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PubMed1988

Low chloride-dependent release of taurine by a furosemide-sensitive process in the in vivo rat hippocampus.

Extracellular amino acid levels and field potentials evoked by perforant pathway stimuli were studied in vivo by means of a dialysis device, perfusing the rat dentate gyrus with low chloride solutions. When balanced with acetate, these perfusions enhanced the granule cell population spike amplitude. A specific extracellular taurine enhancement occurred whenever Cl- was replaced by acetate solution, reaching an increase of 20-fold over the basal taurine levels when 125 mM Cl- was replaced, whereas other amino acids remained unchanged. A considerable degree of Cl- replacement with iodide was needed, however, to obtain significant increases of extracellular taurine. Perfusions with bromide instead of Cl- did not cause any change in levels of extracellular amino acids including taurine. Furosemide, an inhibitor of Cl- transport, greatly reduced the taurine increase evoked by the low extracellular concentration of permeant anions. This drug also inhibited the taurine release induced by perfusion with 9 mM K+. These findings indicate that the extracellular increase of taurine, evoked by low permeant anion concentrations, may result from the taurine release through a furosemide-sensitive process.

Amino Acids↗
PubMed1988

Electrophysiological analysis of the dorsal hippocampal commissure projections to the entorhinal area.

Synaptic effects evoked in the entorhinal area by dorsal hippocampal commissure (dorsal psalterium) projections were analysed in anesthetized adult guinea-pigs by means of a field potential analysis. Stimuli applied to the caudal part of the dorsal psalterium evoked a complex response in the dorsal third of the entorhinal area. The early part of the entorhinal response consisted of a slow wave interrupted by a spike potential. The electrophysiological characteristics and the laminar distribution of the slow wave and of the spike potential, together with the presence of time-locked unit activity, suggested that dorsal psalterium projections evoke monosynaptic excitatory postsynaptic potentials leading to cellular discharge in radially oriented neurons of layers II and III. The commissural fibers responsible for these effects originate in the contralateral presubiculum. The early part of the entorhinal response was followed by three waves in close temporal sequence. These waves were polysynaptically generated and associated with excitatory and inhibitory synaptic effects. Inhibition was demonstrated for the monosynaptically generated spike potential. Whether these effects were mediated by intracortical circuits and/or extrinsic projections cannot be stated from the present results. Causal relations were observed between the entorhinal monosynaptic response and that evoked by dorsal psalterium stimulation in the ipsilateral dentate gyrus, previously shown to be relayed by perforant path fibers. The results indicate that presubicular commissural projections to the entorhinal area monosynaptically activate neurons of the perforant pathway, whose discharge brings about activation of the ipsilateral dentate gyrus.

Action Potentials↗
PubMed1989

Histochemical changes in enzymes of energy metabolism in the dentate gyrus accompany deafferentation and synaptic reorganization.

The dentate gyrus of adult rats was examined histochemically for cytochrome oxidase and lactate dehydrogenase activity after unilateral lesions of the entorhinal cortex. In normal animals, synaptic terminal fields of the perforant pathway from the entorhinal cortex show high levels of cytochrome oxidase activity (the other two-thirds dentate molecular layer), whereas terminal zones of the commissural and associational fibers show high levels of lactate dehydrogenase activity (the inner one-third dentate molecular layer). Lesions of the entorhinal cortex result in a significant reduction in staining for cytochrome oxidase in the deafferented outer molecular layer of the dentate gyrus. The changes become prominent at 16-24 h after the lesion and persist until 90 days, the longest post-lesion survival time studied. In the non-deafferented inner zones ipsilateral to the lesion, there is an increase in staining for cytochrome oxidase and lactate dehydrogenase at 24 h post-lesion that disappears by days 2-4. From 8 to 90 days post-lesion, the band of high reactivity for lactate dehydrogenase in the inner molecular layer spreads approximately 40 microns into the overlying deafferented zone. This expansion parallels the expansion of the commissural and associational terminal fields into the adjacent deafferented molecular layer. Thus, lesion-induced synaptogenesis in the dentate gyrus is accompanied by a corresponding change in enzyme activity. The results indicate that the pattern of activity of enzymes involved in energy metabolism in the dentate gyrus depends on the distribution of pathway-specific synaptic input.

Animals↗
PubMed1989

The effect of blocking sodium influx on anoxic damage in the rat hippocampal slice.

The in vitro rat hippocampal slice was used to study the effect of tetrodotoxin, a sodium channel blocker, on anoxic damage. Tetrodotoxin improved recovery of the evoked population spike after anoxia and reduced the fall in adenosine 5'-triphosphate during anoxia. Electrophysiological responses to perforant pathway stimulation were recorded in the dentate granule cell layer before, during and after 10 min of anoxia, with and without tetrodotoxin. Preincubation with tetrodotoxin permitted recovery of the evoked population spike to 43 +/- 10% (mean +/- standard error) in the post-anoxic period; this compared to 3 +/-3% recovery in untreated tissue (P less than 0.005). Similar studies of the CA1 pyramidal cells, which are more sensitive to anoxia, showed that tetrodotoxin improved recovery of the postsynaptic response after 5 min of anoxia. The recovery was 69 +/- 15% of its pre-anoxic level when treated with tetrodotoxin. This compares to no recovery in untreated tissue (P less than 0.005). Biochemical studies demonstrated a significantly reduced fall in adenosine 5'-triphosphate levels during levels in the dentate granule cell layer fell to 1.4 nM/mg dry wt, whereas following treatment with tetrodotoxin they only fell to 2.2 nM/mg. Since it required only 5 min of anoxia to damage the CA1 pyramidal cells, adenosine 5'-triphosphate levels were measured in this region after 5 min of anoxia. Adenosine 5'-triphosphate levels in the CA1 region fell to 2.2 nM/mg in untreated tissue after 5 min of anoxia, compared to 2.9 nM/mg in the tetrodotoxin-treated tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1991

Regional and laminar distributions of alpha 1-adrenoceptors and their subtypes in human and rat hippocampus.

The distributions of the alpha 1-adrenoceptor and its subtypes (alpha 1A and alpha 1B) in human and rat hippocampus are analysed by quantitative receptor autoradiography. alpha 1-Adrenoceptors are labelled by [3H]prazosin. The alpha 1A subtype is visualized by [3H]prazosin after irreversible blockade of alpha 1B adrenoceptors with chloroethylclonidine or directly by [3H]5-methyl-urapidil. The alpha 1B subtype is investigated by [3H]prazosin binding in the presence of the alpha 1A antagonist 5-methyl-urapidil. Considerable differences in the regional and laminar patterns of alpha 1-adrenoceptors are found between rat and human hippocampi. The rat hippocampus is characterized by a low overall density and a rather homogeneous regional and laminar distribution. This is in contrast to the human pattern, which shows a much higher overall level of alpha 1 receptor density and a restriction of alpha 1 receptors to the CA3 region of Ammon's horn and the dentate gyrus. Moreover, alpha 1A and alpha 1B receptors of the human hippocampus are differentially distributed with the alpha 1A subtype concentrated in the hilus and lucidum layer of CA3, and the alpha 1B subtype concentrated in the molecular layer of the dentate gyrus. Additionally, the distribution of alpha 1 receptors is compared with the distribution of 5-hydroxytryptamine 1A receptors. The subtype specific pattern is correlated with the distribution of glutamatergic systems in the human (but not in the rat) hippocampus. alpha 1A Receptor localization coincides with the target area of the mossy fibre system, and alpha 1B receptors are preferentially localized in the target area of the hippocampal associational fibres and partly of the perforant pathway. This result points to possible interactions between noradrenaline- and glutamate-mediated neurotransmission differentiated by topographically segregated alpha 1-adrenoceptor subtypes.

Adrenergic alpha-Antagonists↗
PubMed1993

Parvalbumin immunoreactivity in the hippocampus of the gerbil after transient forebrain ischaemia: a qualitative and quantitative sequential study.

Parvalbumin immunoreactivity is examined in the hippocampus of the Mongolian gerbil (Meriones unguiculatus) in controls and in animals subjected to 20 min of forebrain ischaemia produced by bilateral clipping of the carotids. In comparison with other species, the hippocampus of the gerbil is characterized by strong immunoreactivity of the (presumably excitatory) perforant pathway, and weak immunoreactivity (low numbers of neurons and scarce dendritic arbors) in nonpyramidal nerve cells (inhibitory neurons) of the CA1 area. These properties may play some role in the development and maintenance of seizures in this susceptible species. Parvalbumin immunoreactivity is rapidly and ephemerally increased in the hippocampus 15 min after reperfusion. Later on, there is a transitory decrease of parvalbumin immunoreactivity which is followed by an increase 6 h later in the stratum granulare hilus and CA3 area, and not until the first and second days in the CA1 area. This increase significantly surpasses the number of immunoreactive neurons in control animals in CA1 and CA3 from 48 h after reperfusion onwards. The effect is similar using different anaesthetics and does not occur in sham-operated animals. In contrast with these findings, the number of parvalbumin-immunoreactive neurons in the somatosensory cortex is not affected in our model of forebrain ischaemia. On the other hand, GABA-immunoreactive neurons in CA1 are preserved during the first week after reperfusion, although an increase in the number of these cells occurs at the end of this period. Delayed neuronal death occurs in the CA1 area 48 h after ischaemia, and marked reduction in the number of CA1 neurons is found by the end of the first week. Eighty per cent of the remaining cells in CA1 at day 7, and 83% at day 15, are parvalbumin-immunoreactive nonpyramidal neurons in contrast to 3% parvalbumin-immunoreactive cells in control animals. These findings indicate that GABAergic neurons in CA1 are preserved after forebrain ischaemia, and that parvalbumin in CA1 neurons is associated with survival.

Animals↗
PubMed1993

Entorhinal cortex lesion induces differential responses in [125I]insulin-like growth factor I, [125I]insulin-like growth factor II and [125I]insulin receptor binding sites in the rat hippocampal formation.

The hippocampus can be induced by deafferentation to selectively reorganize its neuronal input. Entorhinal cortex lesion, which causes degeneration of the perforant pathway, evokes sprouting of septal afferents as well as glutamatergic commissural/associational fibers in the deafferentated zone of the molecular layer of the dentate gyrus. Although the process of reactive synaptogenesis that follows deafferentation has been extensively studied, at present little is known about its molecular basis and the mechanism of initiation. In this study, following unilateral lesion of the entorhinal cortex, the time-course of possible alterations of insulin-like growth factors I and II, and insulin binding sites were evaluated by in vitro quantitative receptor autoradiography. [125I]Insulin-like growth factor I receptor binding sites did not exhibit any significant variation between the contralateral and ipsilateral hippocampal formation at any time periods following lesion except in the molecular layer of the dentate gyrus (P < 0.05) at day 8. However, when compared with the unlesioned animals, a differential time-dependent response of [125I]insulin-like growth factor I binding sites was noted in selective layers of the hippocampus. [125I]Insulin-like growth factor II receptor binding sites showed a significant decrease (P < 0.05) in the ipsilateral granular cell layer of the dentate gyrus only at day 14 post lesion. Interestingly, compared to controls, a dramatic bilateral increase (P < 0.05) in [125I]insulin-like growth factor II binding was evident between days 1 and 8 in most layers of the hippocampal formation. A lesion-induced bilateral increase (P < 0.05) in [125I]insulin binding sites was evident in all layers of the hippocampus between two to eight days and at 30 days post lesion. In selective layers, however, a significant increase (P < 0.05) in [125I]insulin binding sites was also observed at days 1 and 14 after lesion. These results, which are compatible with the process of degeneration and/or sprouting of the terminal fibers, suggest possible involvement of insulin-like growth factors and insulin in the sequence of molecular events that occur to facilitate neuronal repair and to promote neuronal survival following entorhinal cortex lesion.

Afferent Pathways↗
PubMed1994

Specific [3H]L-glutamate binding and [3H]D-aspartate release in the hippocampus of rat after pentylenetetrazol kindling and long-term potentiation.

In the present study, the time-course of changes in glutamate binding and aspartate release in the rat hippocampus following tetanization of perforant pathway and of pentylenetetrazol-induced kindling was investigated. The K+ (48 mM)-stimulated [3H]D-aspartate release from hippocampal slices and the specific [3H]L-glutamate binding to crude synaptic membranes of the hippocampus were measured 1, 4 and 24 h after the last tetanization train or one, five and nine weeks after the last pentylenetetrazol injections, respectively. The tetanization of the fascia dentata was followed by a significant increase in K(+)-stimulated [3H]D-aspartate release from hippocampal slices only 1 h after the last tetanization train, but the specific [3H]L-glutamate binding was enhanced 4 h afterwards. No further deviations from controls have been seen 24 h after tetanization. After pentylenetetrazol kindling, the K(+)-stimulated amino acid release from hippocampal slices was not changed. However, at one week as well as at five and nine weeks after the pentylenetetrazol kindling the specific [3H]L-glutamate binding in the hippocampus was significantly increased by about 50% compared to controls. From these findings it can be assumed that after long-term potentiation induction presynaptic transmitter release and post- (and/or pre-)synaptic glutamate binding are elevated with a different time course only in the early phase of potentiation. In contrast, kindling results in a long lasting increase in activity state of glutamatergic transmission. Therefore, it can be concluded that differences of the synaptic excitability following long-term potentiation and kindling are reflected by a different activation of glutamatergic system in the central nervous system.

Animals↗
PubMed1994

Dynamics of synapsin I gene expression during the establishment and restoration of functional synapses in the rat hippocampus.

Synapse development and injury-induced reorganization have been extensively characterized morphologically, yet relatively little is known about the underlying molecular and biochemical events. To examine molecular mechanisms of synaptic development and rearrangement, we looked at the developmental pattern of expression of the neuron-specific gene synapsin I in granule cell neurons of the dentate gyrus and their accompanying mossy fibers during the main period of synaptogenic differentiation in the rat hippocampus. We found a significant difference between the temporal expression of synapsin I messenger RNA in dentate granule somata and the appearance of protein in their mossy fiber terminals during the postnatal development of these neurons. Next, to investigate the regulation of neuron-specific gene expression during the restoration of synaptic contacts in the central nervous system, we examined the expression of the synapsin I gene following lesions of hippocampal circuitry. These studies show marked changes in the pattern and intensity of synapsin I immunoreactivity in the dendritic fields of dentate granule cell neurons following perforant pathway transection. In contrast, changes in synapsin I messenger RNA expression in target neurons, and in those neurons responsible for the reinnervation of this region of the hippocampus, were not found to accompany new synapse formation. On a molecular level, both developmental and lesion data suggest that the expression of the synapsin I gene is tightly regulated in the central nervous system, and that considerable changes in synapsin I protein may occur in neurons without concomitant changes in the levels of its messenger RNA. Finally, our results suggest that the appearance of detectable levels of synapsin I protein in in developing and sprouting synapses coincides with the acquisition of function by those central synapses.

Acetylcholinesterase↗
PubMed1995

Hippocampal homosynaptic long-term depression/depotentiation induced by adrenal steroids.

The effects of adrenal steroids on synaptic plasticity were investigated in the dentate gyrus of the hippocampus. Experiments were performed in either adrenalectomized or intact (non-adrenalectomized), anesthetized rats. High-frequency stimulation was applied to the medial perforant pathway at three different frequencies; 100, 200 or 400 Hz, either post- or pre- and post-administration of the specific Type-II adrenal steroid receptor agonist RU 28362. High-frequency stimulation prior to RU 28362 administration produced a frequency-dependent long-term potentiation of the population spike, with 100 Hz showing no long-term potentiation and 400 Hz the highest degree of potentiation. In contrast, following administration of RU 28362, high-frequency stimulation produced a long-term depression (in comparison to baseline). In the experiments in which high-frequency stimulation was applied both pre- and post-RU 28362 administration, the size of the population spike was initially potentiated and then depotentiated after the RU 28362 injection. This effect was also frequency dependent, although opposite to the long-term potentiation effect. That is, 400 Hz was the least effective frequency for inducing long-term depression/depotentiation, while 100 Hz was the most effective. Long-term depression/depotentiation was immediate following high-frequency stimulation and lasted for the extent of the recording session, in some cases longer than 1 h. Similar to the finding reported in the accompanying paper, induction of long-term potentiation was substantially suppressed by RU 28362. However, in a number of experiments long-term potentiation could still be induced after RU 28362 administration, even after long-term depression/depotentiation had been established. In these cases, stimulation at the higher frequencies was necessary.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex Hormones↗
PubMed1983

Aminergic blockade modulates long-term potentiation in the dentate gyrus of freely moving rats.

Long-term potentiation (LTP) was induced in the dentate gyrus of freely moving rats by tetanic stimulation of the medial entorhinal cortex under conditions of catecholamine depletion by 200 mg/kg alpha-Methyl-para-tyrosine (AMPT) or blockade of alleged dopamine receptors by 0.5 mg/kg haloperidol. Both substances did not change significantly the normal excitability of the glutamatergic perforant pathway, but affected the establishment of LTP. Whereas the potentiation effect on the EPSP component of the monosynaptic field potential was not changed by both substances when compared to the potentiation of controls, the potentiation of the population spike was prolonged and enhanced. These results point to an effect of catecholaminergic blockade on postsynaptic membranes of the target cells or on other components of the neuronal network but not to a specific influence on the homosynaptic mechanisms of LTP.

Animals↗
PubMed1992

Pattern of neuronal death in the rat hippocampus after status epilepticus. Relationship to calcium binding protein content and ischemic vulnerability.

The pattern of hippocampal cell death has been studied following hippocampal seizure activity and status epilepticus induced by 110-min stimulation of the perforant pathway in awake rats. The order of vulnerability of principal cells in the different hippocampal subfields--as determined by silver impregnation--was found to be very similar to the pattern found in ischemia; i.e., dentate hilus greater than CA1, subiculum greater than CA3c greater than CA3a,b greater than dentate granule cells. The hilar somatostatin-containing cells were the most vulnerable cell type, whereas all other subpopulations of nonprincipal neurons--visualized by immunocytochemistry for the calcium binding proteins parvalbumin and calbindin--were remarkably resistant. Pyramidal cells in the CA3 region containing neither of the examined calcium binding proteins were more resistant to overexcitation than CA1 pyramidal cells, most of which do contain calbindin. This indicates that no simple relationship exists between vulnerability in status epilepticus and neuronal calcium binding protein content, and that local and/or systemic hypoxia during status epilepticus may be responsible for the ischemic pattern of cell death.

Animals↗
PubMed1996

Neonatal isolation alters LTP in freely moving juvenile rats: sex differences.

We have previously reported that neonatal isolation significantly enhanced the magnitude of hippocampal long-term potentiation (LTP) recorded from freely moving male rats tested at 30 days of age. The present study extends this work to examine the effects of neonatal isolation on hippocampal LTP in male and female juvenile rats. Changes in dentate granule cell population measures, i.e., EPSP slope and population spike amplitude (PSA), evoked by tetanization of the medial perforant pathway were used to assess the effects of neonatal isolation on LTP over a period of 96 hrs. Prior to tetanization, significant sex differences were obtained for input/output (I/O) response measures of EPSP slope and PSA, with males showing consistently higher values than females. No significant effect of treatment was obtained within either sex for baseline measures. Following tetanization significant sex differences were also obtained for both measures, with males showing significantly greater enhancement than females. Comparisons made at 1 hr post-tetanization (establishment of LTP) indicated that isolated males showed significantly greater enhancement than any other group. On the other hand, treatment differences were not obtained from females. At 96 hrs (maintenance of LTP), however, both neonatally isolated males and females showed significantly greater enhancement than either non-isolated siblings or unhandled controls. These results indicate that males and females exhibit different enhancement profiles with respect to both the magnitude and duration of LTP, and that neonatal isolation alters these profiles in a sex-specific manner.

Animals↗
PubMed1993

Allosteric potentiation by diazoxide of AMPA receptor currents and synaptic potentials.

Diazoxide (100-560 microM) reversibly increased the amplitude and duration of excitatory post-synaptic field potentials recorded in the dentate gyrus of hippocampal slices following stimulation of the perforant pathway. In rat cortex mRNA-injected Xenopus oocytes diazoxide (1-1000 microM) alone had little effect on membrane current, but rapidly and reversibly increased (up to 5-fold) current responses to (R,S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA, 30 microM), L-glutamate (100 microM), quisqualate (3 microM), kainate (100 microM) and domoate (3 microM), an effect that was neither mimicked by other activators of ATP-sensitive potassium channels nor blocked by glibenclamide. Diazoxide increased current amplitudes for all concentrations of the 'inactivating' ligands, AMPA, L-glutamate and quisqualate but had little effect on their EC50 values. In contrast, diazoxide increased the apparent potency of the 'non-inactivating' ligands, kainate and domoate, but increased the efficacy of saturating concentrations by only 10-20%. Diazoxide did not modify the competitive inhibition of AMPA and kainate currents by 6-nitro-7-sulfamoylbenzo[f]quinoxaline-2,3-dione (NBQX) and thus does not compete for the agonist site as do AMPA and kainate. Similarly, diazoxide neither inhibited the binding of [3H]AMPA or [3H]kainate to rat cortical membranes in competition experiments nor consistently modified the apparent [3H]AMPA affinity (Kd) or receptor density (Bmax) in saturation experiments. These data suggest that diazoxide acts at an allosteric site on the AMPA receptor/channel to potentiate activation in a manner dependent upon the properties of the excitatory agonist.

Allosteric Regulation↗
PubMed1991

Modulation by adrenal steroids of limbic function.

The effects of various steroid hormones on the long-term potentiation (LTP) of the rat hippocampus were evaluated. LTP was elicited in the dentate gyrus of adrenalectomized animals with priming tetanic stimulation (200 Hz-0.03 cps) of its main afferent, the perforant pathway. Single pulse EPSP (excitatory post-synaptic potential) slope, and PS (population spike) amplitude values were compared before and after the i.v. injection of the hormones and subsequently after the priming stimulation every 15 min up to 1 h. 18-OH-deoxycorticosterone (18-OH-DOC) produced a significant decrease of the EPSP LTP and arrested the PS enhancement in comparison with vehicle at every time post-tetanic stimulation. Its 21-acetate derivative produced a moderate decrease of the EPSP and had no effect on the PS LTP in comparison with vehicle. Deoxycorticosterone (DOC) exhibited similar effects on the EPSP although less marked than with 18-OH-DOC while the PS only decreased in the first 30 min post-train. Corticosterone decreased both EPSP and PS for the first 15 and 30 min after priming stimulation, respectively, matching values with those of vehicle afterwards. Its 21-acetate produced an initial decrease of the EPSP and had no effect on the PS LTP. Allo-tetrahydro-DOC produced little, if any, initial enhancement of the PS LTP in comparison with vehicle. These results show that the adrenal steroids tested can modulate hippocampal LTP, a plastic phenomenon in the mammalian CNS which is known to be related to memory and learning processes. Moreover, adrenal steroids can independently modify the PS or EPSP components of the LTP, suggesting different loci of action at the neuronal level.

Adrenal Glands↗
PubMed1991

Effects of adrenal steroids and their reduced metabolites on hippocampal long-term potentiation.

We studied the effects of steroid hormones on the hippocampal long-term potentiation (LTP), a putative mechanism of neuronal plasticity and memory storage in the CNS. In vivo experiments were performed in rats under chloral hydrate anesthesia (0.4 mg/kg i.p.). All animals were adrenalectomized 48 h before recording. LTP was induced after priming tetanic stimulation at the perforant pathway (PP) and single pulse field potentials were obtained from the dentate gyrus (DG). The excitatory post-synaptic potential (EPSP) slope and population spike (PS) amplitude were analyzed before and after the i.v. injection of the steroids and after the induction of LTP, and followed up to 1 h. Results obtained with the hormones were compared with matched control animals injected with vehicle alone, Nutralipid 10%. Previous results from our laboratory showed that deoxycorticosterone (DOC) decreased the magnitude of the EPSP at all times after priming stimulation and the PS decreased during the first 30 min of the LTP. Corticosterone decreased the EPSP in the first 15 min and the PS during the first 30 min after priming stimuli. In these experiments the mineralocorticoids aldosterone and 18-OH-DOC elicited a decrease of the EPSP at all times post-train; and no significant difference against vehicle was observed in the PS. Post-injection values were not changed except for 18-OH-DOC at a dose of 1 mg, where a decrease of both the EPSP (P less than 0.01) and the PS (P less than 0.02) was observed against vehicle. ATH-progesterone at 0.1 mg/rat also decreased the EPSP values significantly after priming stimulation and no significant changes against vehicle were observed in the PS. These results show that adrenal steroids can modulate hippocampal LTP, that they can act at different neuronal loci and with different time courses in the development of the phenomena.

Adrenal Glands↗
PubMed2006

The antioxidant N-acetyl-L-cysteine does not prevent hippocampal glutathione loss or mitochondrial dysfunction associated with status epilepticus.

Hippocampal reduced glutathione (GSH) levels diminish after status epilepticus (SE), which precedes damage to mitochondrial enzymes, which is associated with cell death. The rat perforant pathway stimulation model was used to assess whether intraperitoneal administration of the GSH precursor N-acetyl-L-cysteine (NAC) protected against these changes. NAC (300 mg/kg) treated animals exhibited the same GSH decrease post SE as vehicle treated. Furthermore, NAC treatment had no protective effects on mitochondrial dysfunction.

Acetylcysteine↗
PubMed2006

Administration of levetiracetam after prolonged status epilepticus does not protect from mitochondrial dysfunction in a rodent model.

Neuronal death and dysfunction occur after status epilepticus (SE), and is associated with mitochondrial enzyme damage. We previously showed, using the rat perforant pathway stimulation model, that levetiracetam administration (LEV; 1000 mg/kg intraperitoneal) during established SE reduces seizure severity and prevents mitochondrial dysfunction. We now show that administration of the same dose of LEV after 5h SE, does not protect from mitochondrial dysfunction.

Animals↗