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PubMed1998

Induction of LTD by increasing extracellular Ca2+ from a low level in the dentate gyrus in vitro.

Long-term depression (LTD) of field excitatory postsynaptic potentials was induced in the medial path of the dentate gyrus in juvenile rats in vitro by a protocol involving returning the Ca2+ concentration of the external media to the control level (2 mM) following a period (30 min) in low Ca2+ (1.2 mM), with stimulation at the test frequency throughout. Directly increasing Ca2+ from the control level did not induce LTD (or long-term potentiation). Such LTD showed mutual occlusion with low frequency stimulation (LFS, 1 Hz, 900 stimuli)-induced LTD. The Ca2+-induced LTD was shown to be induced by the procedure of elevating the Ca2+ from the low to the control concentration, and not by the procedure of lowering of Ca2+, as full amplitude LFS induced LTD could be induced in the low Ca2+ media. Ca2+-induced LTD was inhibited by Ni2+ (25 microM) and 2-amino-5-phosphonopentanoate (50 microM), demonstrating the necessity for activation of T/R-type voltage-gated Ca2+ channels and N-methyl-D-aspartate receptors, respectively.

2-Amino-5-phosphonovalerate↗
PubMed2000

Age- and species-dependent maturation of synaptic transmission in the superficial superior colliculus.

Both neonatal maturity and postnatal maturation are known to be species dependent. For instance, guinea pigs are born with their eyes open, while eye opening takes place 2 weeks after birth in rats. Moreover, several abnormalities have been observed in albino compared to pigmented species. The pigment melanin is proposed to play a protective role and its absence is thought to contribute to neuronal deficits. In the present study, we aimed to investigate functional differences in synaptic transmission in the visual, superficial layers of the superior colliculus (SC) of albino and pigmented rats and pigmented guinea pigs, at eye opening and 1 month after birth. This was achieved by analysing evoked field excitatory postsynaptic potentials (fEPSPs) in vitro, and by investigating the ability of these responses to express gamma-aminobutyric acid (GABA)-induced long-term potentiation (LTPG), an enduring increase in synaptic efficacy resulting from bath application of GABA. Guinea pigs did not show any obvious differences with respect to overall fEPSP characteristics and synaptic plasticity at both ages studied, indicating that maturation must have occurred prenatally. Rats, however, underwent synaptic maturation and refinement to produce stronger fEPSPs and a more robust level of synaptic plasticity 1 month after birth compared to the conditions at eye opening. The state of pigmentation was found to have a crucial influence, with albino rats showing less enhancement of the strength of synaptic transmission in the SC. It can therefore be concluded that profound developmental differences in pre- and postnatal maturation of the superficial SC exist between guinea pigs and rats, and that the state of pigmentation is a crucial factor in this process.

Age Factors↗
PubMedDate not supplied

[The potentiation of postsynaptic potentials under the influence of glutamate and agonists in the motoneurons of the frog Rana ridibunda].

Effects of glutamate and agonists (aspartate, NMDA, quisqualate, AMPA, kainate) on dorsal root and reticulomotoneuronal excitatory postsynaptic potentials (EPSPs), as well as on spontaneous postsynaptic potentials (PSP), were studied in the motoneurons of isolated frog spinal cord. Depolarizing responses were evoked by glutamate or agonists bath application. Amplitude of the response decreased in conditions of TTX-block or replacement of Ca2+ by Mn2+, Mg2+ or Co2+ in perfusing solution. Excitatory amino acid antagonists (kynurenate, CNQX, APV, argiopine) also reduced depolarizing response amplitude. DR and RF EPSPs significantly increased in amplitude (and spontaneous PSP in amplitude and frequency) during depolarization, evoked by glutamate or agonists. The potentiation reached up to 300 %. Potentiation diminished with depolarization decay. Sometimes several minutes depression of EPSPs was observed after the depolarizing response. There was no potentiation of the spontaneous PSPs in conditions of TTX-block or replacement of Ca2+ by Mn2+ in perfusing solution. The data obtained suggest rather presynaptic, than postsynaptic mechanism of the potentiation. We found no depressant effect of glutamate or agonists on postsynaptic glutamate receptors, at least for 10 minutes contact. Effects of more prolonged applications and some changes of EPSP amplitude after depolarizing response appear to be associated with other types of glutamate receptors.

Animals↗
PubMed2005

Functional characterization of des-IGF-1 action at excitatory synapses in the CA1 region of rat hippocampus.

Insulin-like growth factor-1 (IGF-1) and growth hormone play a major role in the growth and development of tissues throughout the mammalian body. Plasma IGF-1 concentrations peak during puberty and decline with age. We have determined that chronic treatments to restore plasma IGF-1 concentrations to adult levels attenuate spatial learning deficits in aged rats, but little is known of the acute actions of IGF-1 in the brain. To this end, we utilized hippocampal slices from young Sprague-Dawley rats to characterize the acute effects of des-IGF-1 on excitatory synaptic transmission in the CA1 region. We observed a 40% increase in field excitatory postsynaptic potential (fEPSP) slope with application of des-IGF-1 (40 ng/ml) and used whole cell patch-clamp recordings to determine that this enhancement was due to a postsynaptic mechanism involving alpha-amino-3-hydroxyl-5-methyl-4-isoxazolepropionate (AMPA) but not N-methyl-D-aspartate receptors. Furthermore, the enhancement was completely blocked by the broad-spectrum tyrosine kinase inhibitor, genistein (220 microM), and significantly reduced by the PI3K blockers wortmannin (1 microM) and 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (10 microM), suggesting that the effect was predominantly dependent on PI3K activation. This characterization of the acute actions of des-IGF-1 at hippocampal excitatory synapses may provide insight into the mechanism by which long-term increases in plasma IGF-1 impart cognitive benefits in aged rats. Increases in AMPA receptor-mediated synaptic transmission may contribute directly to cognitive improvement or initiate long-term changes in synthesis of proteins such as brain-derived neurotrophic factor that are important to learning and memory.

Androstadienes↗
PubMed2003

Long-lasting facilitation by dehydroevodiamine. HClof synaptic responses evoked in the CA1 region of rat hippocampal slices.

We tested the effects of dehydroevodiamine.Cl (DHED) on field excitatory postsynaptic potentials (fEPSPs) evoked by the electrical stimulation of Schaffer collaterals-commissural fibres in the CA1 region of rat hippocampal slices. Bath applications of 10 microM DHED for 20 or 40 min induced long-lasting facilitation of fEPSPs, which outlasted the presence of DHED. A 10 min treatment with a higher concentration (100 microM) also induced long-lasting facilitation. The long-lasting facilitation was blocked either by 10 microM atropine, the muscarinic receptor antagonist, or by 50 microM D-2-amino-5-phosphonopentanoic acid (D-AP5), an NMDA receptor antagonist. These results show that DHED produces long-lasting facilitation of synaptic transmission, and that this facilitation depends upon the activation of both the muscarinic and NMDA receptors.

2-Amino-5-phosphonovalerate↗
PubMed2001

Regeneration of phasic synapses on a crayfish slow muscle following allotransplantation of a mixed phasic-tonic nerve.

Separate phasic or tonic nerves allotransplanted to reinnervate a denervated slow superficial flexor muscle (SFM) in the abdomen of adult crayfish regenerate synaptic nerve terminals with phasic or tonic properties. To test competitive interactions between tonic and phasic axons, we allotransplanted the sixth abdominal ganglion with its third nerve root containing a mixture of phasic and tonic axons onto the denervated SFM. The resulting reinnervation of the SFM was compared to the normal innervation on the contralateral intact SFM, which receives innervation only from tonic motoneurons. Variable sizes of excitatory postsynaptic potentials indicated that 2-3 axons innervated each muscle fiber of the SFM in both the allotransplant and normal preparations. Compared to the normal tonic terminals on the intact contralateral side, the allotransplanted synaptic terminals had more phasic-like properties; specifically, they gave rise to larger synaptic potentials, had a lower mitochondrial content and contained a higher density of active zone dense bars per synapse. Moreover, prolific sprouting of the axons in the regenerated nerve, typical of phasic axons, points to more vigorous regeneration of phasic rather than tonic axons to the denervated SFM. In keeping with this prolific axon sprouting, there was both a much higher density of innervation in the allotransplanted SFM compared to the normal SFM, and a higher frequency of extrasynaptic active zones in regenerated terminals of the mixed nerve compared to those of the tonic nerve. Thus, an allotransplanted mixed nerve regenerates mainly phasic axons and synapses on the slow denervated SFM, demonstrating the instructive nature of the neuron in synapse specification, as well as the permissive nature of the target muscle.

Animals↗
PubMed2005

Role of AMPA receptor desensitization and the side effects of a DMSO vehicle on reticulospinal EPSPs and locomotor activity.

Activation of the vertebrate locomotor network is mediated by glutamatergic synaptic drive, normally initiated by the brain stem. Previous investigations have studied the role of glutamate receptors, especially NMDA receptors, in generating and regulating locomotor pattern generation. Few studies, however, have focused on the role of AMPA receptors in shaping network activity, especially with regard to their rapid desensitization. It is important to determine whether AMPA receptor desensitization plays a role in regulating neuronal network activity. We examined this question on both the network and synaptic levels in the lamprey (Lampetra fluviatilis) spinal cord using a selective and potent inhibitor of AMPA receptor desensitization, cyclothiazide (CTZ). The solvent dimethyl sulfoxide (DMSO) is commonly used to dissolve this drug, as well as many others. Unexpectedly, the vehicle alone already at 0.02%, but not at 0.01%, caused significant increases in excitatory postsynaptic potential (EPSP) amplitudes and NMDA-induced locomotor frequency. The results indicate that DMSO may have a profound influence when used > or = 0.02%, a concentration 10-50 times less than that most commonly used. Subsequently we applied CTZ concentrations < or =10 microM (DMSO < or =0.01%). CTZ (1.25-5 microM) caused an appreciable and significant increase in EPSPs mediated by non-NMDA receptors and in both AMPA- and NMDA-induced locomotor frequency, but no effects on EPSPs mediated by NMDA receptors. From the effects of CTZ it is apparent that AMPA receptor desensitization plays an important role in determining locomotor frequency and that this is likely a result of its limiting function on AMPA receptor-mediated EPSPs.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2005

Analysis and comparison of morphological reconstructions of hippocampal field CA1 pyramidal cells.

Morphological reconstructions have become a routine and valuable tool for neuroscientists. The accuracy of reconstructions is a matter of considerable interest given that they are widely used in computational studies of neural function. Despite their wide usage, comparisons of reconstructions obtained using various methodologies are lacking. We reviewed reconstructions of hippocampal CA1 pyramidal cells from five published studies and found marked differences in some of the most basic measurements. For four of the five studies means of total cell length clustered in the 11,479-13,417-microm range. The remaining study had a significantly larger value for this index at 16,992+/-5,788 microm. Surface area means varied more than 4-fold from 16,074 to 67,102 microm2. Volume means varied more than 8-fold from 3,828 to 30,384 microm3. Simulated passive input resistance means varied from 38.0 to 172.1 MOmega, reflecting the variability in cell dimensions. Estimates of the electrotonic length varied from 1.26 to 1.56. In two reconstructions used in previously published studies, simulated somatic excitatory postsynaptic potentials (EPSPs) varied 2-4-fold in amplitude, time to peak and half-width, for synaptic inputs at similar locations. Substantial jitter on the z-axis was identified as one likely source of the discrepancy in total cell length, while substantial differences in diameter measurements across studies, and sometimes within the same study, accounted for the variability in surface area and volume. While some part of the observed variability is surely due to the diversity of CA1 pyramidal cells, our analysis suggests that a substantial portion stemmed from methodological inconsistencies and from technological limitations. Suggestions are made for improving the quality and usefulness of morphological reconstructions. We conclude that reconstructions across studies have substantial variability in measures that are very relevant to neuronal function. Consequently, modelers are advised to use more than just one reconstructed cell in their simulations of neural function.

Animals↗
PubMed2003

Ionic currents underlying rhythmic bursting of ventral mossy cells in the developing mouse dentate gyrus.

The electrophysiological properties of mossy cells were examined in developing mouse hippocampal slices using whole-cell patch-clamp techniques, with particular reference to the dorsoventral difference. Dorsal mossy cells exhibited a higher spontaneous excitatory postsynaptic potential (EPSP) frequency and larger maximal EPSP amplitude than ventral mossy cells. On the other hand, the blockade of synaptic inputs with glutamatergic and GABAergic antagonists disclosed a remarkable dorsoventral difference in the intrinsic activity: none (0/27) of the dorsal mossy cells showed intrinsic bursting, whereas the majority (35/47) of the ventral mossy cells exhibited intrinsic rhythmic bursting. To characterize the ionic currents underlying the rhythmic bursting of mossy cells, we used somatic voltage-clamp recordings in the subthreshold voltage range. Ventral bursting cells possessed both hyperpolarization-activated current (Ih) and persistent sodium current (INaP), whereas dorsal and ventral nonbursting cells possessed Ih but no INaP. Blockade of Ih with cesium did not affect the intrinsic bursting of ventral mossy cells. In contrast, the blockade of INaP with tetrodotoxin or phenytoin established a stable subthreshold membrane potential in ventral bursting cells. The current-voltage curve of ventral bursting cells showed a region of tetrodotoxin-sensitive negative slope conductance between -55 mV and a spike threshold ( approximately -45 mV). On the other hand, no subthreshold calcium conductances played a significant role in the intrinsic bursting of ventral mossy cells. These observations demonstrate the heterogeneous electrophysiological properties of hilar mossy cells, and suggest that the subthreshold INaP plays a major role in the intrinsic rhythmic bursting of ventral mossy cells.

2-Amino-5-phosphonovalerate↗
PubMed2004

Altered hippocampal short-term plasticity and associative memory in synaptotagmin IV (-/-) mice.

Synaptotagmin IV (Syt IV) is an activity-inducible, secretory vesicle protein that is thought to function as an inhibitor of neurotransmitter release (Littleton et al. Nature 400:757-760, 1999). To test this hypothesis in neurons of the mammalian CNS, we measured field excitatory postsynaptic potentials (fEPSPs) in hippocampal slice preparations from Syt IV (-/-) mice. At Schaffer collateral synapses, the basal properties of neurotransmission are largely normal. However, two forms of short-term plasticity, paired-pulse facilitation (PPF) and post-tetanic potentiation (PTP), are significantly enhanced in area CA1 of Syt IV (-/-) slices. Similarly, the early stages of long-term potentiation (LTP) are also enhanced at these synapses. Consistent with the low levels of Syt IV observed in dentate granule cells, the mossy fiber synapses in Syt IV (-/-) slices display largely normal PPF and LTP. In addition, we find that Syt IV (-/-) mice have deficits in the associative passive avoidance memory paradigm, but are normal in the novel object recognition paradigm. The synaptic architecture and connectivity of Syt IV (-/-) brains is indistinguishable from wild-type mice as indicated by immunohistochemical analysis. These results suggest Syt IV is a presynaptic negative regulator of short-term plasticity in area CA1 of the hippocampus and is required for some, but not all, forms of hippocampus-dependent memory.

Animals↗
PubMed2002

Neuronal hyperexcitability induced by repeated brief episodes of hypoxia in rat hippocampal slices: involvement of ionotropic glutamate receptors and L-type Ca(2+) channels.

Repeated exposures of rat hippocampal slices to short episodes of hypoxia induce a sustained decrease in the threshold of the development of stimulus-evoked epileptiform discharges in CA1 pyramidal neurons. We have previously demonstrated that the K(+)(o)-induced hyperexcitability required functional L-type voltage-dependent Ca(2+) channels and NMDA-receptors, but was independent of AMPA/kainate-receptor activation. As hypoxia/ischaemia can lead to increased K(+)(o), the epileptiform activity observed after exposure to these challenges could also result from high K(+)(o). The purpose of this study was: (i) to determine whether ionotropic glutamate receptors and L-type Ca(2+) channels are involved in the development of epileptiform activity induced by repeated exposures of hippocampal slices to hypoxia; and (ii) to compare the properties of hypoxia- and high K(+)(o)-induced hyperexcitability. Population spike of presynaptic fibres with field excitatory postsynaptic potential from the stratum radiatum, and population spike of CA1 pyramidal neurons from the stratum pyramidale, were recorded simultaneously in the CA1 area of rat hippocampal slices in response to electrical stimulation of the Schaffer collateral/commissural fibres. Repeated, brief hypoxic episodes induced a sustained decrease in the threshold for development of evoked epileptiform discharges that was associated with long-term potentiation of the CA3-CA1 synapses, but without EPSP-spike potentiation (i.e. in contrast to high K(+)(o)-induced hyperexcitability). The selective antagonist of NMDA receptors, D-APV (25 microM), and the selective blocker of L-type Ca(2+) channels, nifedipine (10 microM) depressed the development of hypoxia-induced hyperexcitability. However, in contrast to high K(+)(o)-induced hyperexcitability, hypoxia-induced hyperexcitability was also blocked by the AMPA/kainite-receptor antagonist, CNQX (5 microM). The present findings confirm that repeated, brief episodes of hypoxia, like exposure to high extracellular K(+), can induce a pro-epileptic state in the CA1 neuronal network, but that the mechanisms leading to hyperexcitability are different for the two stimuli.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2006

Spike-timing-dependent plasticity at resting and conditioned lateral perforant path synapses on granule cells in the dentate gyrus: different roles of N-methyl-D-aspartate and group I metabotropic glutamate receptors.

We examined the mechanisms underlying spike-timing-dependent plasticity induction at resting and conditioned lateral perforant pathway (LPP) synapses in the rat dentate gyrus. Two stimulating electrodes were placed in the outer third of the molecular layer and in the granule cell layer in hippocampal slices to evoke field excitatory postsynaptic potentials (fEPSPs) and antidromic field somatic spikes (afSSs), respectively. Long-term potentiation (LTP) of LPP synapses was induced by paired stimulation with fEPSP preceding afSS. Reversal of the temporal order of fEPSP and afSS stimulation resulted in long-term depression (LTD). Induction of LTP or LTD was blocked by D,L-2-amino-5-phosphonopentanoic acid (AP5), showing that both effects were N-methyl-D-aspartate receptor (NMDAR)-dependent. Induction of LTP was also blocked by inhibitors of calcium-calmodulin kinase II, protein kinase C or mitogen-activated/extracellular-signal regulated kinase, suggesting that these are downstream effectors of NMDAR activation, whereas induction of LTD was blocked by inhibitors of protein kinase C and protein phosphatase 2B. At LPP synapses previously potentiated by high-frequency stimulation or depressed by low-frequency stimulation, paired fEPSP-afSS stimulation resulted in 'de-depression' at depressed LPP synapses but had no effect on potentiated synapses, whereas reversal of the temporal order of fEPSP-afSS stimulation resulted in 'de-potentiation' at potentiated synapses but had no effect on depressed synapses. Induction of de-depression and de-potentiation was unaffected by ap5 but was blocked by 2-methyl-6-(phenylethynyl) pyridine hydrochloride, a group I metabotropic glutamate receptor blocker, showing that both were NMDAR-independent but group I metabotropic glutamate receptor-dependent. In conclusion, our results show that spike-timing-dependent plasticity can occur at both resting and conditioned LPP synapses, its induction in the former case being NMDAR-dependent and, in the latter, group I metabotropic glutamate receptor-dependent.

Animals↗
PubMed1988

Norepinephrine decreases synaptic inhibition in the rat hippocampus.

The effects of norepinephrine (NE) on inhibitory synaptic potentials were studied on CA1 pyramidal neurons in the hippocampal slice in vitro. Norepinephrine caused the appearance of multiple population spikes in the CA1 region of the hippocampal slice, reminiscent of the actions of gamma-aminobutyric acid (GABA) antagonists. Intracellular recording revealed that NE causes a marked and reversible reduction in inhibitory postsynaptic potentials (IPSPs) recorded in CA1 pyramidal cells. This reduced IPSP results in a larger intracellular excitatory postsynaptic potential (EPSP), which can cause the cell to fire more than one action potential. This disinhibitory effect of NE appears to be mediated by an alpha-receptor, and occurs at a site presynaptic to the pyramidal cell, since NE does not change the reversal potential of the IPSP nor does it affect the amplitude or the reversal potential of iontophoretic GABA responses. In addition to reducing evoked IPSPs, NE causes an increase in the frequency of spontaneous IPSPs, suggesting that inhibition of interneuronal firing may not account for this disinhibitory action of NE.

Action Potentials↗
PubMed1989

Postnatal development of GABA-mediated synaptic inhibition in rat hippocampus.

Developmental alterations in GABAergic synaptic transmission were examined physiologically and biochemically in hippocampus of rats from 3 days of age to adulthood. Neither antidromic nor orthodromic stimulation could elicit identifiable inhibitory postsynaptic potentials in CA1 neurons in slices from rats 5 or 6 days of age. In contrast, at this age these stimuli result in large inhibitory postsynaptic potentials in CA3 pyramidal cells. In the latter cells orthodromic stimulation produced a brief monosynaptic excitatory postsynaptic potential which was followed by a large prolonged biphasic hyperpolarization. These signals were strikingly similar to those recorded in 1-month-old rats. In addition, large recurrent inhibitory postsynaptic potentials were produced by antidromic stimulation. By postnatal day 9 similar inhibitory postsynaptic potentials could be elicited in a majority of neurons of the CA1 subfield. As in mature pyramidal cells, application of GABA antagonists, such as bicuculline, selectively eliminated the antidromic inhibitory postsynaptic potential and the first component of the biphasic inhibitory postsynaptic potential generated by stimulation of stratum radiatum. In the CA3 subfield, this blockade of GABA receptors resulted in prolonged afterdischarges in slices from immature but not month-old rats. Measurements of the equilibrium potential and the conductance of antidromic inhibitory postsynaptic potentials in CA3 neurons were very similar when made during the first postnatal week and at 1 month of age. While on days 10-11 the equilibrium potential was very similar to measurements made at these other ages, the conductance was 3-4 times greater. The activity of glutamate decarboxylase, the synthetic enzyme for GABA, was very low at 3 days in hippocampus, and increased until 30 days of age at which time adult values were obtained. By comparison, hippocampal GABA levels were high early in postnatal life. Glutamate decarboxylase activities in microdissected CA3 and CA1 subfields were similar in immature hippocampus. These results demonstrate dramatic differences in the ontogenesis of functional GABAergic inhibitory synaptic transmission in the CA1 and CA3 subfields of rat hippocampus. The late development of GABA-mediated synaptic inhibition in the CA1 subfield could play a role in the susceptibility of immature hippocampus to seizures. However, the large GABA-mediated inhibitory postsynaptic potentials present in the CA3 subfield at the same age have a critical role in dampening neuronal excitability.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMedDate not supplied

The GluR5 subtype of kainate receptor regulates excitatory synaptic transmission in areas CA1 and CA3 of the rat hippocampus.

Activation of kainate receptors depresses excitatory synaptic transmission in the hippocampus. In the present study, we have utilised a GluR5 selective agonist, ATPA [(RS)-2-amino-3-(3-hydroxy-5-tert-butylisoxazol-4-yl)propanoic acid], and a GluR5 selective antagonist, LY294486 [(3SR,4aRS,6SR,8aRS)-6-([[(1H-tetrazol-5-y l)methyl]oxy]methyl)-1,2,3,4,4a,5,6,7,8,8a-decahydroisoquinoline-3 -carboxylic acid], to determine whether GluR5 subunits are involved in this effect. ATPA mimicked the presynaptic depressant effects of kainate in the CA1 region of the hippocampus. It depressed reversibly AMPA (alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) receptor-mediated field excitatory postsynaptic potentials (field EPSPs) with an IC50 value of approximately 0.60 microM. The dual-component excitatory postsynaptic current (EPSC) and the pharmacologically isolated NMDA (N-methyl-D-aspartate) receptor-mediated EPSC were depressed to a similar extent by 2 microM ATPA (61 +/- 7% and 58 +/- 6%, respectively). Depressions were associated with an increase in the paired-pulse facilitation ratio suggesting a presynaptic locus of action. LY294486 (20 microM) blocked the effects of 2 microM ATPA on NMDA receptor-mediated EPSCs in a reversible manner. In area CA3, 1 microM ATPA depressed reversibly mossy fibre-evoked synaptic transmission (by 82 +/- 10%). The effects of ATPA were not accompanied by any changes in the passive properties of CA1 or CA3 neurones. However, in experiments where K+, rather than Cs+, containing electrodes were used, a small outward current was observed. These results show that GluR5 subunits comprise or contribute to a kainate receptor that regulates excitatory synaptic transmission in both the CA1 and CA3 regions of the hippocampus.

Animals↗
PubMed1998

Generation of theta and gamma rhythms in the hippocampus.

In the behaving rat, theta rhythm was dominant during walking and rapid-eye-movement sleep, while irregular slow activity predominated during immobility and slow-wave sleep. Oscillatory evoked potentials of 20-50 Hz and spontaneous fast (gamma) waves were more prominent during theta compared with non-theta behaviors. The oscillations were simulated by a systems model with recurrent inhibition. The model also predicts a behaviorally dependent inhibition, which was confirmed experimentally using paired-pulse responses. Paired-pulse facilitation (PPF) of the population spikes in CA1 was larger during walking than immobility, mostly mediated by a cholinergic input. Spike responses in vitro were characterized by a relative lack of inhibition or disinhibition compared with the behaving rat. The two-input, two-dipole model of the theta rhythm in CA1 is reviewed. Afferents to the CA1 pyramidal cells are assumed to be rhythmic and consist of atropine-sensitive and atropine-resistant inputs driving the somata and distal dendrites, respectively. The atropine-sensitive theta rhythm was mainly caused by a series of Cl- mediated inhibitory postsynaptic potentials (IPSPs) on pyramidal cells. It is suggested that previous claims of the participation of excitatory postsynaptic potentials (EPSPs) and not IPSPs in the intracellular recordings in vivo were flawed. Single cell recordings in vitro suggested that intrinsic voltage-dependent membrane potential oscillations modulate the response to a theta-frequency driving. Membrane potentials of pyramidal cells in vitro showed resonance in the theta frequency range.

Animals↗
PubMed2006

Ileitis alters neuronal and enteroendocrine signalling in guinea pig distal colon.

BACKGROUND AND AIMS: Intestinal inflammation alters neuronal and enteroendocrine signalling, leading to functional adaptations in the inflamed bowel. Human studies have reported functional alterations at sites distant from active inflammation. Our aims were to determine whether neuronal and enteroendocrine signalling are altered in the uninflamed colon during ileitis. METHODS: We used neurophysiological, immunohistochemical, biochemical and Ussing chamber techniques to examine the effect of 2,4,6-trinitrobenzene sulphonic acid (TNBS)-induced ileitis on the properties of submucosal neurones, enteroendocrine cells and epithelial physiology of the distal colon of guinea pigs. RESULTS: Three days after TNBS administration, when inflammation was restricted to the ileum, the properties of colonic enteric neurones were altered. Submucosal AH neurones were hyperexcitable and had reduced after hyperpolarisations. S neurones received larger fast and slow excitatory postsynaptic potentials, due to an increase in non-cholinergic synaptic transmission. Despite the absence of inflammation in the colon, we found increased colonic prostaglandin E(2) content in animals with ileitis. Ileitis also increased the number of colonic 5-hydroxytryptamine (5-HT)- and GLP-2-immunoreactive enteroendocrine cells. This was accompanied by an increase in stimulated 5-HT release. Functional alterations in epithelial physiology occurred such that basal short circuit current was increased and veratridine-stimulated ion transport was reduced in the colon of animals with ileitis. CONCLUSION: Our data suggest that inflammation at one site in the gut alters the cellular components of enteric reflex circuits in non-inflamed regions in ways similar to those at sites of active inflammation. These changes underlie altered function in non-involved regions during episodes of intestinal inflammation.

Animals↗
PubMed1994

Age-dependent long-term potentiation of inhibitory synaptic transmission in rat visual cortex.

Long-term potentiation (LTP) of inhibitory synaptic transmission in rat visual cortex was investigated using intracellular recording in slice preparations. The inhibitory postsynaptic potential (IPSP) of layer V cells evoked monosynaptically by layer IV stimulation was recorded while excitatory postsynaptic potentials (EPSPs) were blocked by adding NMDA and non-NMDA receptor antagonists to the perfusate. Separate presynaptic fiber groups were activated by two stimulating electrodes placed in layer IV. One electrode was used to test the effect of conditioning stimulation; the other served as a control. Trains of high-frequency stimulation (50 Hz, 1 sec) were applied at an interval of 10 sec as a conditioning stimulation. The LTP of IPSP induced by the conditioning stimulation had properties similar to those known for LTP of EPSP in hippocampal CA1: (1) it was specific to the conditioned pathway; (2) repetitive application of the conditioning stimulation saturated the LTP; (3) LTP was induced by conditioning stimulation at intensities higher than a threshold; (4) weak conditioning stimulation to one pathway, which alone failed to induce LTP, induced associative LTP when strong conditioning stimulation was simultaneously applied to the other pathway; (5) weak conditioning stimulation sometimes induced short-term potentiation. In contrast to these similarities, LTP of IPSP was induced by a wider range of stimulus frequencies than that capable of generating LTP of EPSPs in CA1. It was induced not only by a brief high-frequency stimulation but also by an intermediate-frequency (2 Hz) stimulation continued for 5 min. In addition, the LTP induction was not dependent on postsynaptic membrane potential. Finally, the LTP of IPSP was more easily induced in developing than in mature rats. This age dependence suggests that LTP of IPSPs may contribute to the improvement of response selectivity of visual cortical cells through visual experience during postnatal development.

Aging↗