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PubMed2003

Pyridostigmine enhances glutamatergic transmission in hippocampal CA1 neurons.

Pyridostigmine, a carbamate acetylcholinesterase (AChE) inhibitor, is routinely employed in the treatment of the autoimmune disease myasthenia gravis. Due to its positively charged ammonium group, under normal conditions pyridostigmine cannot cross the blood-brain barrier (BBB) and penetrate the brain. However, several studies have suggested that under conditions in which the BBB is disrupted, pyridostigmine enters the brain, changes cortical excitability, and leads to long-lasting alterations in gene expression. The aim of this study was to characterize the mechanisms underlying pyridostigmine-induced changes in the excitability of central neurons. Using whole cell intracellular recordings in hippocampal neurons we show that pyridostigmine decreases repetitive firing adaptation and increases the appearance of excitatory postsynaptic potentials. In voltage clamp recordings, both pyridostigmine and acetylcholine (ACh) increased the frequency but not the amplitude of excitatory postsynaptic currents. These effects were reversible upon the administration of the muscarinic receptor antagonist, atropine, and were not blocked by tetrodotoxin. We conclude that pyridostigmine, by increasing free ACh levels, causes muscarinic-dependent enhancement of excitatory transmission. This mechanism may explain central side effects previously attributed to this drug as well as the potency of AChE inhibitors, including nerve-gas agents and organophosphate pesticides, in the initiation of cortical synchronization, epileptic discharge, and excitotoxic damage.

Acetylcholine↗
PubMed1998

Synaptic inhibition in the isolated respiratory network of neonatal rats.

Gramicidin-perforated patch-clamp recording revealed phasic Cl(-)-mediated hyperpolarizations in respiratory neurons of the brainstem-spinal cord preparation from newborn rats. The in vitro respiratory rhythm persisted after block of gamma-aminobutyric acid (GABA), i.e. GABAA, receptor-mediated inhibitory postsynaptic potentials (IPSPs) with bicuculline and/or glycinergic IPSPs with strychnine. In one class of expiratory neurons, bicuculline unmasked inspiration-related excitatory postsynaptic potentials (EPSPs), leading to spike discharge. Bicuculline also blocked hyperpolarizations and respiratory arrest due to bath-applied muscimol, whereas strychnine antagonized similar responses to glycine. The reversal potential of respiration-related IPSPs and responses to GABA, muscimol or glycine was not affected by CO2/HCO3(-)-free solutions, but shifted from about -65 mV to values more positive than -20 mV upon dialysis of the cells with 144 instead of 4 mM Cl-. Impairment of GABA uptake with nipecotic acid or glycine uptake with sarcosine evoked a bicuculline- or strychnine-sensitive decrease of respiratory frequency which could lead to respiratory arrest. Also, the GABAB receptor agonist baclofen led to reversible suppression of respiratory rhythm. This in vitro apnoea was accompanied by a K+ channel-mediated hyperpolarization (reversal potential -88 mV) of tonic cells, whereas membrane potential of neighbouring respiratory neurons remained almost unaffected. Both baclofen-induced hyperpolarization and respiratory depression were antagonised by 2-OH-saclofen, which did not affect respiration-related IPSPs per se. The results show that synaptic inhibition is not essential for rhythmogenesis in the isolated neonatal respiratory network, although (endogenous) GABA and glycine have a strong modulatory action. Hyperpolarizing IPSPs mediated by GABAA and glycine receptors provide a characteristic pattern of membrane potential oscillations in respiratory neurons, whereas GABAB receptors rather appear to be a feature of non-respiratory neurons, possibly providing excitatory drive to the network.

Action Potentials↗
PubMed1997

Differential effects of a benzodiazepine on synaptic transmissions in rat hippocampal neurons in vitro.

The effects of midazolam, one of the most popular benzodiazepines, on synaptic transmissions were compared with intracellular recordings between CA1 pyramidal cells (CA1-PCs) and dentate gyrus granule cells (DG-GCs) in rat hippocampal slices. First, we studied the effects of midazolam on orthodromically evoked spikes, membrane properties and synaptic potentials. Secondly, the effects of a GABA(A) receptor agonist, muscimol, were examined on membrane properties to determine whether or not the densities of GABA(A) receptors are different between CA1-PCs and DG-GCs. Midazolam (75 microM) markedly depressed orthodromically evoked spikes in CA1-PCs, compared with those in DG-GCs. A GABA(A) receptor antagonist, bicuculline (10 microM), almost completely antagonized the depressant effects of midazolam on spike generation in CA1-PCs, whereas it had little effect on midazolam in dentate gyrus granule cells. Midazolam produced either depolarizing or hyperpolarizing effects on resting membrane potentials (Vm) with an input resistance decrease in CA1-PCs, whereas it produced depolarized Vm in DG-GCs. Midazolam significantly increased the amplitude of monosynaptic inhibitory postsynaptic potentials in CA1-PCs, whereas midazolam slightly decreased these in DG-GCs. Midazolam significantly decreased the amplitude of excitatory postsynaptic potentials both in CA1-PCs and DG-GCs. Muscimol (100 microM) produced either depolarizing or hyperpolarizing effects on Vm with an input resistance decrease in CA1-PCs, and it depolarized Vm with an input resistance decrease in DG-GCs. These results demonstrate that midazolam has differential effects on excitatory and inhibitory synaptic transmissions in hippocampal neurons. The mechanism of this difference could be partly due to the different types of GABA(A) receptors between CA1-PCs and DG-GCs.

2-Amino-5-phosphonovalerate↗
PubMed1995

Acute tolerance to the excitatory effects of opioids in the rat hippocampus.

Prolonged iontophoretic administrations of delta- and mu-selective opioid receptor agonists were conducted in the hippocampus of rats, in order to study the possible development of acute tolerance to the excitatory effects of the opioids. Acute tolerance (AT) to the excitatory effects of the delta-selective opioid receptor agonist Tyr-D-Ser-Gly-Phe-Leu-Thr (DSLET) was observed when the drug was applied locally for 3-5 min in the CA1 hippocampal pyramidal neurons. The acute tolerance was expressed as a decrease in the commissurally evoked spike responsiveness during peptide's administration and led to a long-lasting potentiation of the population spike (PS) upon its withdrawal. In all cases, where AT and spike potentiation were evident, the population excitatory postsynaptic potential (pEPSP) remained unaltered. Pharmacological studies of AT and long-lasting spike potentiation showed the following: (1) the nonselective opioid receptor antagonist, naloxone, while effective in blocking the excitatory effects of DSLET when applied prior and during the application of the latter, failed to exhibit any effect on the long-lasting potentiating effect of the opioid; and (2) during the spike potentiation phase, administration of DSLET exhibited a depressant effect towards baseline values. This depressant effect of the opioid was evident 2-3 min from the beginning of the application and was completely antagonized by naloxone. The above results show that the development of acute tolerance to the excitatory effects of the DSLET led to long-lasting spike potentiation, which manifests a withdrawal phenomenon.

Analgesics↗
PubMed2000

The effect of pyramidal stimulation upon tail muscle motoneurons in the decerebrate cat.

This study aimed to determine the effects of the corticospinal tract (CST) on the motoneurons innervating the tail muscles in cats. The stimulation of the pyramidal tract predominantly evoked excitatory postsynaptic potentials (EPSPs; 48/90 motoneurons: 53%). Single-pulse stimulation produced EPSPs in 18 of 48 motoneurons, but double shocks evoked postsynaptic potentials in most of the remaining cells (26/48). Monosynaptic excitatory connections between pyramidal tract fibers and tail motoneurons were confirmed in 4 motoneurons. Inhibitory postsynaptic potentials (IPSPs) were recorded from motoneurons innervating long tendinous tail muscles (7/90: 8%) and the shortest neuronal pathways of IPSPs were shown to be disynaptic pathways. Interactions between the CST and reflex pathways from low-threshold muscle and cutaneous afferents innervating the tail and hindlimbs were observed.

Animals↗
PubMed2002

Spontaneous, low frequency (approximately 2-3 Hz) field activity generated in rat ventral hippocampal slices perfused with normal medium.

This study demonstrates that transverse slices taken from the ventral hippocampus of adult rats perfused with a medium of normal ionic composition sustain spontaneous periodic field potentials due to the synchronous activity of a population of neurons. This ventral hippocampus spontaneous synchronous activity (VHSSA) in CA1 stratum pyramidale consisted of positive potentials (approximately 0.12 mV, 55 ms) occurring at a frequency of 2.8 +/- 0.2 Hz for hours without interruption. VHSSA was most frequently observed in slices taken 1-3 mm from the ventral end of hippocampus, and was absent in slices taken from tissue more than 4.5 mm away from it. Stimulation of Schaffer collaterals primed the appearance of potentials, which were similar to VHSSA and clearly distinguishable from excitatory postsynaptic potentials. In view of the known relative proneness of ventral hippocampus to epilepsy, we perfused ventral slices with high-[K(+)](o) medium (8 mM). Albeit reduced in amplitude, VHSSA persisted during the high-[K(+)](o) induced interictal-like epileptiform activity. We could not document any temporal relationship between the two phenomena. Low concentrations of the antagonist of gamma-amino-butyric acid receptors, type A, bicuculline (2-3 microM), which enhanced the high-[K(+)](o) induced epileptiform activity, reversibly blocked the VHSSA. We conclude that under standard in vitro conditions small circuits in the ventral hippocampus are most often and for long periods of time engaged in synchronous quasi-rhythmic low-frequency activity, generated locally by mechanisms substantially differing from those supporting epileptiform discharges.

Animals↗
PubMed1990

Mutual Re-excitation with Post-Inhibitory Rebound: A Simulation Study on the Mechanisms for Locomotor Rhythm Generation in the Spinal Cord of Xenopus Embryos.

We have used computer simulations as one way to test the hypothesis that locomotor rhythm production for swimming in frog embryo spinal cord depends on rebound from inhibition and is sustained by mutual re-excitation among spinal excitatory interneurons. All simulations were based on physiological and anatomical data on the neurons and circuitry of Xenopus embryo spinal cord. Model 'neurons' had resistively coupled axon, soma, and dendrite compartments. Membrane properties were based on Hodgkin - Huxley equations with resting potential at - 75 mV and where soma and dendrite had reduced K+ and Na+ conductance and slowed K+ conductance. These 'neurons' fired a single non-overshooting spike both to depolarizing current and after hyperpolarizing current given during imposed depolarization. Synapses were made on to the dendrite. Inhibitory and excitatory synaptic channels had Nernst potentials of - 80 and 0 mV, time constants for opening of 1 ms, and closing of 6 and 75 ms. When the short inhibitory postsynaptic potential occurred on the long (N-methyl-D-aspartate-type) excitatory postsynaptic potential, it led to rebound firing. A four 'neuron' symmetrical network was built with reciprocal inhibition and where excitatory 'neurons' re-excited themselves and the inhibitory 'neuron' on their own side. The rhythmic alternating activity with one spike per cycle produced reliably by this network was self-sustaining, initiated by a brief synaptic input, and closely resembled the spinal cord motor pattern during swimming. The robustness of this activity pattern was investigated by varying cellular and synaptic parameters, initiating inputs, and network connectivity. We conclude that cellular, synaptic, and network properties are all important and that mutual re-excitation, a form of positive feedback, could sustain motor rhythm production in the Xenopus embryo spinal cord.

Journal Article↗
PubMed2003

Enhanced excitability of myenteric AH neurones in the inflamed guinea-pig distal colon.

The electrical and synaptic properties of myenteric neurones in normal and inflamed guinea-pig distal colons were evaluated by intracellular microelectrode recording. Chronic inflammation was established 6 days following administration of trinitrobenzene sulfonic acid (TNBS). In S neurones, inflammation only altered synaptic inputs as the amplitude of fast excitatory postsynaptic potentials were significantly larger (31 +/- 2 mV compared to 20 +/- 1 mV) and they were more likely to receive slow excitatory synaptic input (85% compared to 55%). AH neurones displayed altered electrical properties in colitis compared to control tissues: they generated more action potentials during a maximal depolarising current pulse (7 +/- 1 compared to 1.6 +/- 0.2); they had a smaller after hyperpolarisation (9 +/- 2 mV s compared to 20 +/- 2 mV s); and they were more likely to receive fast excitatory synaptic input (74% compared to 17%), possess spontaneous activity (46% compared to 3%), and generate anodal break action potentials (58% compared to 19%). Although the resting membrane potential, input resistance and action potential characteristics were unaltered in AH neurones from inflamed tissues, they exhibited an enhanced Cs+-sensitive rectification of the current-voltage relationship. This suggests that the increase in excitability of AH neurones may involve a colitis-induced augmentation of the hyperpolarisation-activated cation current (Ih) in these cells. An increased excitability, selectively in AH neurones, suggests that the afferent limb of intrinsic motor reflexes is disrupted in the inflamed colon and this may contribute to dysmotility associated with inflammatory diseases.

Action Potentials↗
PubMed2004

Experimental evidence and modeling studies support a synchronizing role for electrical coupling in the cat thalamic reticular neurons in vivo.

Thalamic reticular (RE) neurons are crucially implicated in brain rhythms. Here, we report that RE neurons of adult cats, recorded and stained intracellularly in vivo, displayed spontaneously occurring spikelets, which are characteristic of central neurons that are coupled electrotonically via gap junctions. Spikelets occurred spontaneously during spindles, an oscillation in which RE neurons play a leading role, as well as during interspindle lulls. They were significantly different from excitatory postsynaptic potentials and also distinct from fast prepotentials that are presumably dendritic spikes generated synaptically. Spikelets were strongly reduced by halothane, a blocker of gap junctions. Multi-site extracellular recordings performed before, during and after administration of halothane demonstrated a role for electrical coupling in the synchronization of spindling activity within the RE nucleus. Finally, computational models of RE neurons predicted that gap junctions between these neurons could mediate the spread of low-frequency activity at great distances. These experimental and modeling data suggest that electrotonic coupling within the RE nucleus plays an important role in the generation and synchronization of low-frequency (spindling) activities in the thalamus.

Action Potentials↗
PubMedDate not supplied

A generalized Hebbian rule for activity-dependent synaptic modifications.

In this paper our previous model of activity-dependent synaptic modification is extended and applied to a model neuron with active dendrites and is used in computer simulations to examine in detail the dependence of synaptic modifications on the interval between the onset of excitatory postsynaptic potentials (EPSPs) and postsynaptic action potentials (APs). The EPSP amplitude is increased when the action potentials occur within 20 ms after EPSPs and is reduced when the action potentials occur within 20 ms before EPSPs. Furthermore, the absolute value of changes in the EPSP amplitude tends to increase as the interval between APs and EPSPs decreases. A learning rule for synaptic modifications described in this paper may, hence, further generalize the Hebbian rule which requires conjunctive presynaptic and postsynaptic activity for synaptic modification to occur. Functional roles for such a generalized Hebbian rule are also considered.

Action Potentials↗
PubMed2003

Involvement of GABA(B) receptors in presynaptic inhibition of fibers of the descending projections of the spinal cord in the frog Rana ridibunda.

Isolated spinal cord preparations from Rana ridibunda frogs were used for studies of the effects of the GABA(B) receptor agonists (-)-baclofen (50 and 100 microM) and GABA (4-8 mM) and the specific GABA(B) receptor antagonist 2-hydroxysaclofen (100 microM) on the transmission of signals from fibers of the ventral columns monosynaptically connected with motoneurons in segments 9 and 10. These experiments showed that (-)-baclofen (50 and 100 microM) produced significant and dose-dependent suppression of excitatory postsynaptic potentials (EPSP) in motoneurons and ventral root potentials evoked by stimulation of fibers of the ipsi- and contralateral ventral columns. The inhibitory effect of (-)-baclofen (100 microM) on descending EPSP was 35-50% blocked by the GABA(B) receptor antagonist 2-hydroxysaclofen (0.2 mM). The inhibitory effect of GABA (4-8 mM) on descending EPSP was 60% blocked by the GABA(A) receptor antagonist picrotoxin (0.05 mM). (-)-Baclofen (50 microM) and GABA (4 and 6 mM) were found to have inhibitory effects on ventral root potentials evoked by stimulation of the ipsi- and contralateral ventral columns. The data obtained here, as well as data obtained by pharmacological analysis and conditioning by stimulation of the ipsi- and contralateral ventral columns, are regarded as a significant argument supporting the existence of GABA(B) receptor-mediated presynaptic inhibition of descending fibers connected monosynaptically to spinal cord motoneurons in the frog Rana ridibunda.

Action Potentials↗
PubMed1998

Regional differences in hippocampal excitability manifested by paired-pulse stimulation of genetically epileptic El mice.

Hippocampal excitability in El mice was studied by analyzing paired-pulse responses of population excitatory postsynaptic potentials (EPSPs) and population spikes (PSs). In vitro slice preparations from seizure-susceptible adult (15 weeks old) and non-seizure susceptible young (5 weeks old) El mice were compared with age-matched mother strain ddY mice. In CA1 area, paired-pulse inhibition of PSs was reduced by about 50% at 10 ms interpulse interval (IPI) in both 5 and 15 weeks old El mice when compared to ddY mice. Phenobarbital (200 microM) decreased paired-pulse ratio (PPR) by 30% in El mice, and bicuculline (1 microM) increased PPR by 80% in ddY mice at 10 ms IPI. These results suggest an intrinsic existence of decreased GABA(A) receptor-mediated inhibition in CA1 of El mice. In dentate gyrus (DG), an increase in paired-pulse facilitation of PSs was observed at intermediate IPIs (50-200 ms) in El mice at both ages, especially at 15 weeks of age, when 52%-increased PPR was recorded. The facilitation was not due to GABA(A) receptor-mediated inhibition and was not age-dependent. In CA3 area, increased paired-pulse facilitation of PSs and EPSPs over the range of 10-1000 ms IPIs was observed only in the 15-week-old El mice. The age-dependent appearance of seizure susceptibility was associated with the increase in excitatory synaptic transmission in CA3. Our results show that El mice possess excitatory/inhibitory synaptic transmission abnormalities in the hippocampus that could contribute to seizure predisposition.

Action Potentials↗
PubMed2004

Long-term potentiation of transmitter exocytosis expressed by Ca2+-induced Ca2+ release from thapsigargin-sensitive Ca2+ stores in preganglionic nerve terminals.

We have studied whether Ca(2+)-induced Ca(2+) release (CICR) is involved in the mechanism of long-term potentiation (LTP) at nicotinic synapses of bullfrog sympathetic ganglia. Fast excitatory postsynaptic potentials (fast EPSPs) were recorded in a low-Ca(2+), high-Mg(2+) solution and quantal analysis was applied. The conditioning stimulation of the B-type preganglionic nerve at 20 Hz for 4 min consistently enhanced the amplitude and quantal content of fast EPSP for > 2 h, but only sometimes enhanced the quantal size. The LTP of quantal content produced by the conditioning tetanus was blocked by thapsigargin, a blocker of Ca(2+) pumps at Ca(2+) stores, applied before or after the conditioning tetanus, and by Xestospongin C, a blocker of inositoltrisphosphate (IP(3)) receptors, applied before the tetanus. It was not, however, blocked by ryanodine, a blocker and/or activator of ryanodine receptors, or by propranolol, a blocker of beta-adrenergic receptors. Thus the long-lasting activity of the preganglionic nerve at a high frequency causes the LTP of impulse-evoked transmitter release by the activation of CICR from thapsigargin-sensitive Ca(2+) stores in the nerve terminals. It is likely that a large Ca(2+) entry into the nerve terminals during tetanic activity primes ryanodine-insensitive Ca(2+) release channels for activation.

Adrenergic beta-Antagonists↗
PubMed2001

Mechanism for increased hippocampal synaptic strength following differential experience.

Exposure to novel environments or behavioral training is associated with increased strength at hippocampal synapses. The present study employed quantal analysis techniques to examine the mechanism supporting changes in synaptic transmission that occur following differential behavioral experience. Measures of CA1 synaptic strength were obtained from hippocampal slices of rats exposed to novel environments or maintained in individual cages. The input/output (I/O) curve of extracellularly recorded population excitatory postsynaptic potentials (EPSPs) increased for animals exposed to enrichment. The amplitude of the synaptic response of the field potential was related to the fiber potential amplitude and the paired-pulse ratio, however, these measures were not altered by differential experience. Estimates of biophysical parameters of transmission were determined for intracellularly recorded unitary responses of CA1 pyramidal cells. Enrichment was associated with an increase in the mean unitary synaptic response, an increase in quantal size, and a trend for decreased input resistance and reduction in the stimulation threshold to elicit a unitary response. Paired-pulse facilitation, the percent of response failures, coefficient of variance, and estimates of quantal content were not altered by experience but correlated well with the mean unitary response amplitude. The results suggest that baseline synaptic strength is determined, to a large extent, by presynaptic release mechanisms. However, increased synaptic transmission following environmental enrichment is likely due to an increase in the number or efficacy of receptors at some synapses and the emergence of functional synaptic contacts between previously unconnected CA3 and CA1 cells.

Action Potentials↗
PubMedDate not supplied

[Functional organization of the vestibulospinal system in amphibians].

In experiments on the preparation of a frog perfused brain, using recording of intracellular potentials the vestibulospinal neurons were identified on the basis of excitatory postsynaptic potentials evoked by the stimulation of the ipsilateral vestibular nerve and antidromic activation from the stimulation of the cervical and lumbar enlargements of the spinal cord. The average conduction velocity determined for axons of C neurons was 10.67 m/s and for L neurons 15.84 m/s. The ratio of C and L neurons over the vestibular nuclear complex was very stimular to each other: 52% C neurons and 48% L neurons. The majority of both types of neurons were localized in the lateral vestibular nucleus (58.6%), to the lesser extent in the descending vestibular nucleus (30.7%) and very little in the medial vestibular nucleus (10.6%). Fast and slow cells were detected among the vestibulospinal neurons. The fast neurons of L cells did not prevail greatly over the slow ones, whereas the slow neurons of C cells prevailed comparatively largely over the fast neurons. Thus, it became possible to reconstruct spatial distribution of the identified vestibulospinal neurons. The results of spatial distribution of C and L vestibulospinal neurons in the frogs failed to conform to definite somatotopy, which is characteristic for mammalian vestibular nuclei. C and L neurons in the frog's vestibular nuclei as a source of vestibulospinal fibres, are scattered separately or more frequently in groups, so that they establish a "patch-like" somatotopy and do not form a distinctly designed fields as in mammals.

Amphibians↗
PubMed2000

Effects of lamotrigine on field potentials and long-term potentiation in guinea pig hippocampal slices.

PURPOSE: To investigate the effects of lamotrigine (LTG), a new anticonvulsant, on neuronal excitability, synaptic transmission, and long-term potentiation (LTP) in guinea pig hippocampal slices. METHODS: Electrically evoked field excitatory postsynaptic potentials (fEPSPs) and population spikes (PSs) were investigated in the CA1 region of the hippocampus. RESULTS: The concentration-response curves showed different actions of LTG in concentrations near therapeutic plasma levels (10 microM) on fEPSPs and PSs. The initial slopes of fEPSPs were not affected, whereas the amplitudes of PSs were significantly decreased. Higher concentrations of LTG decreased both fEPSP slopes and PS amplitudes; however, the effects on PSs were much stronger. Also, there were no differences in fEPSP slopes or PS amplitudes compared with controls when LTP was induced in the presence of LTG (10 microM). CONCLUSIONS: Our data are in contrast to previous findings that suggest LTG acts primarily on presynaptic sites by blocking the release of excitatory amino acids. Further, LTP was not affected by LTG.

Animals↗
PubMed2002

The influence of developmental period of aluminum exposure on synaptic plasticity in the adult rat dentate gyrus in vivo.

Previous studies from our group have demonstrated that chronic aluminum exposure from parturition throughout life impairs both long-term potentiation (LTP) and long-term depression (LTD) of the excitatory postsynaptic potential (EPSP) slope and reduces the population spike (PS) amplitude in the rat dentate gyrus in vivo. The present study sought to extend these findings by evaluating the developmental periods critical for aluminum-induced impairment of synaptic plasticity. Rats were exposed to aluminum (gestational, lactational and postlactational) through drinking 0.3% aluminum chloride in water over different developmental intervals: (1) prenatal exposure; (2) beginning from birth and terminating at weaning; (3) beginning at weaning throughout life; (4) beginning at birth and continuing throughout life. As adults (postnatal day 80-100), field potentials were measured in the dentate gyrus of hippocampus in response to stimulation applied to the lateral perforant path. The results showed: (1) Prenatal aluminum exposure had no effect on the magnitude of LTP as measured by the EPSP slope and LTD as measured for the PS amplitude, while it had a small effect on the magnitude of LTP as measured for the PS amplitude and LTD as measured by the EPSP slope. (2) Lactational, postlactational and throughout life exposure to aluminum impaired both LTP and LTD of the EPSP slope and PS amplitude, except that LTD of PS amplitude was not significantly changed in animals postlactationally exposed. (3) Aluminum exposure from parturition throughout life caused the greatest impairment of the range of synaptic plasticity, while prenatal aluminum exposure caused the least. From these results we conclude that the lactational period was the most susceptible to aluminum-induced impairment of synaptic plasticity and that chronic aluminum exposure from parturition throughout life is extremely disruptive to synaptic plasticity and should be avoided.

Aluminum↗
PubMed2006

Representation of auditory signals in the M-cell: role of electrical synapses.

The teleost Mauthner (M-) cell mediates a sound-evoked escape behavior. A major component of the auditory input is transmitted by large myelinated club endings of the posterior VIIIth nerve. Paradoxically, although nerve stimulations revealed these afferents have mixed electrical and glutamatergic synapses on the M-cell's distal lateral dendrite, paired pre- and postsynaptic recordings indicated most individual connections are chemically silent. To determine the sensory information encoded and the relative contributions of these two transmission modes, M-cell responses to acoustic stimuli in air were recorded intracellularly. Excitatory postsynaptic potentials (EPSPs) evoked by both short 100- to 900-Hz "pips" and longer-lasting amplitude- and frequency-modulated sounds were dominated by fast, repetitive EPSPs superimposed on an underlying slow depolarization. Fast EPSPs 1) have kinetics comparable to presynaptic action potentials, 2) are maximal on the distal lateral dendrite, and 3) are insensitive to GluR antagonists. They presumably are coupling potentials, and power spectral analysis indicated they constitute a high-pass signal that accurately tracks sound frequency and amplitude. The spatial profile of the slow EPSP suggests both proximal and distal dendritic sources, a result supported by predictions of a multicompartmental model and the effects of AMPAR antagonists, which preferentially reduced the proximal component. Thus a second class of afferents generates a portion of the slow EPSP that, with sound stimuli, demonstrate that the dominant mode of transmission at LMCE synapses is electrical. The slow EPSP is a dynamic, low-pass representation of stimulus strength. Accordingly, amplitude and phase information, which are segregated in other systems, are faithfully represented in the M-cell.

Acoustic Stimulation↗