synaptic stimulation. Similar observations were made on six cells from the CA2/3 region, although these cells were affected by lower doses of KA. The mechanism of IPSP depression was studied by using KCl-filled electrodes to invert spontaneous IPSPs and make them readily visible. In nine CA1 cells the rate and amplitude of spontaneous IPSPs transiently increased but then decreased in conjunction with evoked IPSP depression. Possible KA effects on postsynaptic GABA responses were investigated by applying GABA locally to cells. KA did not significantly affect GABA responses. Prolonged exposure of CA1 cells to KA in doses of 1 microM or higher depressed intracellularly and extracellularly recorded EPSPs and all field potential activity. This depression was not apparently due to depolarization block in CA1, however. We conclude that KA induces epileptiform activity in hippocampus principally by a presynaptic block of IPSP pathways.

Action Potentials↗
PubMed1998

Development of spontaneous synaptic transmission in the rat spinal cord.

Dorsal root afferents form synaptic connections on motoneurons a few days after motoneuron clustering in the rat lumbar spinal cord, but frequent spontaneous synaptic potentials are detected only after birth. To increase our understanding of the mechanisms underlying the differentiation of synaptic transmission, we examined the developmental changes in properties of spontaneous synaptic transmission at early stages of synapse formation. Spontaneous postsynaptic currents (PSCs) and tetrodotoxin (TTX)-resistant miniature PSCs (mPSCs) were measured in spinal motoneurons of embryonic and postnatal rats using whole cell patch-clamp recordings. Spontaneous PSC frequencies were higher than mPSC frequencies in both embryonic and postnatal motoneurons, suggesting that even at embryonic stages, when action-potential firing rate was low, presynaptic action potentials played an important role in triggering spontaneous PSCs. After birth, the twofold increase in spontaneous PSC frequency was attributed to an increase in action-potential-independent quantal release rather than to a higher rate of action-potential firing. In embryonic motoneurons, the fluctuations in peak amplitude of spontaneous PSCs were normally distributed around single peaks with modal values similar to those of mPSCs. These data indicated that early in synapse differentiation spontaneous PSCs were primarily composed of currents generated by quantal release. After birth, mean mPSC amplitude increased by 50% but mean quantal current amplitude did not change. Synchronous, multiquantal release was apparent in postnatal motoneurons only in high-K+ extracellular solution. Comparison of the properties of miniature excitatory and inhibitory postsynaptic currents (mEPSCs and mIPSCs) demonstrated that mean mEPSC frequency was higher than mIPSC frequency, suggesting that either excitatory synapses outnumbered inhibitory synapses or that the probability of excitatory transmitter release was higher than the release of inhibitory neurotransmitters. The finding that mIPSC duration was several-fold longer than mEPSC duration implied that despite their lower frequency, inhibitory currents could modulate motoneuron synaptic integration by shunting incoming excitatory inputs for prolonged time intervals.

2-Amino-5-phosphonovalerate↗
PubMed1990

The adenosine antagonist 8-cyclopentyltheophylline reduces the depression of hippocampal neuronal responses during hypoxia.

Exposure of rat hippocampal slices to hypoxic conditions for 15 min produced a rapid, profound, but completely reversible depression of evoked synaptic potentials. The specific A1 adenosine receptor antagonist 8-cyclopentyltheophylline (8-CPT) significantly reduced hypoxia-induced synaptic depression in a concentration-dependent manner. It is concluded that adenosine, which is neuroprotective when exogenously applied during severe hypoxia because of its ability to depress synaptic transmission, may have an important and exploitable endogenous role in the protection of sensitive neurons.

Action Potentials↗
PubMed1993

Bilateral inhibition by glycinergic afferents in the medial superior olive.

1. Coincidence-detection of excitatory synaptic potentials has long been considered to be the mechanism by which medial superior olivary (MSO) neurons compute interaural time differences. Here we demonstrate the contribution of synaptic inhibition in this circuit using a gerbil brain slice preparation. 2. Nearly all cells exhibited excitatory postsynaptic potentials (EPSPs) and action potentials (APs) after stimulation of either the ipsilateral or contralateral afferent pathway. In 44% of cells, the latency of APs depended on stimulus amplitude, exhibiting shifts of 0.25-2 ms. 3. Nearly all neurons (89%) exhibited stimulus-evoked synaptic inhibition. The inhibitory effects were enhanced at greater stimulus amplitudes and were usually able to block synaptically evoked APs. In addition, APs and EPSPs were reversibly blocked by delivering the inhibitory transmitter glycine in almost all tested cells (91%). 4. In the presence of the glycine antagonist strychnine, the effects of synaptic inhibition were suppressed. 5. The stimulus level-dependent inhibitory potentials influenced the probability that an MSO neuron would fire an AP, as well as the precise timing. Therefore, the present results have implications for the processing of interaural time differences by the MSO and at higher auditory centers.

Animals↗
PubMed2003

Sensory deprivation changes the pattern of synaptic connectivity in rat barrel cortex.

We examined whether sensory deprivation during formation of the cortical circuitry influences the pattern of intracortical single-cell connections in rat barrel cortex. Excitatory postsynaptic potentials from layer 5 pyramidal neurons were recorded in vitro using patch-clamp techniques. In order to evoke such postsynaptic potentials presumptive presynaptic neurons were stimulated by photolytically applied glutamate thus generating action potentials. Synaptic connections between the stimulated and the recorded neuron were identified by the occurrence of postsynaptic potentials following photostimulation. Sensory deprivation altered the projections from layer 2/3 neurons to layer 5 pyramidal cells (L2/3-->L5 projections). In slices of non-deprived rats the input probability of L2/3-->L5 projections showed a periodic pattern with more synaptic connections originating from the borders of the barrel columns, and less synaptic connections originating from the centres. After whisker clipping this periodic pattern disappeared completely and the input probability declined monotonically with increasing distance between stimulated and recorded neuron. These results indicate that sensory input is a prerequisite to establish a synaptic projection pattern which is correlated to the columnar organisation of the anatomical barrel structure.

Animals↗
PubMed1973

Acquisition and retention of long-term habituation in Aplysia: correlation of behavioral and cellular processes.

To examine the cellular mechanisms responsible for transition from a short-term to a long-term behavioral modification, a rapid training procedure was developed for producing long-term habituation of the defensive withdrawal of gill and siphon in Aplysia. Four ten-trial training sessions, with 1(1/2)-hour intersession intervals, produced habituation that was retained for more than 1 week. This 5-hour procedure could be applied to a test system in the isolated abdominal ganglion where the cellular changes accompanying the acquisition of long-term habituation can be examined. During acquisition, intracellular recordings were obtained from L7, a major gill and siphon motor neuron, and the pattern of stimulation used in the behavioral experiments was applied to an afferent nerve. Acquisition was associated with a progressive decrease in the complex excitatory synaptic potential produced in L7 by afferent nerve stimulation. When retention was tested 24 hours later, the synaptic decrement was still evident. Thus, a behaviorally meaningful stimulus sequence, consisting of only 40 patterned stimuli, leads to changes in synaptic effectiveness lasting one or more days in a neural pathway involved in short-term habituation of this reflex.

Action Potentials↗
PubMed1998

Pharmacological modulation of GABA(A) receptor-mediated postsynaptic potentials in the CA1 region of the rat hippocampus.

It is unclear whether GABA(A) receptor-mediated hyperpolarizing and depolarizing synaptic potentials (IPSP(A)s and DPSP(A)s, respectively) are evoked by (a) the same populations of GABAergic interneurones and (b) exhibit similar regulation by allosteric modulators of GABA(A) receptor function. We have attempted to address these questions by investigating the effects of (a) known agonists for presynaptic receptors on GABAergic terminals, and (b) a range of GABA(A) receptor ligands, on each response. The GABA uptake inhibitor NNC 05-711 (10 microM) enhanced whereas bicuculline (10 microM) inhibited both IPSP(A)s and DPSP(A)s. (-)-Baclofen (5 microM), [D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin (DAGO; 0.5 microM), and carbachol (10 microM) caused substantial depressions (up to 99%) of DPSP(A)s that were reversed by CGP 55845A (1 microM), naloxone (10 microM) and atropine (5 microM), respectively. In contrast, 2-chloroadenosine (CADO; 10 microM) only slightly depressed DPSP(A)s. Quantitatively, the effect of each agonist was similar to that reported for IPSP(A)s. The neurosteroid ORG 21465 (1 - 10 microM), the anaesthetic propofol (50-500 microM), the barbiturate pentobarbitone (100-300 microM) and zinc (50 microM) all enhanced DPSP(A)s and IPSP(A)s. The benzodiazepine (BZ) agonist flunitrazepam (10-50 microM) and inverse agonist DMCM (1 microM) caused a respective enhancement and inhibition of both IPSP(A)s and DPSP(A)s. The BZomega1 site agonist zolpidem (10-30 microM) produced similar effects to flunitrazepam. The anticonvulsant loreclezole (1-100 microM) did not affect either response. These data demonstrate that similar populations of inhibitory interneurones can generate both IPSP(A)s and DPSP(A)s by activating GABA(A) receptors that are subject to similar allosteric modulation.

Animals↗
PubMed2005

Maturation of escape circuit function during the early adulthood of cockroaches Periplaneta americana.

During postembryonic development of insects, sensorimotor pathways, which generate specific behaviors, undergo maturational changes. It is less clear whether such pathways are typically stable, or undergo further maturation, during the adult stage. In the present study, we have examined this issue by multilevel analysis of a simple model system, the escape behavior of the cockroach, from identified synapses to behavior. We show that the escape system is highly responsive immediately after the molt to adulthood, but that the latency of escape responses was not at its typical value immediately after the molt to adult. The latency of escape behavior increased over the first 30 days of adult life, perhaps indicating maturational adjustments of the escape sensorimotor pathway. The first station in the escape circuitry is the synaptic connections between the cercal wind receptors and the giant interneurons. We measured unitary excitatory synaptic potentials between single sensory neurons and an identified giant interneuron (GI(2)). We found a decrease in the synaptic strength between identified cercal hairs from a single column and GI(2) over the first month after the adult molt. Consequently, the latency and the number of action potentials of GI(2) in response to natural stimuli increased and decreased respectively during this time. Thus, we show that both behavioral performance and the wind sensitivity of GI(2) decreased over the first month after molt. We conclude that the cockroach escape system undergoes further sensorimotor maturation over a period of 1 month, and that cellular changes correlate with, or predict, some changes in behavioral performance.

Action Potentials↗
PubMed2005

Synaptic contacts between an identified type of ON cone bipolar cell and ganglion cells in the mouse retina.

We surveyed the potential contacts between an identified type of bipolar cell and retinal ganglion cells in the mouse. By crossing two existing mouse strains (line 357 and line GFP-M), we created a double transgenic strain in which GFP is expressed by all members of a single type of ON cone bipolar cell and a sparse, mixed population of retinal ganglion cells. The GFP-expressing bipolar cells appear to be those termed CB4a of Pignatelli & Strettoi [(2004) J. Comp. Neurol., 476, 254-266] and type 7 of Ghosh et al. [(2004) J. Comp. Neurol., 469, 70-82 and J. Comp. Neurol., 476, 202-203]. The labelled ganglion cells include examples of most or all types of ganglion cells present in the mouse. By studying the juxtaposition of their processes in three dimensions, we could learn which ganglion cell types are potential synaptic targets of the line 357 bipolar cell. Of 12 ganglion cell types observed, 10 types could be definitively ruled out as major synaptic targets of the line 357 bipolar cells. One type of monostratified ganglion cell and one bistratified cell tightly cofasciculate with axon terminals of the line 357 bipolar cells. Double labelling for kinesin II demonstrates colocalization of bipolar cell ribbons at the sites of contact between these two types of ganglion cell and the line 357 bipolar cells.

Animals↗
PubMed1981

Effects of efferent stimulation on the saccule of goldfish.

1. The effect of single or repetitive stimulation applied to efferent nerve fibres on afferent nerve activity and microphonic potentials was studied in the saccule of goldfish. 2. The sound-evoked excitatory post-synaptic potentials (e.p.s.p.s) recorded intracellularly from afferent eighth nerve fibres were reduced in size or completely abolished by efferent stimulation. The maximum inhibitory effect produced by repetitive efferent stimulation was equivalent to reducing the sound intensity by 10-25 db. Spontaneous miniature e.p.s.p.s were also suppressed by efferent stimulation. 3. The effect of single efferent stimulation appeared with a delay of 607 msec and lasted for about 40 msec, reaching its peak at about 12 msec. The slow and prolonged time course makes a sharp contrast with the very fast time course of afferent synaptic action. 4. The application of hyperpolarizing current through the recording micro-electrode revealed no sign of a post-synaptic increase in membrane conductance during inhibition. Hence, the inhibition was mostly attributable to a presynaptic action, i.e. to a suppression of transmitter release from hair cells. 5. Individual e.p.s.p.s were evoked in response to each wave of sound without any change in latency, but reached their peak much earlier during inhibition than in the control period. A likely explanation for this finding is that transmitter is released from hair cells during inhibition only in the early part of the stimulatory phase of the sound wave. 6. The extracellularly recorded microphonic potentials showed a slight increase in amplitude during efferent stimulation. 7. The nature and site of action of efferent nerve action are discussed along with some drug effects.

Action Potentials↗
PubMed1982

The actions of 3,4-diaminopyridine in bullfrog sympathetic ganglia.

The effects of 3,4-diaminopyridine (3,4-DAP) on isolated sympathetic ganglia were studied by means of intracellular and extracellular recording techniques. 3,4-DAP in micromolar concentrations caused a single orthodromic stimulus to generate a brief burst of repetitive postganglionic discharges. Such stimulus-bound repetition (SBR) appeared to represent a presynaptic action of 3,4-DAP, as no repetitive firing could be evoked by antidromic or direct stimulation of ganglion cells. 3,4-DAP also increased the latency to the onset of the synaptic potential at concentrations paralleling those responsible for SBR. The actions of 3,4-DAP on synaptic transmission extended over a 10,000-fold concentration range, beginning with synaptic facilitation at micromolar concentrations (1-500 microM), and proceeding to depressant effects at millimolar concentrations (0.5-10 mM). The postganglionic repetitive discharges (SBR) induced by 3,4-DAP could be selectively suppressed by D-tubocurarine (D-Tc) or tetraethylammonium (TEA), at concentrations of these antagonists below those required to block transmission. 3,4-DAP had significant anti-curare effects, producing a four-fold shift of the D-Tc concentration-effect curve for transmission block. In contrast, 3,4-DAP neither antagonized nor enhanced the transmission block produced by TEA. These results are incompatible with traditional concepts of ganglionic blockade by D-Tc and TEA, and suggest the possibility of presynaptic sites of action in ganglion block.

4-Aminopyridine↗
PubMed1983

Functional elimination of afferent pathways and decreased safety factor during postembryonic development of cockroach giant interneurons.

The giant interneurons (GIN) from the cockroach CNS undergo two major physiological changes during the postembryonic developmental period: (A) a marked decrease in the number of afferent pathways innervating the GIN at the metathoracic ganglion (Ts); and (B) a gradual decrease in the safety factor for impulse propagation along the intraganglionic segment in T3. In 100% of the experiments (n greater than 100) performed on GIN from early developmental stages, spontaneous postsynaptic potentials (SPSPs) were recorded; in adults, on the other hand. SPSPs have been recorded in only 34% of the experiments (n = 74). Evoked synaptic potentials can be elicited in nymphal stages by stimulation of 8 nerves of T3, the contralateral connectives, ipsi- and contralateral nerve roots 2, 3, 5, and by stimulation of adjacent GINs. In adult, PSPs can be evoked by stimulation of adjacent GINs, and contralateral thoracic connectives, but not from nerves 2, 3 and 5. The functional disappearance of synaptic inputs to the GINs does not reflect a general phenomenon of reduction in synaptic transmission efficacy. In previous studies it was demonstrated that high frequency stimulation of adult GIN leads to blockage of impulse propagation in T3. In nymphal stages, the safety factor for propagation of impulses along T3 is higher. The reduction in safety factor appears gradually during the postembryonic developmental period. From analysis of the mechanisms underlying the elimination of functional afferent pathways and the appearance of low safety factor (see consecutive paper by Yarom and Spira) it is concluded that the functional elimination of afferents is a consequence of decreased transmission efficacy, while the appearance of low safety regions for impulse propagation is a consequence of morphological changes of the GIN segment within ganglion T3.

Afferent Pathways↗
PubMedDate not supplied

Atropine inhibits associative potentiation in the hippocampus.

The effects of the muscarinic receptor blocker atropine on associative long-term potentiation were studied in the CA1 region of the rat hippocampus. Focal excitatory post-synaptic potentials (EPSP) were recorded in living slices. Local application of atropine (0.1 mM) significantly inhibited associative long-term potentiation (40-60 min after tetanization) in the "weak" input (str. radiatum 128 +/- 10% compared with 168 +/- 9% in controls). Long-term potentiation at the "strong" input (str. oriens) was increased relative to the control (from 137 +/- 13% to 158 +/- 4%). These results indicate that endogenous acetylcholine aids the development of long-term potentiation in synapses with low levels of activation.

Animals↗
PubMed1994

Interaction between adenosine and GABAA receptors on hippocampal neurones.

Extracellular recordings were made from the CA1 pyramidal cell layer of hippocampal slices in response to stimulation of Schaffer collateral fibres in stratum radiatum. Adenosine and muscimol induced concentration-dependent reductions in the amplitude of orthodromically induced population potentials. In order to eliminate effects of these agents on potassium channels, experiments were performed in the presence of barium, 1 mM. This concentration increased potential size, and reduced the inhibitory effect of adenosine on population spike size, but not synaptic potential size. This profile is consistent with the blockade of potassium channels associated only with the postsynaptic effects of adenosine. Muscimol responses were unaffected. Adenosine potentiated the ability of muscimol to inhibit evoked potentials in the absence or presence of barium. The potentiation was prevented by the A1 selective antagonist 8-cyclopentyltheophylline. The effects of adenosine as well as muscimol were reduced by the chloride channel blockers DIDS, which also prevented the adenosine potentiation of muscimol. The results indicate the ability of adenosine to operate chloride channels in hippocampal neurones, and suggest a potentiative interaction between adenosine and muscimol which may also involve chloride channels.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1996

Hypoxia triggers neuroprotective alterations in hippocampal gene expression via a heme-containing sensor.

Sublethal ischemia or hypoxia triggers adaptive changes that protect the brain against future hypoxic/ischemic damage. Preexposure of in vitro hippocampal slices to brief periods of hypoxia increases the resistance of Schaffer collateral-CA1 synaptic potentials to further, longer periods of hypoxia that would otherwise cause an irreversible loss of synaptic transmission. Since hypoxia has been shown to cause alterations in the patterns of protein synthesis, we hypothesized that newly-expressed proteins might mediate hypoxia-induced neuroprotection. We report here that the induction of neuroprotection by hypoxic preconditioning in rat hippocampal slices is blocked by either cycloheximide, a protein synthesis inhibitor, or by Actinomycin D, an inhibitor of RNA synthesis. In contrast, pharmacological blockade of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) and N-methyl-D-aspartate (NMDA) subtypes of glutamate receptors did not prevent the induction of neuroprotection by hypoxia. Carbon monoxide (CO), which can lock heme moieties in their oxygenated configurations, did prevent hypoxia from inducing neuroprotection. We conclude that hypoxia activates protective mechanisms via deoxygenation of a heme moiety, triggering expression of gene products which protect synaptic function from subsequent hypoxic damage.

Adaptation, Physiological↗
PubMed1989

Histamine H2 receptor mediates postsynaptic excitation and presynaptic inhibition in submucous plexus neurons of the guinea-pig.

Intracellular recordings were made from submucous plexus neurons of the guinea-pig cecum maintained in vitro. Histamine (0.3-10 microM) produced a dose-dependent membrane depolarization (congruent to 13 mV with 3 microM) in about 28% of the cells tested; most of these cells showed a prominent calcium-activated potassium conductance (AH cells). The depolarization was due primarily to an inactivation of potassium conductance which is available at the resting membrane potential of -60 mV. Peak amplitude of the fast excitatory postsynaptic potential was depressed by histamine (0.1-10 microM) in a dose-dependent manner (congruent to 62% depression with 1 microM). This was observed even in those cells in which histamine did not produce any membrane depolarizations (mostly S cells). The depression of the fast excitatory postsynaptic potential resulted from the presynaptic inhibition of acetylcholine release. Histamine also reduced the amplitude of the non-cholinergic, presumably peptidergic, slow excitatory postsynaptic potential by suppressing peptide release from presynaptic nerve terminals. Peak amplitude of the adrenergic inhibitory synaptic potential was not depressed by histamine suggesting that histamine receptors are not present on presynaptic terminals of sympathetic nerve fibres. Both postsynaptic and presynaptic actions of histamine were blocked by cimetidine or ranitidine but not by pyrilamine implying that H2 receptors are involved.

Action Potentials↗
PubMed1969

Microelectrode studies in the frog isolated spinal cord during depression by general anaesthetic agents.

1. Extracellular and intracellular potentials have been recorded from the isolated spinal cord of the frog during depression of synaptic transmission by volatile and barbiturate general anaesthetic agents.2. Volatile agents did not impair conduction in presynaptic terminals in concentrations which completely blocked synaptic transmission.3. Methohexitone consistently impaired conduction in presynaptic terminals long before transmission through polysynaptic pathways was blocked.4. Volatile agents depressed the excitability of the motoneurone membrane, as evidenced by impaired antidromic invasion, reduced excitability to direct stimulation, depression of the synaptic potential and elevation of firing threshold. It is concluded that these actions are responsible for the depressant effect of volatile agents on spinal reflexes.5. Methohexitone produced an increase in the excitability of the motoneurone membrane, as evidenced by enhanced antidromic invasion, increased excitability to direct stimulation and potentiation of short latency responses. Despite this excitatory action, the polysynaptic pathways through the cord were depressed by an action of the drug on conduction in presynaptic terminals.6. It is suggested that the sensitivity of the motoneurone membrane to volatile agents may contribute to the good muscle relaxant properties of these drugs in clinical use.

Anesthetics↗