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PubMed2003

Requirement of a critical period of GABAergic receptor blockade for induction of a cAMP-mediated long-term depression at CA3-CA1 synapses.

Previous reports show that bath application of the adenosine 3' : 5'-cyclic monophosphate (cAMP) analog, Sp-cAMPS, induces a protein kinase A (PKA)-dependent and protein synthesis-dependent long-term potentiation (LTP) at hippocampal CA3-CA1 synapses. Recently, we reported a novel form of long-term depression (LTD) induced by concurrent application of Sp-cAMPS and picrotoxin, the gamma-aminobutyric acid type A (GABA(A)) receptor antagonist. In the present study, we further investigated the mechanisms underlying such cAMP-mediated LTD. Synaptically connected CA3 and CA1 cells of hippocampal slice cultures were impaled by sharp electrodes. Excitatory postsynaptic potentials recorded from a CA1 pyramidal cell were evoked by single action potentials in a CA3 cell. Picrotoxin was applied to slices at various time points after Sp-cAMPS was perfused. We found that Sp-cAMPS-induced potentiation could be converted to depression when picrotoxin was applied within 30 min after perfusion of Sp-cAMPS. Picrotoxin applied 1 h after perfusion of Sp-cAMPS had no effect on Sp-cAMPS-induced synaptic potentiation. Once LTP was induced by Sp-cAMPS and expressed for 1 h, the subsequent application of Sp-cAMPS and picrotoxin produced no new changes in synaptic strength. Also, once LTD was induced and expressed for 1 h, subsequent Sp-cAMPS produced no new changes in synaptic strength. These findings suggest that a synapse is committed irreversibly to cAMP-mediated LTP or LTD during a critical period and that later signals cannot interconvert these two fates.

Animals↗
PubMed1997

Epileptogenesis following neocortical trauma from two sources of disinhibition.

Epileptogenesis following neocortical trauma from two sources of disinhibition. J. Neurophysiol. 78: 2804-2810, 1997. Intracellular and field potential recordings were obtained from superficial and deep neurons from both intact coronal rat somatosensory slices, and from slices which had been acutely divided into a superficial strip of cortex ( approximately 450 micron from the pia) and a deep segment. Membrane properties for cells in the traumatized slices were similar to those of their counterparts in intact slices. However, synaptic hyperexcitability developed in the deep segments in which a majority of cells likely underwent dendrotomy. This hyperexcitability was manifested by epileptiform activity in 54% of traumatized slices. Measurements of fastGABAergic inhibitory strength showed these slices were disinhibited. Superficial delivery of tetrodotoxin to the upper 450 micron of intact slices led to disinhibition of fast GABAergic transmission as well as an attendant increase in excitatory postsynaptic potential strength but not epileptogenesis. Pharmacological maneuvers aimed at preventing glutamate-triggered increases in intracellular calcium [glutamate ionotropic antagonists, dantrolene, and bis-(o-aminophenoxy)-N,N,N', N'-tetraacetic acid (BAPTA)-AM] showed that a 1 h treatment in these agents conferred protection against epileptogenesis. These results demonstrate that the seizure-like activity developing in deep dendrotomized cortical segments resulted from two sources of GABAergic disinhibition: the physical removal of important superficial inhibitory circuits and glutamate-triggered increases in intracellular calcium.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1993

Anoxic depression of excitatory and inhibitory postsynaptic potentials in rat neocortical slices.

1. The effects of brief anoxia (4-6 min replacement of O2 by N2) on synaptic potentials evoked from layer IV and/or the white matter were studied in pyramidal neurons of layers II-III from rat neocortical slices. 2. The early and late components of excitatory postsynaptic potentials (EPSPs) showed differential sensitivity to anoxia: within 2 min the late EPSP (lEPSP) disappeared, whereas the amplitude of the early EPSP (eEPSP) decreased by 70% at 5 min of anoxia. Recovery was complete within 4-11 min. 3. Both fast and slow inhibitory postsynaptic potentials (IPSPs) were extremely sensitive to lack of O2 and were abolished earlier than the lEPSP evoked by the same stimulus. As well, recovery of the IPSPs was always more delayed than that of the EPSPs. 4. A transient increase in excitability during early anoxia and/or midrecovery, manifested as enhanced probability of spiking in 25% of neurons, is attributed to the higher sensitivity of IPSPs compared with EPSPs. 5. The anoxic-induced depression of the lEPSP and IPSPs, which are generated close to the soma, is not due to depolarization-induced occlusion; however, occlusion may cause an attenuation of the eEPSP at dendritic sites. 6. The depression of the EPSPs is not a result of a decreased transmembrane Na+ gradient after inactivation of Na-K-adenosine triphosphatase (Na-K-ATPase). Although ouabain induced a depolarization similar to that of anoxia, it did not affect EPSP amplitude.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Slow excitatory synaptic transmission mediated by P2Y1 receptors in the guinea-pig enteric nervous system.

Electrophysiological recording was used to study a type of slow excitatory postsynaptic potential (slow EPSP) that was mediated by release of ATP and its action at P2Y1 receptors on morphologically identified neurones in the submucosal plexus of guinea-pig small intestine. MRS2179, a selective P2Y1 purinergic receptor antagonist, blocked both the slow EPSP and mimicry of the EPSP by exogenously applied ATP. Increased conductance accounted for the depolarization phase of the EPSP, which occurred exclusively in neurones with S-type electrophysiological behaviour and uniaxonal morphology. The purinergic excitatory input to the submucosal neurones came from neighbouring neurones in the same plexus, from neurones in the myenteric plexus and from sympathetic postganglionic neurones. ATP-mediated EPSPs occurred coincident with fast nicotinic synaptic potentials evoked by the myenteric projections and with noradrenergic IPSPs evoked by sympathetic fibres that innervated the same neurones. The P2Y1 receptor on the neurones was identified as a metabotropic receptor linked to activation of phospholipase C, synthesis of inositol 1,4,5-trisphosphate and mobilization of Ca2+ from intracellular stores.

Adenosine Diphosphate↗
PubMed1998

Microinjection of mRNA encoding rat synapsin Ia alters synaptic physiology in identified motoneurons of the crayfish, Procambarus clarkii.

Studies of identified neurons have made important contributions to our understanding of cellular neurophysiology. We have developed a technique for modifying gene expression in identified motoneurons of the crayfish Procambarus clarkii in the isolated nervous system as well as in the intact animal through the injection of exogenously synthesized RNAs. mRNA suitable for injection was transcribed in vitro from cDNA templates cloned into a plasmid, pSEM. Initially, mRNAs encoding green fluorescent protein (GFP) and beta-galactosidase were injected into the soma of the motor giant neuron (MoG) to determine whether these mRNAs could be successfully translated into protein. Both proteins were expressed. Measurements of GFP fluorescence increase indicated that GFP mRNA was stable and translated into protein for at least 3 days postinjection. We then examined the effects of expression of GFP, AASP-168 (an endogenous crayfish axonal protein), and rat synapsin Ia on MoG synaptic physiology. The mRNA injection procedure did not appear to directly influence synaptic physiology based on the results of the AASP-168 and GFP injections. Injection of mRNA encoding rat synapsin Ia resulted in a significant increase in peak excitatory postsynaptic potential (EPSP) amplitude during repetitive stimulation. These data are consistent with previous studies that have shown that synapsin deficiency reduces synaptic vesicle numbers. The translation of mRNAs with diverse functions and species of origin suggests that this approach will prove useful for studying the function of a wide variety of endogenous and exogenous genes in identified neurons.

Animals↗
PubMed2001

Clinical electrophysiology of the upper and lower motor neuron in amyotrophic lateral sclerosis.

Electrophysiology is important in amyotrophic lateral sclerosis (ALS). It helps in the assessment of disease severity and rate of progression, and it plays a role in evaluating the efficacy of therapeutic trials. Presently, electrophysiology is the only means of confirming suspected ALS, and this has been incorporated into the El Escorial criteria. Needle electromyography identifies disease in clinically "unaffected muscles" including bulbar musculature, confirms involvement of anterior horn cells, and can detect early involvement of respiratory muscles (intercostals and diaphragm). Conduction studies are imperative to rule out motor neuropathy with multifocal conduction block. Various techniques (cortical threshold, cortical silent period, double stimulation) employing transcranial magnetic stimulation have demonstrated that the motor cortex in ALS is hyperexcitable. Central motor conduction is normal in ALS but uniquely slow in the D9OA SOD1 mutation. Using peristimulus time histograms (PSTHs) it is possible to estimate the size of a unitary excitatory postsynaptic potential (EPSP). In ALS the EPSP is typically desynchronized. With time it becomes reduced in amplitude and a slow conducting component becomes recognizable in the primary peak of the PSTH. This reflects conduction through a slow motor pathway. Abnormalities of the PSTH are not seen in Kennedy's disease, implying that the changes seen in ALS are due to supraspinal mechanisms.

Amyotrophic Lateral Sclerosis↗
PubMed2002

Ifenprodil and ethanol enhance NMDA receptor-dependent long-term depression.

Long-term alterations in synaptic transmission are thought to underlie various types of alcohol-related brain disorders. While ethanol effects on synaptic potentiation are well documented, ethanol effects on synaptic depression have not been addressed. Herein, we performed experiments to assess the role of ethanol on long-term depression (LTD) formation. In rat hippocampal slices, prolonged low-frequency stimulation (LFS) of CA1 Schaffer collaterals (1 Hz for 7 min) induced saturable, long-lasting, reversible N-methyl-D-aspartate (NMDA) receptor-dependent LTD of stimulus-evoked dendritic population excitatory postsynaptic potentials. This depression (-26% LTD amplitude) was observed in young rats (12-20 days old), but not adult rats (28-35 days old). Induction of LTD was blocked (-3% LTD amplitude) when the LFS was delivered in the presence of the NMDA receptor antagonist D-2-amino-5-phosphonovaleric acid. When the conditioning LFS was delivered in the presence of ethanol, there was a significant enhancement in the induction of NMDA receptor-dependent LTD versus control LTD (-36% LTD amplitude). Ifenprodil, an N-methyl-D-aspartate receptor subunit 2B (NR2B)-selective antagonist, also significantly facilitated the induction of LTD (-40% LTD amplitude). Consistent with this result, ifenprodil did not affect the NMDA receptor-dependent component of the baseline synaptic response, whereas D-2-amino-5-phosphonovaleric acid caused significant depression of the NMDA component. These data indicate that whereas ethanol is known to inhibit NMDA receptor function in a variety of systems, it significantly enhances the induction of NMDA receptor-dependent LTD. Furthermore, since ifenprodil is known to select for ethanol-sensitive subtypes of NR2B-NMDA receptors, these data also suggest that NR2B-containing NMDA receptor subpopulations do not contribute to LTD, but instead may actually play inhibitory roles in LTD induction.

Animals↗
PubMed1997

A fast synaptic potential mediated by NMDA and non-NMDA receptors.

A fast synaptic potential mediated by NMDA and non-NMDA receptors. J. Neurophysiol. 78: 2693-2706, 1997. Excitatory synaptic transmission in the CNS often is mediated by two kinetically distinct glutamate receptor subtypes that frequently are colocalized, the N-methyl--aspartate (NMDA) and non-NMDA receptors. Their synaptic currents are typically very slow and very fast, respectively. We examined the pharmacological and physiological properties of chemical excitatory transmission at the mixed electrical and chemical synapses between auditory afferents and the goldfish Mauthner cell, in vivo. Previous physiological data have suggested the involvement of glutamate receptors in this fast excitatory postsynaptic potential (EPSP), the chemical component of which decays with a time constant of <2 ms. We demonstrate here that the pharmacological and voltage-dependent characteristics of the synaptic currents are consistent with glutamatergic transmission and that both NMDA and non-NMDA receptors are involved. The two components surprisingly exhibit quite similar kinetics even at resting potential, with the NMDA response being only slightly slower. Due to its fast kinetics and characteristic voltage dependence, NMDA receptor-mediated transmission at these first-order synapses contributes significantly to paired pulse and frequency-dependent facilitation of successive fast EPSPs during high-frequency repetitive firing, a presynaptic impulse pattern that induces activity-dependent homosynaptic changes in both electrical and chemical transmission. Thus NMDA receptor kinetics in this intact preparation are suited to its functional requirements, namely speed of information transmission and the ability to trigger changes in synaptic efficacy.

2-Amino-5-phosphonovalerate↗
PubMed1997

Calcium-dependent plateau potentials in rostral ambiguus neurons in the newborn mouse brain stem in vitro.

Calcium-dependent plateau potentials in rostral ambiguus neurons in the newborn mouse brain stem in vitro. J. Neurophysiol. 78: 2483-2492, 1997. The nucleus ambiguus contains vagal and glossopharyngeal motoneurons and preganglionic neurons involved in respiration, swallowing, vocalization, and control of heart beat. Here we show that the rostral compact formation's ambiguus neurons, which control the esophageal phase of swallowing, display calcium-dependent plateau potentials in response to tetanic orthodromic stimulation or current injection. Whole cell recordings were made from visualized neurons in the rostral nucleus ambiguus using a slice preparation from the newborn mouse. Biocytin-labeling revealed dendritic trees with pronounced rostrocaudal orientations confined to the nucleus ambiguus, a morphological profile matching that of vagal motoneurons projecting to the esophagus. Single-stimulus orthodromic activation, using an electrode placed in the dorsomedial slice near the nucleus tractus solitarius, evoked single excitatory postsynaptic potentials (EPSPs) or short trains of EPSPs (500 ms to 1 s). However, tetanic stimulation (5 pulses, 10 Hz) induced voltage-dependent afterdepolarizations or long-lasting plateau potentials (>1 min) with a constant firing pattern. Depolarizing or hyperpolarizing current pulses elicited voltage-dependent afterdepolarizations or plateau potentials lasting a few seconds to several minutes. Constant spike activity accompanied the long-lasting plateau potentials, which ended spontaneously or could be terminated by weak hyperpolarizing current pulses. Current-induced afterdepolarizations and plateau potentials were dependent on extracellular and intracellular Ca2+, as they were blocked completely by extracellular Co2+, Cd2+, or intracellular bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid (BAPTA). Orthodromically induced afterdepolarizations and plateau potentials were blocked by intracellular BAPTA. Afterdepolarizations and plateau potentials were completely blocked by substitution of extracellular Na+ with choline. Afterdepolarizations persisted in tetrodotoxin. We conclude that rostral ambiguus neurons have a Ca2+-activated inward current carried by Na+. Synaptic activation of this conductance may generate prolonged spike activity in these neurons during the esophageal phase of swallowing.

Animals↗
PubMed2005

Beta-Amyloid peptide25-35 depresses excitatory synaptic transmission in the rat basolateral amygdala "in vitro".

The effects of beta-amyloid peptide25-35 on resting membrane potential, spontaneous and evoked action potential and synaptic activity have been studied in basolateral amygdaloid complex on slices obtained from adult rats. Intracellular recordings reveal that perfusion with beta-amyloid peptide25-35 at concentrations of 400 nM and less did not generate any effect on resting membrane potential. However, concentrations in the range of 800-1200 nM produced an unpredictable effect, depolarization and/or hyperpolarization, which were blocked by tetrodotoxin or 6-cyano-7-nitroquinoxaline-2,3-dione+D-(-)-2-amino-5-phosphonopentanoic acid together with bicuculline. Excitatory and inhibitory evoked responses mediated by glutamic acid or gamma-aminobutyric acid decreased in amplitude after beta-amyloid peptide25-35 perfusion. Additionally, results obtained using the paired-pulse protocol offer support for a presynaptic mode of action. To determine which type of receptors and/or channels are involved in the presynaptic mechanism of action, a specific blocker of alpha-7 nicotinic receptors (methyllycaconitine citrate) or L-type calcium channel blockers (calcicludine or nifedipine) were used. beta-amyloid petide25-35 decreased excitatory postsynaptic potentials amplitude in control conditions and also in slices permanently perfused with methyllycaconitine citrate. However, this effect was blocked in slices perfused with calcicludine or nifedipine suggesting the involvement of the L-type calcium channels. On the whole, these experiments provide evidence that beta-amyloid peptide25-35 affects neurotransmission in basolateral amygdala and its action is mediated through L-type calcium channels.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2001

Pre- and postsynaptic actions of ATP on neurotransmission in rat submandibular ganglia.

The pre- and postsynaptic actions of exogenously applied ATP were investigated in intact and dissociated parasympathetic neurones of rat submandibular ganglia. Nerve-evoked excitatory postsynaptic potentials (EPSPs) were not inhibited by the purinergic receptor antagonists, suramin and pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS), or the desensitising agonist, alpha,beta-methylene ATP. In contrast, EPSPs were abolished by the nicotinic acetylcholine receptor antagonists, hexamethonium and mecamylamine. Focal application of ATP (100 microM) had no effect on membrane potential of the postsynaptic neurone or on the amplitude of spontaneous EPSPs. Taken together, these results suggest the absence of functional purinergic (P2) receptors on the postganglionic neurone in situ. In contrast, focally applied ATP (100 microM) reversibly inhibited nerve-evoked EPSPs. Similarly, bath application of the non-hydrolysable analogue of ATP, ATP gamma S, reversibly depressed EPSPs amplitude. The inhibitory effects of ATP and ATP gamma S on nerve-evoked transmitter release were antagonised by bath application of either PPADS or suramin, suggesting ATP activates a presynaptic P2 purinoceptor to inhibit acetylcholine release from preganglionic nerves in the submandibular ganglia. In acutely dissociated postganglionic neurones from rat submandibular ganglia, focal application of ATP (100 microM) evoked an inward current and subsequent excitatory response and action potential firing, which was reversibly inhibited by PPADS (10 microM). The expression of P2X purinoceptors in wholemount and dissociated submandibular ganglion neurones was examined using polyclonal antibodies raised against the extracellular domain of six P2X purinoceptor subtypes (P2X(1-6)). In intact wholemount preparations, only the P2X(5) purinoceptor subtype was found to be expressed in the submandibular ganglion neurones and no P2X immunoreactivity was detected in the nerve fibres innervating the ganglion. Surprisingly, in dissociated submandibular ganglion neurones, high levels of P2X(2) and P2X(4) purinoceptors immunoreactivity were found on the cell surface. This increase in expression of P2X(2) and P2X(4) purinoceptors in dissociated submandibular neurones could explain the increased responsiveness of the neurones to exogenous ATP. We conclude that disruption of ganglionic transmission in vivo by either nerve damage or synaptic blockade may up-regulate P2X expression or availability and alter neuronal excitability.

Acetylcholine↗
PubMed2005

Blockade of nicotinic acetylcholine receptors suppresses hippocampal long-term potentiation in wild-type but not ApoE4 targeted replacement mice.

Both impaired nicotinic neurotransmission and the inheritance of apoE4 are associated with increased risk for Alzheimer disease (AD) as well as other deficiencies in memory-related behavior. Long-term potentiation (LTP), a cellular model of memory, is known to be altered by nicotinic agents. Recent studies also support an emergent role for apoE in LTP. We compared the effects of mecamylamine, a nonspecific antagonist of nicotinic acetylcholine receptors (nAChRs), on basal synaptic transmission and LTP in hippocampal slices from wild-type (wt) mice and targeted replacement mice expressing human apoE4 (apoE4-TR). Field excitatory postsynaptic potentials (EPSPs) were recorded in the dentate gyrus (DG) in response to medial perforant path activation, and theta burst stimulation was used to induce LTP. Bath application of mecamylamine (3 microM) did not alter input-output relationships or paired pulse depression in either mouse strain. Under control conditions, apoE4-TR mice showed significantly less LTP than wt mice (17.5% +/- 3.2%, n = 9, vs. 30.1% +/- 3.9%, n = 11, P < 0.02). Mecamylamine reduced LTP in wt mice to a level that was similar to control levels for apoE4-TR mice (15.7% +/- 3.4%, n = 9), whereas apoE4-TR showed no further reduction of LTP (16.6% +/- 3.7%, n = 8) by mecamylamine. Thus mice expressing human apoE4 differ from wt mice both in their capacity for LTP and in the effect on LTP of nicotinic cholinergic blockade. It is possible that nicotinic neurotransmission is already compromised in apoE4-TR mice and, hence, that interference with the integrity of this cholinergic system represents a mechanism by which inheritance of the apoE4 allele contributes to cognitive risk.

Analysis of Variance↗
PubMed2005

Protection by a taurine supplemented diet from lead-induced deficits of long-term potentiation/depotentiation in dentate gyrus of rats in vivo.

Previous studies have demonstrated that synaptic plasticity, which includes long-term potentiation (LTP) and depotentiation (DP) in hippocampus, is important for learning and memory. The purpose of this study is to evaluate the effect of taurine via drinking water on the lead-induced impairments of LTP and DP in rat dentate gyrus (DG) in vivo. The experiments were carried out in four groups of rats (control, lead-exposed, control and lead-exposed with a taurine-supplement diet, respectively). The input-output (I/O) function, excitatory postsynaptic potential (EPSP) and population spike (PS) amplitude were measured in the DG area of adult rats (60-90 days) in response to stimulation applied to the lateral perforant path. The results show that: 1. chronic lead exposure impaired LTP/DP measured on both EPSP slope and PS amplitude in DG area of the hippocampus; 2. in control rats, taurine had no effect on LTP/DP; 3. the amplitudes of LTP/DP of lead-exposed group were significantly increased by applying taurine. These results suggest that dietary taurine supplement could protect rats from the lead-induced impairments of synaptic plasticity and might be a preventive medicine to cure the cognitive deficits induced by lead.

Animals↗
PubMed1998

Frequency-dependent synaptic depression modifies postsynaptic firing probability in cats.

1. The influence of stimulus trains applied to single I a axons on the firing behaviour of single motoneurones was assessed in anaesthetized cats. The change in motoneurone firing probability associated with a single I a afferent spike was measured from short-latency peaks in peristimulus time histograms or cross-correlograms. Some synapses showed frequency-dependent depression of the short-latency peak, which is consonant with the frequency-dependent depression reported for the I a-motoneurone excitatory postsynaptic potential (EPSP). 2. Where they could be measured, EPSPs superimposed on the depolarizing ramps of potential recorded from motoneurones as they fired repetitively showed frequency-dependent changes in amplitude that parallelled those of the simultaneously recorded histograms. 3. Thus it appears that at synapses with small EPSPs, which are typical in the mammalian CNS, modulation of the EPSP should result in similar modulation of cell firing.

Afferent Pathways↗
PubMed1998

Serotonin reduces polysynaptic inhibition via 5-HT1A receptors in the superficial entorhinal cortex.

The superficial cells of the entorhinal cortex (EC), main input to the hippocampus, receive a serotonergic input from the raphe nuclei and express 5-hydroxytryptamine creatine sulfate complex (5-HT) receptors at high density. With the use of intracellular recordings, we investigated the effects of serotonin on synaptic inhibition of layer II and III neurons of the EC. Serotonin reduced both polysynaptic fast and slow inhibitory postsynaptic potentials (IPSPs) in projection neurons of the superficial EC. Polysynaptic fast and slow IPSPs were depressed by serotonin in a dose-dependent manner (0.1-100 microM). Serotonin in a concentration of 1 microM reduced the amplitudes of polysynaptic fast and slow IPSPs by approximately 40 and 50%, respectively. To identify the subtype of the 5-HT-receptor mediating the effects on polysynaptic IPSPs, we applied various 5-HT-receptor agonists and antagonists. Although the serotonin agonists for the 5-HT1B,2C,3 receptors were ineffective, the effects were mimicked by the 5-HT1A-receptor agonists (8-OH-DPAT, 5-CT) and prevented by the 5-HT1A-receptor antagonist NAN-190. To look at the direct effects of 5-HT on inhibitory interneurons, we elicited monosynaptic IPSPs in the absence of excitatory synaptic transmission. In contrast to the polysynaptic IPSPs, monosynaptic IPSPs were not significantly affected by serotonin. Recordings from putative inhibitory interneurons revealed that their excitatory postsynaptic potentials (EPSPs) were reversibly reduced by serotonin. We conclude that serotonin suppresses polysynaptic inhibition in projection neurons of layers II and III of the EC by depression of EPSPs on inhibitory interneurons via 5-HT1A receptors.

2-Amino-5-phosphonovalerate↗
PubMed2000

Saccular and utricular inputs to single vestibular neurons in cats.

Saccular and utricular organs are essential for postural stability and gaze control. Although saccular and utricular inputs are known to terminate on vestibular neurons, few previous studies have precisely elucidated the origin of these inputs. We investigated the saccular and utricular inputs to single vestibular neurons in whole vestibular nuclei of decerebrated cats. Postsynaptic potentials were recorded from vestibular neurons after electrical stimulation of the saccular and utricular nerves. Ascending and descending axonal projections were examined by stimulating the oculomotor/trochlear nuclei and the cervical segment of the spinal cord, respectively. After each experiment, locations of recorded neurons were identified. The recorded neurons (140) were classified into vestibulo-spinal (79), vestibulo-oculo-spinal (9), and vestibulo-ocular (3) neurons based on antidromic responses; 49 other vestibular neurons were unidentified. The majority of recorded neurons were mainly located in the lateral vestibular nucleus. Most of the otolith-activated vestibular nuclei neurons seemed to participate in vestibulospinal reflexes. Of the total 140 neurons recorded, approximately one third (51) received saccular and utricular inputs (convergent neurons). The properties of these 51 convergent neurons were further investigated. Most (33/51) received excitatory postsynaptic potentials (EPSPs) after saccular and utricular nerve stimulation. These results implied that most of the convergent neurons in this study additively coded mixed information for vertical and horizontal linear acceleration. Based on the latencies of convergent neurons, we found that an early integration process for vertical and horizontal linear acceleration existed at the second-order level.

Acceleration↗
PubMed2006

Enriched environment exposure regulates excitability, synaptic transmission, and LTP in the dentate gyrus of freely moving rats.

Performance in hippocampus-dependent and other tasks can be improved by exposure to an enriched environment (EE), but the physiological changes in neural function that may mediate these effects are poorly understood. To date, there have been conflicting reports regarding potential mechanisms, such as an increase in basal synaptic transmission, an increase in cell excitability, or altered synaptic plasticity. Here, we reexamined in freely moving animals the conditions under which varying degrees of EE exposure might lead to increases in synaptic or neural function in the dentate gyrus of the hippocampus. Adult male Sprague-Dawley rats were chronically implanted with stimulating and recording electrodes in the perforant path and dentate gyrus, respectively, and housed singly in standard cages. After stable recordings were established for field excitatory postsynaptic potentials (fEPSPs) and population spikes (PSs), the effects of various degrees of periodic novel environment exposure for 19 days were assessed. Exposure to an EE increased fEPSPs, but only when animals were kept in nominally low-stress housing conditions. An increase in granule-cell excitability, as evidenced by PS increases, was induced by all environmental treatments with the greatest effect being induced by overnight EE exposure. EE exposure did not change the level of long-term potentiation (LTP) induced by a moderate high-frequency tetanus, but continued EE exposure post-tetanus produced a significantly faster decay of LTP relative to control animals. These results suggest that, in adult animals, EE exposure may augment hippocampal information processing, but may also speed turnover of information in the hippocampus during the maintenance period.

Animals↗
PubMed2002

Deficit in hippocampal long-term potentiation in monosodium glutamate-treated rats.

Rats subjected to monosodium glutamate (MSG) administration during the neonatal period present chronic neuroendocrine dysfunction associated with marked cognitive deficits. Long-term potentiation (LTP) in the hippocampus provides a model suited for the study of mammalian brain plasticity and memory formation. In the present work, we used the LTP protocol to investigate the synaptic plasticity in the hippocampal CA1 area of adult rats subjected to MSG treatment during the first 10 days of life. Synaptic transmission in CA1 area was analyzed using extracellular field recordings in response to Schaffer's collateral fiber stimulation in hippocampal slices. Animals injected with MSG exhibited a dramatic decrement of LTP field excitatory postsynaptic potentials (fEPSPs) compared to control group. Analysis of percent enhancement of fEPSP slope at 2 min after high frequency stimulation (HFS) increased by 189.3 +/- 33.2% in slices from control rats and 129.45 +/- 18.5% (p < 0.01) in slices from MSG-treated rats. Additionally, MSG-treated animals failed to maintain or consolidate LTP as revealed by a significant reduction in fEPSP slope enhancement over time after HFS. The mean fEPSP slope, 60 min after HFS, was 154.28 +/- 21% of the average baseline slope in control slices versus only 124.4 +/- 15% in MSG-treated rats (p < 0.01). At 90 min after HFS, slices from controls reached a potentiation of 44.5 +/- 2.9%, whereas the MSG group displayed an overall response enhancement of 17.65 +/- 2.7% of basal levels (p < 0.01). These findings indicate that MSG-treated rats display a chronic impairment of CA1 synaptic plasticity.

Aging↗