Rat Kindling Model Of Epilepsy Research Articles

Effect of adenovirus-mediated overexpression of PTEN on brain oxidative damage and neuroinflammation in a rat kindling model of epilepsy.

Background:Epilepsy is a chronic and severe neurological disorder. Phosphatase and tensin homolog deleted on chromosome ten (PTEN)-deficient mice exhibit learning and memory deficits and spontaneous epilepsy. The aim of this study was to investigate the role of PTEN in brain oxidative damage and neuroinflammation in a rat model of epilepsy.Methods:An adenovirus (Ad)-PTEN vector was constructed, and status epilepticus (SE) was induced in 41 model rats using lithium chloride-pilocarpine. Thirty-six SE rats were then allocated into the Ad-PTEN, Ad-LacZ, and SE groups, those were administered intracerebroventricular injections of Ad-PTEN, Ad-enhanced green fluorescent protein, and phosphate buffer saline, respectively. The normal group was comprised of healthy Sprague-Dawley rats. Nissl staining was conducted to evaluate neuronal damage, and immunohistochemistry was conducted to observe the morphology of cells in the hippocampal CA1 region and the distribution of ionized calcium-binding adaptor molecule 1 (Iba1) and ED1 (rat homologue of human CD68). Levels of apoptosis-related proteins, inflammatory-related factors, and oxidative stress-related markers (reactive oxygen species [ROS], glutathione [GSH], superoxide dismutase [SOD], and malondialdehyde [MDA]) were measured. Comparisons between multiple groups were conducted using one-way analysis of variance (ANOVA), and pairwise comparisons after ANOVA were conducted using the Tukey multiple comparisons test.Results:After SE induction, PTEN expression in the rat brain exhibited a four-fold decrease (P = 0.000) and the expression of both Iba1 and ED1 increased. Furthermore, significant neuronal loss, oxidative damage, and neuroinflammation were observed in the SE rat brain. After intracerebroventricular injection of Ad-PTEN, PTEN expression exhibited a three-fold increase (P = 0.003), and the expression of both Iba1 and ED1 decreased. Additionally, neurons were restored and neuronal apoptosis was inhibited. Furthermore, ROS and MDA levels decreased, GSH level and SOD activity increased, and neuroinflammation was reduced.Conclusion:Our study demonstrated that brain oxidative damage and neuroinflammation in SE rats were ameliorated by intracerebroventricular injection of Ad-PTEN.

Influence of Xingnaojing Injection on the Expression of c-fos and c-jun Proteins in Brains of Rats in a Kindling Model of Epilepsy Chronically Induced by Pentetrazol

Objective: To investigate the molecular biological mechanism of the antiepileptic effect of Xingnaojing (XNJ) injection on a rat kindling model of epilepsy (KME). Methods: Fifty healthy 6-week-old male Sprague-Dawley rats were divided into the following five groups: blank control (BC) group, model (M) group, XNJ injection (XI) group, phenobarbital injection (PI) group and XNJ combined with phenobarbital (XP) group. There were 10 rats in each group. The intervention drugs were administered 30 min before the model-building drugs once a day for 5 weeks. The model-building drug pentetrazol was given to each group as an intraperitoneal injection 30 min after the use of the intervention drug once a day for 4 weeks for KME establishment (except for the BC group). The BC group was given physiological saline instead. All drugs were injected intraperitoneally. The behaviors of each group of rats were observed after the use of the model-building drugs for 1 h every day. The last kindling test was carried out at the end of week 5. Then, c-fos and c-jun protein expressions in the rat brains of each group were observed and analyzed by immunohistochemistry at the end of the experiment. Results: There was a large number of cells positive for the c-fos and c-jun proteins in the rat brains of the M group. Compared with the M group, the expression level of the c-fos and c-jun proteins was lower in the rat brains of the XI and PI groups (p < 0.01). There was no statistical difference between the XI and PI groups (p > 0.05). The number of positive cells in the rat brains of the XP group was even smaller than that of the XI or PI groups. Conclusion: The antiepileptic effect of the XNJ injection on the rat KME is probably related to its interruption function on the expression of the c-fos and c-jun proteins in rat brains.

Suppression of fully kindled seizure and retardation of kindling acquisition by YM928 in the rat kindling model of epilepsy

We investigated the effects of 2-[ N-(4-chlorophenyl)- N-methylamino]-4 H-pyrido[3.2-e]-1,3-thiazin-4-one (YM928), a selective α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor antagonist, in the rat kindling model of complex partial seizures. YM928 (10 and 30 mg/kg p.o.) markedly suppressed the motor seizures and afterdischarge induced by electrical stimulation of the amygdala at generalized seizure-triggering threshold intensity. YM928 (10 mg/kg p.o.) did not induce apparent abnormal behavior, but did induce sedation at a dose of 30 mg/kg p.o. YM928 (30 mg/kg p.o.) showed a similar anticonvulsant effect at twice the threshold intensity as it did at threshold intensity. Diazepam (10 mg/kg p.o.) and phenobarbital (60 mg/kg p.o.) also exerted anticonvulsant activities. Diazepam (10 mg/kg) showed a similar effect at twice the threshold as at threshold, but the anticonvulsant effect of phenobarbital (60 mg/kg p.o.) was reversed when the stimulus was doubled. When YM928 (10 mg/kg p.o.) was administered 60 min before daily stimulation of the amygdala, the development of kindling seizure was significantly retarded. These results indicate that YM928 has anticonvulsant effects and suppresses kindling acquisition without sedative effects, and may be suitable as an antiepileptic drug for the treatment of complex partial seizures in humans.

Seizure suppression by adenosine-releasing cells is independent of seizure frequency.

Intraventricular cellular delivery of adenosine was recently shown to be transiently efficient in the suppression of seizure activity in the rat kindling model of epilepsy. We tested whether the suppression of seizures by adenosine-releasing grafts was independent of seizure frequency. Adenosine-releasing cells were encapsulated and grafted into the lateral brain ventricle of rats kindled in the hippocampus. During 4 weeks after grafting, electric test stimulations were delivered at a frequency of either once a week or 3 times per week. Seizure activity was evaluated by visual scoring of seizure severity and by the recording of EEGs. Adenosine released from encapsulated cells exerted potent antiepileptic activity for >/=2 weeks. One week after grafting, treated rats displayed a complete protection from clonic seizures, and a protection from focal seizures was observed in the majority of animals. Seizure suppression was accompanied by a reduction of afterdischarges in EEG recordings. The protective efficacy of the grafted cells was the same irrespective of whether electrical test stimulations were delivered 1 or 3 times per week. Rats receiving control grafts continued to display full clonic convulsions. This study demonstrated that the frequency of test stimulations did not influence the seizure-suppressive potential of adenosine-releasing grafts. Thus the local delivery of adenosine is likely to be effective in seizure control over a threefold range of seizure-discharge frequency.

The insular but not the perirhinal cortex is involved in the expression of fully-kindled amygdaloid seizures in rats

We have previously reported an important excitatory role of the perirhinal cortex (PRC) in rat kindling development using an immunohistochemistry technique. In this study, we investigated the roles of the PRC and the insular cortex (INS) located rostral to the PRC, in fully-kindled amygdaloid seizures, using a microinjection technique in the rat kindling model of epilepsy. Following the establishment of daily kindling, we investigated the effects of microinjections of procaine hydrochloride, 2-amino-5-phosphonovalerate (APV; an N-methyl- d-aspartate (NMDA) receptor antagonist) and 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(f)-quinoxaline (NBQX; an α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA) receptor antagonist). Microinjections of these drugs into the ipsilateral PRC did not suppress kindled seizures. The possibility is that the process of kindling development forms novel seizure-generalization pathways that do not require further activation of the PRC. On the other hand, procaine and APV injected into the ipsilateral INS significantly suppressed kindled seizures. The manner of suppression appeared to be ‘all or none’. It is therefore possible that at least the activation of NMDA receptors in the INS is necessary to express generalized kindled amygdaloid seizures.

Increases in mRNA levels for Tα1-tubulin in the rat kindling model of epilepsy

The expression of mRNA for Tα1-tubulin, a cytoskeletal protein, was studied in the rat kindling model of epilepsy. The Tα1-tubulin mRNA level increased significantly in the dentate gyrus (DG) and CA3 of hippocampus ipsilateral to stimulation from 8 h to 4 weeks after amygdaloid kindled seizures. The peak increase was observed at 1 week after the last seizures both in the DG and CA3. These results suggest that the microtubule formation contributes to synaptic remodeling and reorganization of neural networks, which may be based on the kindling-inducing epileptogenesity.

Anticonvulsant and proconvulsant effects of tramadol, its enantiomers and its M1 metabolite in the rat kindling model of epilepsy.

1. The centrally acting analgesic tramadol has recently been reported to cause seizures at re-commended dosages in patients, whereas animal experiments had indicated that seizures only occur in high, toxic doses. Tramadol has a dual mechanism of action that includes weak agonistic effects at the mu-opioid receptor as well as inhibition of monoamine (serotonin, norepinephrine) re-uptake. Its major (M1) metabolite mono-O:-desmethyltramadol, which is rapidly formed in vivo, has a markedly higher affinity for mu receptors and may thus contribute to the effects of the parent compound. Furthermore, the pharmacological effects of tramadol appear to be related to the different, but complementary and interactive pharmacologies of its enantiomers. In the present study, we evaluated (+/-)-tramadol, its enantiomers, and its M1 metabolite ((+)-enantiomer) in the amygdala kindling model of epilepsy in rats. Adverse effects determined in kindled rats were compared to those in nonkindled rats. 2. At doses within the analgesic range, (+/-)-tramadol and its enantiomers induced anticonvulsant effects in kindled rats. However, at only slightly higher doses seizures occurred. With (+/-)-tramadol, generalized seizures were observed at 30 mg kg(-1) in most kindled but not in nonkindled rats. The (-)-enantiomer induced myoclonic seizures at 30 mg kg(-1) in most kindled but not in nonkindled rats, although myoclonic seizure activity was observed in some nonkindled rats at 10 or 20 mg kg(-1). Seizures were also observed after the (+)-enantiomer and the (+)-enantiomer of the M1 metabolite, but experiments with higher doses of these compounds were limited by marked respiratory depression. 3. The data demonstrate that kindling enhances the susceptibility of rats to convulsant adverse effects of tramadol and its enantiomers, indicating that a preexisting lowered seizure threshold increases the risk of tramadol-induced seizures.

Increment of synapsin I immunoreactivity in the hippocampus of the rat kindling model of epilepsy.

Synapsin is a vesicle-associated protein that is thought to be involved in synaptogenesis and neurotransmitter release. In this study, we investigated the repeated amygdala kindling-induced changes in levels of synapsin I, a marker of enhanced synaptic activity, using immunohistochemistry. Eight hours after the last seizure, synapsin I immunoreactivity (IR) was increased bilaterally in the polymorphic zone of the dentate gyrus, the hilus and the stratum lucidum in area CA3 of the hippocampus. However, 4 weeks after the last kindled seizures, synapsin I IR was not significantly changed in any of the brain regions studied. Therefore, the increased levels of synapsin I protein observed in these brain regions early after the last seizure may reflect the plastic changes that occur in the specific neural networks of the hippocampus directly after kindling-induced seizure activity.

Effect of dipotassium clorazepate on amygdaloid-kindling and comparison between amygdaloid- and hippocampal-kindled seizures in rats

We examined the effect of dipotassium clorazepate (7-chloro-1,3-dihydro-2-oxo-5-phenyl-1 H-1, 4-benzodiazepine-3-carboxylate potassium hydroxide), an antianxiety drug, on amygdaloid kindling and compared its effects for 7 successive days on amygdaloid- versus hippocampal-kindled seizures, using the rat kindling model of epilepsy. Dipotassium clorazepate at 5 mg/kg significantly delayed amygdaloid kindling. The contralateral cortical after-discharge duration in the dipotassium clorazepate-treated group was significantly shorter than the after-discharge duration in the amygdala in the first seven stimulations, whereas it was significantly shorter only in the first three stimulations in the control group, indicating that dipotassium clorazepate suppressed the spread of seizure activity from focus to contralateral cortex. Dipotassium clorazepate suppressed amygdaloid-kindled seizures at 2 and 5 mg/kg, while 1 mg/kg or more suppressed hippocampal-kindled seizures. Thus, differences in effective dosages in both amygdaloid- and hippocampal-kindled seizures may suggest a difference in the neuronal mechanisms involved in this kindling.

Action of the selective 5-HT4 receptor antagonist SB 204070A in the rat kindling model of epilepsy

Although there has been increasing evidence that the serotonin (5-HT) system plays an important role in regulating clinical and experimentally-induced seizures, no studies have examined the direct action of agents modulating 5-HT4 receptors in seizure models. The present study assessed the effects of the potent and selection 5-HT4 receptor antagonist, (1-butyl-4-piperidinylmethyl)-8-amino-7-chloro-1,4-benzodioxan-5-carboxylate hydrochloride (SB 204070A), on kindled seizures and on the kindling development originating from the rat amygdala. A subcutaneous injection of 1 mg/kg SB 204070A significantly reduced the duration of bilateral forelimb clonus of fully amygdala-kindled seizures. In contrast, daily treatment with SB 204070A at the same dose prior to each electrical stimulation produced no significant effects on behavioral or electrographic seizure development, although the duration of bilateral forelimb clonus of the first generalized seizure was significantly reduced. These results suggest that blockade of 5-HT4 receptors can inhibit the expression of kindled generalized seizures, but not the developmental seizure process of kindling.

Action of the selective 5‐HT4 receptor antagonist SB 204070A in the rat kindling model of epilepsy

Action of the selective 5‐HT4 receptor antagonist SB 204070A in the rat kindling model of epilepsy

Increases in mRNA levels for synapsin I but not synapsin II in the hippocampus of the rat kindling model of epilepsy

We studied brain synapsin I and II mRNA levels using the amygdala kindling model of epilepsy. There were significant increases in the synapsin I mRNA level in the granule cell layer of the hippocampal bilateral dentate gyrus. One to 8 h after seizures, the level in the dentate gyrus ipsilateral to stimulation increased by 44.2-73.2%, compared with the control level. Of the time points investigated, the greatest increase in expression was observed 8 h after the kindled seizures. Furthermore, the synapsin I mRNA levels in the dentate gyrus contralateral to stimulation increased by 28.0% and 51.1%, 2 and 8 h, respectively, after the kindled seizures. Expression of this mRNA, however, did not change significantly in other areas examined, including CA1, CA2, CA3 and the polymorphic layer of the hippocampus and the perirhinal and temporal cortices. Synapsin II mRNA levels did not change significantly in any of the regions studied for up to 24 h after the seizures and synapsin II was presumed to have little involvement in kindling. We considered the locally elevated synapsin I mRNA levels in the bilateral dentate gyrus associated with kindling indicate that excitatory changes occur in the synaptic circuit in which the dentate granule cells participate. Synapsin I may be involved in the presynaptic molecular mechanisms underlying the neuronal plasticity in kindling.

Effects of the 5-HT 3 receptor agonist 1-( m-chlorophenyl)-biguanide in the rat kindling model of epilepsy

This study assessed the action of the serotonin 3 (5-HT 3) receptor agonist, 1-( m-chlorophenyl)-biguanide ( m-CPBG), against both kindled seizures and kindling development from the rat amygdala (AM). The intracerebroventricular (i.c.v.) administration of 40 μg m-CPBG significantly increased the duration of afterdischarge and bilateral forelimb clonus of generalized kindled seizures. In addition, daily i.c.v. treatment with m-CPBG at the same dose prior to each electrical stimulation to the AM significantly facilitated behavioral and electrographic seizure development and reduced the number of stimulations needed to elicit generalized seizures. The present results indicate that m-CPBG increases the duration of fully kindled seizures and facilitates the developmental seizure process, suggesting an excitatory role of 5-HT 3 receptors in the kindling model of epilepsy.

The Anticonvulsant Effect of Deprenyl on Pentylenetetrazol-Induced Seizures in Lewis Rats

There is recent evidence that deprenyl may have anticonvulsant action in a rat kindling model of epilepsy as well as in a maximal electroshock model. We therefore investigated the effect of deprenyl on the brain sensitivity threshold to pentylenetetrazol (PTZ)-induced maximal seizures in Lewis rats, in a model that provides pharmacodynamic information free of pharmacokinetic interference. The novel finding of this investigation was the anticonvulsant effect of deprenyl following repetitive administration whereas a single deprenyl dose did not affect the PTZ concentrations required to induce maximal seizures. The data suggests that the mechanism of this effect is not associated with the dopaminergic activity of deprenyl since pretreatment with both bromocriptine (a dopamine D2 agonist) and haloperidol (dopamine antagonist) did not affect the seizure threshold, whereas levodopa caused a proconvulsant effect. It was also concluded that the mechanism is not related to changes in acetylcholine levels since prolonged pretreatment with deprenyl did not attenuate the brain sensitivity to pilocarpine-induced seizures. The fact that long term administration of deprenyl was needed to produce its anticonvulsant effect may indicate that the anticonvulsant effect of deprenyl may be due to changes in levels of certain endogenous compounds or down or up-regulation of relevant receptor/ effector units.

Anticonvulsant Effects of Tigabine, a New Antiepileptic Drug: The Profile of Action in the Rat Kindling Model of Epilepsy.

Anticonvulsant Effects of Tigabine, a New Antiepileptic Drug: The Profile of Action in the Rat Kindling Model of Epilepsy.

Biphasic action of the histamine precursor l-histidine in the rat kindling model of epilepsy

The effects of the histamine precursor, l-histidine, were examined in the rat kindling model of epilepsy. The intraperitoneal (i.p.) administration of 800 mg/kg l-histidine significantly prolonged the latency to the onset of bilateral forelimb clonus of previously kindled seizures from the amygdala (AM), with no significant effect observed in the behavioral seizure stage or afterdischarge duration. In contrast, daily administration of l-histidine at the same dose prior to each electrical stimulation to the AM significantly facilitated both behavioral and electrographic seizure development of kindling. The present results indicate that although l-histidine can suppress secondary generalization of AM-kindled seizures, it possesses a facilitatory effect on the acquisition of kindling epileptogenesis, suggesting a biphasic action of histamine in kindling.

Antiepileptogenic and anticonvulsant effects of NBQX, a selective AMPA receptor antagonist, in the rat kindling model of epilepsy

To investigate the role of non-NMDA receptors in epileptic seizures, we examined the antiepileptogenic and anticonvulsant effects of NBQX (2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)-quinoxaline), a potent and selective AMPA receptor antagonist, in the rat kindling model. Systemic administration of 10–40 mg/kg NBQX significantly and dose dependently suppressed previously kindled seizures from the amygdala (AM), assessed in terms of the motor seizure stage and afterdischarge (AD) duration. The maximal effects were observed at 0.5–1 h after drug injection. When the intensity of electrical stimulation was increased to twice the generalized seizure-triggering threshold (GST), the anticonvulsant effects of NBQX on AM-kindled seizures were not reversed, suggesting that the effects were not due to non-specific elevation of the GST. In contrast to AM-kindled seizures, 20–40 mg/kg NBQX significantly suppressed only the motor seizure stage without reducing the AD duration of previously hippocampal-kindled seizures. Daily administration of 15 or 30 mg/kg NBQX prior to each electrical stimulation of the AM markedly and significantly suppressed the development of kindling. During drug sessions, the growth of the AD duration was blocked almost completely, while the waveform of ADs became more complex. These results indicate that NBQX has potent antiepileptogenic and anticonvulsant actions on kindling, at least more from the AM and that non-NMDA receptors have an important role in seizure propagation.

The development of changes in hippocampal GABA immunoreactivity in the rat kindling model of epilepsy: A light microscopic study with gaba antibodies

Immunocytochemical techniques were used to study changes of GABA immunoreactivity in the rat hippocampal CA1 region during kindling epileptogenesis, gradually developing over a period of two weeks by daily electrical tetanization of Schaffer collaterals/commissural fibres. The number of GABA-immunoreactive somata per mm 2 was quantified in CA1 region after 6 and 14 stimulus-induced afterdischarges and in fully kindled animals. The absolute values were compared with those obtained from controls and the relative difference between the side where the stimulations were applied and the contralateral side was determined. In comparison to controls the rats showed, after 6 afterdischarges at the ipsilateral, stimulated side, a slight increase in cell density of about 10%; after 14 afterdischarges, there was a significant increase of 38% together with an enhanced labelling density, while in fully kindled rats (34 afterdischarges) there was no significant difference with controls. At the contralateral side, we observed a different pattern of, respectively, a small decrease (17%), no significant difference, and a significant increase of 22% in fully kindled animals. This result is discussed in relation to observations that fully kindled rats, investigated 24 days after the last seizure of the acquisition phase, showed rather a significant decrease by 35% of cell density at the stimulated side and a regional loss of immunoreactivity of varicosities. At this point in time, no significant changes were found at the contralateral side. The complex time-course of GABA immunoreactivity during epileptogenesis consists of a transient increase in the early phase of kindling acquisition followed by a process of gradual reduction that leads to the long-term decrease of GABA immunoreactivity and high excitability.

Decrease in number of hippocampal gamma-aminobutyric acid (GABA) immunoreactive cells in the rat kindling model of epilepsy.

Daily repeated tetanic electrical stimulation (kindling) of hippocampus or other brain structures leads to progressive increase in epileptiform activity. Since kindling may involve changes in the inhibitory neurotransmitter gamma-aminobutyric acid (GABA), the distribution of this amino acid was studied. A significant decrease in number of GABA immunoreactive positive cell bodies in stimulated CA1 region of the rat hippocampus compared to the contralateral side was found.

Potentials evoked by alvear tract in hippocampal CA1 region of rats. II. Spatial field analysis.

ArticlesPotentials evoked by alvear tract in hippocampal CA1 region of rats. II. Spatial field analysisS. W. LeungS. W. LeungPublished Online:01 Nov 1979https://doi.org/10.1152/jn.1979.42.6.1571MoreSectionsPDF (3 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByMechanisms of Gamma Oscillations in the Hippocampus of the Behaving RatNeuron, Vol. 37, No. 2Structural Inhomogeneities Differentially Modulate Action Currents and Population Spikes Initiated in the Axon or DendritesL. López-Aguado, J. M. Ibarz, P. Varona, and O. Herreras1 November 2002 | Journal of Neurophysiology, Vol. 88, No. 5Apical and Basal Orthodromic Population Spikes in Hippocampal CA1 In Vivo Show Different Origins and Patterns of PropagationFabian Kloosterman, Pascal Peloquin, and L. Stan Leung1 November 2001 | Journal of Neurophysiology, Vol. 86, No. 5Macroscopic and Subcellular Factors Shaping Population SpikesP. Varona, J. M. Ibarz, L. López-Aguado, and O. Herreras1 April 2000 | Journal of Neurophysiology, Vol. 83, No. 4Modulation of Dendritic Action Currents Decreases the Reliability of Population SpikesL. López-Aguado, J. M. Ibarz, and O. Herreras1 February 2000 | Journal of Neurophysiology, Vol. 83, No. 2Fast pre-potential generation in rat hippocampal ca1 pyramidal neuronsNeuroscience, Vol. 53, No. 4Long-term potentiation induced by patterned stimulation of the commissural pathway to hippocampal CA1 region in freely moving ratsNeuroscience, Vol. 48, No. 1Current source density of sustained potential shifts associated with electrographic seizures and with spreading depression in rat hippocampusBrain Research, Vol. 570, No. 1-2Methods for studying the conductance changes associated with synaptic activation of forebrain slices: the interpretation of field potentials using CSD profilesJournal of Neuroscience Methods, Vol. 39, No. 1The role of hippocampal commissures in the interhemispheric transfer of epileptiform afterdischarges in the rat: a study using linear and non-linear regression analysisElectroencephalography and Clinical Neurophysiology, Vol. 76, No. 6The development of changes in hippocampal GABA immunoreactivity in the rat kindling model of epilepsy: A light microscopic study with gaba antibodiesNeuroscience, Vol. 23, No. 2Electrical activity of the cingulate cortex. I. Generating mechanisms and relations to behaviorBrain Research, Vol. 407, No. 1Laminar distribution of hippocampal rhythmic slow activity (RSA) in the behaving rat: Current-source density analysis, effects of urethane and atropineBrain Research, Vol. 365, No. 1A simple method for the construction of electrode arraysJournal of Neuroscience Methods, Vol. 11, No. 3Cellular bases of hippocampal EEG in the behaving ratBrain Research Reviews, Vol. 6, No. 2Two types of interictal transients of reversed polarity in rat hippocampus during kindlingElectroencephalography and Clinical Neurophysiology, Vol. 55, No. 3Differential effects of pentobarbital and ether on the synaptic transmission of the hippocampal CA1 region in the ratElectroencephalography and Clinical Neurophysiology, Vol. 51, No. 3Model of behavioral modulation of the hippocampal CA1 region of the ratBrain Research, Vol. 205, No. 1Behavior-dependent evoked potentials in the hippocampal CA1 region of the rat. I. Correlation with behavior and eggBrain Research, Vol. 198, No. 1Behavior-dependent evoked potentials in the hippocampal CA1 region of the rat. II. Effect of eserine, atropine, ether and pentobarbitalBrain Research, Vol. 198, No. 1 More from this issue > Volume 42Issue 6November 1979Pages 1571-1589 Copyright & PermissionsCopyright © 1979 the American Physiological Societyhttps://doi.org/10.1152/jn.1979.42.6.1571PubMed501390History Published online 1 November 1979 Published in print 1 November 1979 Metrics