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PubMed1993

A comparison of rat hippocampal mossy cells and CA3c pyramidal cells.

1. There is a long-standing debate about whether the large spiny cells in the hilar region of the hippocampus should be classified as pyramidal cells of Ammon's horn or as a distinct cell type of the dentate gyrus. The rationale for grouping these hilar neurons (termed "mossy cells") with pyramidal cells of Ammon's horn is shared characteristics. In the present study we have compared the morphological and physiological characteristics of mossy cells and nearby CA3c pyramidal cells with the use of a rat hippocampal slice preparation. 2. Biocytin-labeled neurons were examined on the basis of soma area, location, shape, number of primary dendrites, extent of dendritic spines, dendritic location, and axon trajectories. Mossy cells had larger soma areas than CA3c pyramidal cells, and they had more large complex spines (thorny excrescences) on their proximal dendrites and somata than CA3c pyramidal cells. Mossy cell dendritic trees and axon collaterals ramified in different regions of the hippocampus than dendrites and axons of CA3c pyramidal cells. 3. Intrinsic physiological properties, and spontaneous and evoked synaptic properties, were measured and compared. Mossy cells had significantly higher input resistances, smaller amplitude burst afterhyperpolarizations, smaller amplitude action potentials, less spike-frequency adaptation, and more anomalous rectification than CA3c pyramidal cells. 4. Mossy cells had spontaneous excitatory postsynaptic potentials (EPSPs) that were significantly higher in frequency and larger in amplitude than CA3c pyramidal cells. A larger proportion of mossy cells than CA3c pyramidal cells responded to perforant path stimulation with depolarizing postsynaptic potentials without any apparent hyperpolarization. Conversely, a smaller proportion of mossy cells than CA3c pyramidal cells responded to perforant path stimulation with inhibitory postsynaptic potentials (IPSPs), and spontaneous IPSPs were more difficult to detect in mossy cells. 5. The intrinsic physiological properties of mossy cells endow these cells with potent excitatory mechanisms but relatively fewer inhibitory control processes than CA3c pyramidal cells. Recordings of spontaneous and evoked PSPs suggest that mossy cells receive more excitatory input and less inhibitory input than CA3c pyramidal cells. These intrinsic and synaptic properties of mossy cells may explain this cell type's exceptional vulnerability to excitotoxic damage by intense afferent stimulation. 6. In summary, mossy cells were significantly different from CA3c pyramidal cells in many of their morphological, intrinsic physiological, and synaptic properties.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1992

Whole cell recordings from respiratory neurons in the medulla of brainstem-spinal cord preparations isolated from newborn rats.

In brainstem-spinal cord preparations isolated from newborn rats, a whole cell recording technique was applied to record membrane potentials of inspiratory (Insp) and pre-inspiratory (Pre-I) neurons in the ventrolateral medulla. Labelling of these respiratory neurons with Lucifer Yellow allowed analysis of their locations and morphology. Intracellular membrane potentials from 25 Insp neurons were recorded. Average resting membrane potential was -49 mV (n = 25) and input resistance was 306 M omega. Insp neurons were classified into three types from the patterns of synaptic potentials. Type I neurons (n = 11) had a high probability of excitatory postsynaptic potentials (EPSPs) in the pre- and post-inspiratory phases. Type II neurons (n = 7) showed abrupt transition to the burst phase from the resting potential level without increased EPSPs in the preinspiratory phase. Type III neurons (n = 7) were hyperpolarized by inhibitory postsynaptic potentials (IPSPs) in the pre- and post-inspiratory phases. These Insp neurons, located in the ventrolateral medulla 80-490 microns from the ventral surface, were 10-30 microns in diameter, and had various soma shapes (pyramidal, spherical or fusiform). Intracellular membrane potentials from 24 Pre-I neurons were recorded. The average resting membrane potential was -45 mV (n = 24), and the input resistance was 320 M omega. Typical Pre-I neurons showed fairly great depolarization accompanied by action potentials during their burst phase and repolarization during the inspiratory phase. Most Pre-I neurons appeared to have a high level of synaptic activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

A reflex behavior mediated by monosynaptic connections between hair afferents and motoneurons in the larval tobacco hornworm, Manduca sexta.

In the tobacco hornworm caterpillar, tactile stimulation of sensory hairs located on the tip of a proleg (the planta) evokes ipsilateral or bilateral retraction of the prolegs in that segment. We have used electrophysiological and anatomical methods to investigate the excitatory neural pathways linking the planta hair afferents and the proleg retractor motoneurons (MNs). An important technical innovation was the development of an isolated proleg and desheathed ganglion preparation that permits rapid and reversible ionic manipulations and drug applications. Action potentials (spikes) in individual planta hair afferents produce time-locked excitatory postsynaptic potentials (EPSPs) in ipsilateral proleg MNs which appear to be chemically-mediated and monosynaptic: the EPSPs have a short and constant latency, they follow afferent spikes without failure, they are reversibly abolished in elevated Mg++ saline, and they persist in saline with elevated Mg++ and Ca++ levels. Planta hair afferents also excite ipsilateral MNs by polysynaptic pathways, and their excitation of contralateral proleg MNs is exclusively polysynaptic. Cobalt-staining of the proleg MNs and planta hair afferents shows that the afferents terminate in ventral neuropil, and the proleg MNs have an unusual ventral projection into this region. The ventral projection is on the ipsilateral side, which is consistent with the electrophysiological finding that time-locked EPSPs are found only from ipsilateral hairs. Two factors that contribute to the strong monosynaptic excitation of proleg MNs by ipsilateral planta hairs are the convergence of many hair afferents onto each MN, and the facilitation shown at each afferent-MN synapse. At least 6 afferents converge on each MN, and at short interspike intervals the afferent-evoked EPSPs are enhanced by as much as 400% by homosynaptic facilitation. The EPSP is abolished reversibly by the cholinergic antagonists curare and atropine, suggesting that the neurotransmitter at the synapse is acetylcholine (ACh). This is of particular interest because the ACh receptors of tobacco-feeding Manduca larvae are reported to be less nicotine-sensitive than those of other insects.

Acetylcholine↗

PubMed1991

Delta opioid receptor activation is required to induce LTP of synaptic transmission in the lateral perforant path in vivo.

The role of opioid receptors in long-term potentiation (LTP) of the medial (MPP) and lateral (LPP) divisions of the perforant path-granule cell projection was investigated in urethane anesthetized rats. A stimulating electrode was positioned in the dorsomedial or ventrolateral aspect of the angular bundle for selective activation of the MPP and LPP, respectively. A push-pull cannula served to focally perfuse artificial cerebrospinal fluid (ACSF) across the perforant path terminal zone, while perforant path evoked potentials were monitored in the dentate hilus. Robust LTP of the excitatory postsynaptic potential (EPSP) initial slope and population spike height was induced by high frequency stimulation (400 Hz, 8 bursts of 8 pulses) applied to the medial or lateral perforant path in rats perfused with standard medium. In the lateral perforant path, a putative proenkephalin system, LTP of the EPSP and population spike was blocked when ACSF containing 100 microM of the opioid receptor antagonist naloxone was present during the tetanus, while perfusion with 0.1 microM naloxone prevented EPSP potentiation but only reduced the magnitude of the population spike increase. Naloxone had no effect on LTP induction in the MPP. Importantly, 0.1 microM ICI 174,864, a selective antagonist of delta opioid receptors, blocked LTP of synaptic transmission in the LPP while leaving the population spike increase intact. The results indicate that LTP of synaptic transmission in the LPP requires activation of delta opioid receptors, while 'non-delta' opioid receptors may be involved in augmenting granule cell output. This opioid receptor-dependent LTP illustrates peptidergic regulation of synaptic plasticity in the hippocampus.

Animals↗

PubMed1994

The role of tetrodotoxin-resistant sodium channels of small primary afferent fibers.

Intracellular recordings from neurons in the dorsal root ganglion (DRG) and dorsal horn (DH), in an in vitro spinal cord-dorsal root ganglion preparation, were used to investigate the role of tetrodotoxin-resistant (TTX-R) afferent fibers in the sensory synaptic transmission in the superficial DH. Bath application of 25-50 mM potassium to the DRG depolarized the DRG neurons, blocked action potentials in the large neurons, evoked action potentials in slow conducting neurons, and synaptically excited dorsal horn neurons. Excitatory postsynaptic potentials (EPSP) which were evoked in DH neurons by electrical stimulation of large myelinated fibers, but not those evoked by stimulation of small unmyelinated fibers, were blocked by the potassium treatment of the primary afferents. Tetrodotoxin, when applied to the sensory neurons, abolished the action potentials in fast fibers but had no effect on the action potentials in a population of slow conducting afferents. Peripheral application of TTX blocked the fast EPSPs evoked by electrical stimulation but failed to block the electrically evoked slow EPSPs and the synaptic activation of DH neurons induced by the application of high potassium to sensory neurons. Furthermore, high potassium potentiated electrically evoked, TTX-resistant EPSPs in the majority of neurons. This effect was abolished in Na(+)-free solution. These findings indicate that high [K+]e applied to the DRG, dorsal root and peripheral process selectively activates a primary afferent input to the DH, which is sodium-dependent and tetrodotoxin resistant.

Animals↗

PubMed1988

Orotate improves memory and enhances synaptic long-term potentiation in active avoidance behaviour in rats with perforant path stimulation as the conditioned stimulus.

Male Wistar rats were trained in an active avoidance task with stimulation of the perforant path with impulse trains of 15 Hz as the conditioning stimulus. Immediately after the first training session, methylglucamine orotate (225 micrograms), a memory improving drug, was injected intraventricularly. The retention of the learned behaviour was determined on the following day in a relearning session. Field potentials evoked in the dentate area by test stimuli from the perforant path electrode were recorded at different times after learning and relearning sessions to determine whether there were functional changes in the perforant path-granular cell synapses, which are involved in the conditioning pathway. Untreated control animals exhibited a so-called 'postconditioning potentiation', expressed as a long-lasting increase of both the excitatory postsynaptic potential (EPSP) and the population spike of the granular cells of the evoked test potentials. This finding reproduces previously published results. Methylglucamine orotate-treated rats showed significantly more conditioned reactions in the relearning sessions compared with untreated controls and a significantly more pronounced potentiation of the population spike, whereas the postconditioning potentiation of the field EPSP remained unaffected by the treatment. When both the control animals and the methylglucamine orotate-treated rats were divided into subgroups of good and poor learners according to their learning scores from the first training session, differences between the effect of the drug became evident. In good learners, the treatment with methylglucamine orotate after the learning session slightly, but significantly, improved retention compared with that of untreated good learners.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Inhibitory effect of YM060 on 5-HT3 receptor-mediated depolarization in colonic myenteric neurons of the guinea pig.

We used conventional intracellular recording methods to examine the effects of YM060 [(-)-(R)-5-[(1-methyl-1H-indol-3-yl)carbonyl]-4,5,6,7- tetrahydro-1H-benzimidazole monohydrochloride), a novel 5-HT3 receptor antagonist, on 5-hydroxytryptamine (5-HT, serotonin)-evoked fast membrane depolarization in myenteric neurons of the guinea pig distal colon, and compared its potency to that of other 5-HT3 receptor antagonists. Microapplication of 5-HT from fine-tipped pipettes evoked both fast and slowly activating depolarizing responses in 78% and 40% of colonic myenteric neurons, respectively. The selective 5-HT3 receptor agonist 2-methyl-5-HT applied with short pressure pulses (100-300 ms) mimicked the fast but not the slow response. The 5-HT3 receptor antagonists YM060, granisetron and ondansetron suppressed the 5-HT-evoked fast response in 98% of colonic myenteric neurons in a concentration-dependent manner with pIC50 values of 8.62, 7.77 and 6.90, respectively. Methysergide and GR113808 did not affect the fast responses at concentrations sufficient to block 5-HT1, 5-HT2 and 5-HT4 receptors, respectively. YM060 did not affect the slowly activating response to 5-HT or any other electrophysiological parameter of the neurons including resting membrane potential, input resistance and the amplitude of action potentials evoked by injection of depolarizing current. Stimulus-evoked fast excitatory postsynaptic potentials were unchanged by YM060 at concentrations up to 10(-8) M, excluding any possible local anesthetic or anticholinergic effects of YM060. The results confirm that the fast component of the two depolarizing responses to 5-HT in colonic myenteric neurons is mediated by 5-HT3 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

LTP in hippocampal CA1 of urethane-narcotized rats requires stronger tetanization parameters.

Rats with chronically implanted electrodes in the hippocampal CA1 region were tested in their capacity to express and maintain long-term potentiation (LTP) of the population spike (PS) or of the field excitatory postsynaptic potential (fEPSP). Two different states were compared: a) freely moving animals; b) urethane-anesthetized animals (1 g/kg, IP). We found that a short, high-frequency tetanus (six bursts of 15 pulses; 200 Hz; double-pulse width; interburst interval 10 s) increased PS amplitudes and fEPSP slopes up to 300% in response to test stimuli in double-pulse width; interburst interval 10 s) increased PS amplitudes and fEPSP slopes up to 300% in response to test stimuli in the awake rat. The PS amplitude slowly decreased in time, returning to baseline levels 4 h post-tetanically, whereas the fEPSP slope remained at higher values for 24 h. Urethane injection reduced the fEPSP slope and abolished the PS to normal test pulses. We thus increased the strength of the test stimuli until we again recorded magnitudes of PSs and fEPSPs comparable to those in the awake animal. In conjunction with these stronger stimuli, tetanus-induced LTP was elicited that for the PS was increased in magnitude and prolonged in duration compared to the untreated control group. Although, stronger tetanic stimuli were applied to the narcotized fEPSP group too, no difference was found compared to controls. These results suggest that urethane narcosis influences the sensitivity of CA1 neurons to express LTP. Stronger stimulation was required to induce and maintain a long-lasting potentiation of the fEPSP slope and PS amplitude.

Animals↗

PubMed1993

Chronic effects of trimipramine, an antidepressant, on hippocampal synaptic plasticity.

The effects of trimipramine (TRIM), an antidepressant agent, on both the induction and the maintenance of long-term potentiation (LTP) was investigated in area CA1 of hippocampal slice preparations. Chronic administration (7-9 days) of TRIM in rat caused a large reduction in the magnitude of LTP induced by a theta burst stimulation (TBS) paradigm. Results indicate that the reduction of LTP produced by trimipramine does not seem to result from major changes in the physiological properties of the slice preparations. First, paired-pulse facilitation was not impaired following the drug administration suggesting that transmitter release was not modified in TRIM-treated slices. Second, the burst responses evoked by high-frequency stimulation exhibited the typical buildup of depolarization, which is due to both a reduction of IPSPs and the activation of NMDA receptors. Finally, the treatment did not change the amount of short-term potentiation induced by TBS nor did it modify the component of excitatory postsynaptic potentials (EPSPs) mediated by the activation of NMDA receptors, suggesting that the NMDA receptor functions remained intact in TRIM-treated slices. Taken together the present data suggest that the loss of LTP maintenance in TRIM-treated animals is more likely the result of the disruption by trimipramine of cellular processes that follow LTP induction. In addition, the results provide evidence for a possible correlation between the reduction in LTP expression and learning deficits produced by chronic administration of trimipramine.

Animals↗

PubMed1978

Presynaptic modulation of voltage-dependent Ca2+ current: mechanism for behavioral sensitization in Aplysia californica.

Behavioral sensitization of the gill-withdrawal reflex of Aplysia is the result of a prolonged increase in transmitter release from the presynaptic terminals of sensory neurons. Earlier work suggested that this presynaptic facilitation might be mediated by a serotonin-sensitive adenylate cyclase in the sensory neuron terminals. Here we present evidence that presynaptic facilitation results from a cyclic AMP-dependent increase in the calcium current that underlies action potentials in the sensory neurons. The action potentials of sensory neuron cell bodies have, in addition to a sodium current, a calcium current that is enhanced by blocking the opposing potassium current with tetraethylammonium. Under these conditions, the action potentials show a slowly repolarizing plateau that follows the Nernst potential for a calcium electrode and serves as a sensitive assay for changes in calcium current. Stimulation of the pathway that mediates sensitization, incubation with serotonin or phosphodiesterase inhibitors, or intracellular injection of cyclic AMP produces an increase in the calcium plateau in the presence of tetraethylammonium. In addition, both before and after sensitizing stimulation, the duration of the plateau potential parallels transmitter release as measured by the amplitude of monosynaptic excitatory postsynaptic potentials evoked in the motor neurons by intracellular stimulation of single sensory neurons. These results are consistent with the idea that presynaptic facilitation is caused by a cyclic AMP-mediated increase in a voltage-sensitive calcium current in sensory neuron presynaptic terminals. This synaptic action is novel in that it can produce little or no change in the resting potential, is of long duration, and exerts its influence directly on a conductance triggered by the action potential, rather than on non-voltage-sensitive conductances, as is typical of conventional synaptic actions.

Action Potentials↗

PubMed1991

The effects of trans-ACPD on long-term potentiation in the rat hippocampal slice.

Trans-ACPD, a metabotropic glutamate receptor agonist, enhanced both the short-term potentiation (STP) at 1 and 5 min, and long-term potentiation (LTP) at 20 min, following tetanic stimulation, of the population, excitatory postsynaptic potential (epsp) recorded from CA1 of the rat hippocampal slice. The enhancement of both STP and LTP also occurred in the presence of the protein kinase inhibitor sphingosine, indicating that the enhancement is most likely to occur through the inositol phosphate rather than the protein kinase limb following receptor activation and phosphoinositide hydrolysis. LTP of the low frequency population epsp was not induced by t-ACPD, even at 100 microM. The metabotropic glutamate receptor may have an important role in LTP induction or modulation.

Animals↗

PubMed1997

mGluR II agonist inhibition of LTP induction, and mGluR II antagonist inhibition of LTD induction, in the dentate gyrus in vitro.

The effects of the metabotropic glutamate receptor (mGluR) group II agonist (2S,1'R,2'R,3'R)-2-(2',3'-dicarboxycyclopropyl)glycine (DCG-IV) and the antagonist 2S,1S',2S'-2-methyl-2-(2'-carboxycyclopropyl)glycine (MCCG) on the induction of long-term potentiation (LTP) and long-term depression (LTD) of the field excitatory postsynaptic potential (epsp) in the dentate gyrus of the rat hippocampus were investigated in vitro. In control media, high frequency stimulation (HFS) consisting of a series of trains of stimuli at 200 Hz induced LTP, and low frequency stimulation (LFS) consisting of 900 stimuli at 1 Hz induced LTD. DCG-IV (50 nM) strongly inhibited the induction of LTP. The block of LTP induction was not caused by a frequency-dependent inhibition of the epsp during HFS, as the epsps evoked during HFS were not altered by DCG-IV. MCCG (500 microM) did not inhibit the induction of LTP, but did prevent the block of LTP by DCG-IV. MCCG (500 microM) strongly inhibited the induction of LTD. DCG-IV (50 nM) did not inhibit LTD induction.

Amino Acids, Dicarboxylic↗

PubMed1991

Long-term Potentiation of NMDA Receptor-mediated EPSP in Guinea-pig Hippocampal Slices.

Hippocampal slices from guinea-pigs were used to examine the long-term potentiation (LTP) of the N-methyl-d-aspartate (NMDA)-mediated excitatory postsynaptic potential (EPSP). Intracellular recordings were performed from CA1 pyramidal neurons in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 5 - 10 microM) and picrotoxin (50 microM). In these experimental conditions test stimuli applied at low frequency (0.1 Hz) to the Schaffer collateral - commissural pathway evoked a prolonged EPSP (150 - 200 ms). To obtain this CNQX-resistant EPSP, stimulus intensities had to be raised above the level required to evoke an EPSP of comparable amplitude in physiological solution. Tetanic stimulation (two trains of 100 Hz, 1 s every 20 s) led to a potentiation of the CNQX-resistant EPSP, and this potentiated response was abolished with d-(-)-2-amino-5-phosphonovaleric acid (50 microM). The potentiation of the NMDA receptor-mediated EPSP was more pronounced for strong than for weak test stimuli, and was suppressed when test EPSPs were evoked during membrane hyperpolarization. These results suggest that NMDA receptor-mediated responses can undergo LTP, and hence can contribute to the maintenance of LTP.

Journal Article↗

PubMed1993

Synaptic plasticity in an in vitro slice preparation of the rat nucleus accumbens.

Extra- and intracellular recordings in slices were used to examine what types of synaptic plasticity can be found in the core of the nucleus accumbens, and how these forms of plasticity may be modulated by dopamine. Stimulus electrodes were placed at the rostral border of the nucleus accumbens in order to excite primarily infralimbic and prelimbic afferents, as was confirmed by injections of the retrograde tracer fluoro-gold. In extracellular recordings, tetanization induced long-term potentiation (LTP) of the population spike in 20 out of 53 slices. The presynaptic compound action potential did not change following LTP induction. For the intracellularly recorded excitatory postsynaptic potentiation, three types of synaptic plasticity were noted: long-term potentiation (16 out of 54 cells), decremental potentiation (eight cells) and long-term depression (LTD; six cells). No correlation was found between the occurrence of potentiation or depression and various parameters of the tetanic depolarization (e.g. peak voltage, integral under the curve). The N-methyl-D-aspartate receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid (50 microM; D-AP5) reduced, but did not completely prevent, the induction of LTP. The incidence of LTD was not markedly affected by D-AP5. No difference in LTP was found when comparing slices bathed in dopamine (10 microM) and controls. Likewise, slices treated with a mixture of the D1 receptor antagonist Sch 23390 (1 microM) and the D2 antagonist S(-)-sulpiride (1 microM) generated a similar amount of LTP as controls. In conclusion, both LTP and LTD can be induced in a key structure of the limbic-innervated basal ganglia. LTP in the nucleus accumbens strongly depends on N-methyl-D-aspartate receptor activity, but is not significantly affected by dopamine.

2-Amino-5-phosphonovalerate↗

PubMed1987

The expression of N-methyl-D-aspartate-receptor-mediated component during epileptiform synaptic activity in hippocampus.

1 The possible involvement of N-methyl-D-aspartate (NMDA)-receptors in epileptiform synaptic activity in the kainic acid (KA) lesioned hippocampus was investigated. In this chronic model of epilepsy there is a loss of both the early and the late components of synaptic inhibition as well as changes in the membrane properties of the surviving CA1 pyramidal cells. 2 The action of the specific NMDA-receptor antagonist D-2-amino-5-phosphonovalerate (D-APV) was tested on evoked bursts of action potentials recorded intracellularly from cells of lesioned hippocampi. The effects of D-APV on control synaptic responses from the contralateral, unlesioned hippocampi were also recorded. 3 In the presence of Mg2+ (1 mM), D-APV (20 microM) had a profound effect on the evoked epileptiform activity. Both the number of action potentials in the burst, as well as the area under the excitatory postsynaptic potential (e.p.s.p.) was considerably reduced. Furthermore this D-APV-sensitive component of the epileptiform burst had a very early onset, coincident with the first action potential in the burst. 4 D-APV (20 microM) was ineffective in blocking the e.p.s.p. evoked by Schaffer collateral afferents onto CA1 cells in slices of hippocampus contralateral to the KA lesion. 5 D-APV had no effect on the passive membrane properties of either population of cells. Hyperpolarizing potentials such as the inhibitory postsynaptic potentials (i.p.s.ps) or the afterhyperpolarization following a current-induced burst of action potentials were also unaffected. 6 It appears that an NMDA-receptor component is expressed during synaptically evoked epileptiform activity in this chronic model of epilepsy.

2-Amino-5-phosphonovalerate↗

PubMed1995

Age-dependent inhibition of long-term potentiation by ethanol in immature versus mature hippocampus.

The goal of this study was to assess the effects of ethanol on the induction of long-term potentiation (LTP) in hippocampal slices from immature versus mature rats. Population excitatory postsynaptic potentials (pEPSPs) were recorded from stratum radiatum of area CA1 of hippocampal slices using electrical stimulation of the Schaffer collateral/commissural fiber pathway. The slices were prepared from rats aged 15 to 25 or from 70 to 100 days. Long-term potentiation (LTP) of the pEPSP slope was induced using a single, theta-burst stimulus train in the presence or absence of 60 mM ethanol. Under control conditions, the stimulus train induced LTP in slices from both immature and mature animals. However, the magnitude of LTP was greater in slices from immature rats. When ethanol was present during the stimulus train, the magnitude of LTP in slices from mature animals did not differ significantly from the magnitude of LTP in control slices. However, ethanol virtually blocked the induction of LTP in slices from immature animals. These results indicate that memory-related synaptic plasticity in the hippocampus is attenuated by ethanol to a greater degree in immature versus mature animals.

Age Factors↗

PubMed1981

Presynaptic inhibition of transmission from identified interneurons in locust central nervous system.

1. Intracellular recordings near the output terminals of an identified interneuron (the descending contralateral movement detector, DCMD) in the locust revealed the occurrence of depolarizing synaptic potentials. These presynaptic depolarizing potentials were evoked by spikes in both DCMDs, by auditory stimuli, and by electrical stimulation of the pro- to mesothoracic connectives. The occurrence of the depolarizing potentials decreased the amplitude of the action potentials close to the output terminals. 2. The stimuli that produced depolarizing potentials in the presynaptic terminals reduced the amplitude of the monosynaptic excitatory postsynaptic potentials evoked by the DCMDs in identified follower interneurons. We conclude that at least part of this reduction in transmission from the DCMDs results from presynaptic inhibition and that the presynaptic inhibition is related to a reduction in the amplitude of the presynaptic action potentials. 3. We propose that the function of the presynaptic inhibition of the DCMDs is to ensure that the interneurons triggering a jump are never activated by the DCMDs in the absence of proprioceptive signals from the legs indicating the animal's readiness to jump.

Action Potentials↗

PubMed1997

Bidirectional associative plasticity of unitary CA3-CA1 EPSPs in the rat hippocampus in vitro.

Associative long-term potentiation (LTP) and depression of compound and unitary CA3-CA excitatory postsynaptic potentials (EPSPs) were investigated in rat hippocampal slice cultures. The induction of LTP with synchronous pairing of synaptic activation and postsynaptic depolarization resulted in an increase in the amplitude of EPSPs to the same absolute level, regardless of whether the input was naive or had been previously depressed by asynchronous pairing of pre- and postsynaptic activity. Saturated LTP of compound and unitary EPSPs was reversed by asynchronous pairing and could be reinduced by synchronous pairing. The likelihood that an action potential in a presynaptic CA3 cell failed to trigger an unitary EPSP in a postsynaptic CA1 cell decreased after induction of associative potentiation and increased after induction of associative depotentiation. These changes in the rate of transmission failures were accompanied by large changes in the amplitude of nonfailure EPSPs. We conclude that the same CA3-CA1 synapses can alternatively undergo associative potentiation and depression, perhaps through opposite changes in a single expression mechanism.

Animals↗