Current and voltage-clamp techniques were used to study the effects of kainic (KA) and quisqualic (quis) acids on the slow synaptic inhibition evoked by mossy fibre stimulation in CA3 hippocampal pyramidal neurones in vitro. The K+ conductance underlying the slow synaptic inhibition is coupled to a gamma-aminobutyric acid b (GABAb) receptor by a guanosine-triphosphate (GTP)-binding protein. Both KA and quis reduce (after 7-10 min) the slow inhibitory post-synaptic current (IPSC) without changing the reversal potential. They also reduce the cellular response to exogenously applied (-)baclofen and 5-hydroxytryptamine, which are known to activate a similar K+ conductance. We conclude that KA and quis block the post-synaptic K+ conductance underlying the slow IPSC.

Animals↗

PubMed1990

Subtotal gastrectomy in infancy for perforating necrotizing gastritis.

Necrotizing gastritis is a rare pathology causing a high rate of morbidity and mortality in the infants. A 4-week-old baby, with right hypoplastic kidney and ectopic ureter, was admitted because of profound septic shock and "coffee ground" vomitus. Aggressive treatment was started and hemodynamic stabilization was achieved. On the fourth admission day, ascites was noted and on the eighth day in a plain abdominal x-ray, free air was shown. At urgent explorative laparotomy, double posterior gastric wall perforations with extensive gastric wall necrosis were found, which required subtotal gastrectomy. The etiology and pathophysiology of this rare process are discussed with an emphasis on the difficulty in diagnosis of posterior gastric perforation into the lesser sac.

Escherichia coli Infections↗

PubMed1990

Hippocampal potassium ATP channels and anoxia: presynaptic, postsynaptic or both?

Explore the source record for details and available documents.

Adenosine Triphosphate↗

PubMed1990

Brief seizure episodes induce long-term potentiation and mossy fibre sprouting in the hippocampus.

Much of our present understanding of the cellular mechanisms of learning and memory derives from studies on the hippocampus in which long-term potentiation (LTP) of synaptic transmission is produced by a train of high-frequency electrical stimulation or by potassium channel blockers. The hippocampus is also a seizure-prone region and recent studies have revealed that brief seizure episodes produce remarkably long-lasting changes which are reminiscent of 'classical' LTP. A brief seizure episode also sets in motion a cascade of events that includes changes in gene expression, sprouting of fibres and the establishment of new synaptic contacts. This paper reviews this use-dependent structural rearrangement of the neuronal network and discusses its possible role in epilepsy and as a model of plasticity in the adult nervous system.

Animals↗

PubMed1990

Long-term potentiation in the rat hippocampus induced by the mast cell degranulating peptide: analysis of the release of endogenous excitatory amino acids and proteins.

Using a push-pull device, we have analysed, in vivo, the release of endogenous excitatory amino acids and proteins induced by the mast cell degranulating peptide in the CA1 region of the hippocampus. Local application of the mast cell degranulating peptide (20 microM) for 5 or 10 min produced a long-term potentiation of the slope of the field excitatory postsynaptic potential (70 +/- 40%, 3 h after the drug application). This long-term potentiation was associated with (i) a transient increase (10 min) in the release of endogenous glutamate and aspartate and (ii) a late transient enhanced release of proteins and newly secreted proteins. In cases in which the mast cell degranulating peptide induced recurrent interictal activity, there was a sustained enhanced release of glutamate. These observations suggest that mast cell degranulating peptide induced long-term potentiation is not associated with a sustained enhanced release of excitatory amino acids.

Action Potentials↗

PubMed1990

Activators of ATP-sensitive K+ channels reduce anoxic depolarization in CA3 hippocampal neurons.

In CA3 hippocampal neurons of the rat, brief anoxic episodes produce a depolarization which is probably due to a synaptic release of glutamate. Diazoxide, an activator of ATP-sensitive K+ channels (K+ ATP), blocks the anoxic depolarization and has no effect in control oxygenated artificial cerebrospinal fluid. The hormone somatostatin which activates K+ ATP channels in the pancreas also reduces the anoxic depolarization in CA3 neurons. We suggest that drugs that open K+ ATP channels may constitute a novel approach to selectivity reducing the deleterious effects of excessive release of glutamate during anoxia without producing a generalized blockade of glutamatergic synaptic transmission.

Adenosine Triphosphate↗

PubMed1990

GABAergic mechanisms in the CA3 hippocampal region during early postnatal life.

The developmental pattern of GABAergic neurons in the rat hippocampus during the first week of postnatal life shows several particularities both from a morphological and physiological point of view: (1) GABA immunoreactive neurons which are initially localized in a deep and superficial layer, progressively disappear from these two layers. From the end of the first postnatal week, GABAergic neuronal somata appear throughout the whole hippocampus, but GABA immunoreactive terminal structures are not frequent until the second postnatal week. (2) Intracellular observations in slices reveal the presence in CA3 pyramidal neurons between P0 and P6 (postnatal days) of spontaneous giant depolarizing potentials (GDPs); these are mediated by GABA acting on GABAA receptors and modulated presynaptically by NMDA receptors. During this period of development, GABA and GABAA analogues have a depolarizing action at resting membrane potential. Bicuculline at this developmental stage blocks completely spontaneous and evoked synaptic potentials. During the second postnatal week, when GABA responses shift from depolarizing to hyperpolarizing, bicuculline induces spontaneous interictal discharges. It is suggested that the positive feedback of the GABAergic interneuron on the pyramidal neuron during the first week of life may account for the generation of GDPS which may play an important role in synaptogenesis.

Action Potentials↗

PubMed1990

The allosteric glycine site of the N-methyl-D-aspartate receptor modulates GABAergic-mediated synaptic events in neonatal rat CA3 hippocampal neurons.

We report in this study that, in the presence of magnesium, bath application of micromolar concentrations of glycine have prominent effects on synaptic events and N-methyl-D-aspartate (NMDA) responses in neonatal but not in adult hippocampal slices. Intracellular recordings were made from 71 rat CA3 hippocampal neurons in neonatal slices. In keeping with our earlier study, during the first postnatal week, CA3 neurons exhibited giant depolarizing potentials (GDPs). These GDPs are mediated by gamma-aminobutyric acid (GABA) acting on type A GABA (GABAA) receptors and modulated presynaptically by NMDA receptors. In the majority of cells (18 out of 31), glycine (10-30 microM) increased the frequency of GDPs (from 0.14 to 0.29 Hz). This effect was mimicked by D-serine (10-20 microM) and blocked by the NMDA receptor antagonists D-(-)-2-amino-5-phosphonovalerate (50 microM) and DL-2-amino-7-phosphonoheptanoate (50 microM) and by the GABAA antagonist bicuculline (10 microM) but not by strychnine (1 microM). Subthreshold concentrations of glycine (or D-serine) and NMDA, when given together, enhanced synaptic noise and the frequency of GDPs. In the presence of tetrodotoxin (1 microM), glycine and D-serine (up to 50 microM) did not modify the NMDA-induced inward currents in CA3 pyramidal cells. However the reduction of NMDA-mediated currents by 7-chlorokynurenate (10-20 microM) was reversed by glycine and D-serine (100-200 microM). In contrast, glycine (up to 100 microM) had no effect on membrane potential, input resistance, or NMDA responses after postnatal day 10. It is concluded that GABA-mediated events are facilitated by glycine acting on presynaptically located NMDA receptors.

Aging↗

PubMed1990

Neurogranin: immunocytochemical localization of a brain-specific protein kinase C substrate.

The developmental expression and the cellular localization of neurogranin (formerly designated p17), a brain-specific protein kinase C (PKC) substrate, were investigated. The developmental expression of neurogranin was studied by immunoblotting of rat brain and neuronal cell-culture extracts using neurogranin polyclonal antibodies. Neurogranin synthesis was found to be developmentally regulated, with no expression in the embryonic and neonatal period and an abrupt increase between 2 and 3 weeks of age. By immunohistochemistry, neurogranin was found essentially in the adult rat telencephalon, specifically located in the cell bodies and dendritic processes of neurons of the cerebral cortex, hippocampus, striatum, and a few other discreet areas. Neurogranin immunoreactivity was nearly absent in the thalamus, cerebellum, and brain stem. The late developmental expression and the dendritic localization of neurogranin in neurons are 2 features that also characterize the type I PKC isozyme. The specific localization of the protein in integrative areas of the rat brain suggests a highly specialized function of neurogranin in the CNS. A possible role for neurogranin in the transduction of the PKC activation signals at the postsynaptic level is suggested.

Animals↗

PubMed1989

Anoxic changes in dentate granule cells.

In most of the granule cells recorded, by current clamp and single-electrode voltage-clamp (SEVC), only small depolarizations (or inward currents) and minor conductance increases were observed during brief periods of anoxia (2-3 min). Thus, unlike pyramidal cells, granule cell bodies show little sign of K channel activation by anoxia. Post-anoxic hyperpolarizations were also minimal. Moreover, diazoxide (an activator of ATP-sensitive K conductance (GK(ATP]) had no consistent hyperpolarizing action. The depressant effect of diazoxide on anoxic glutamate release from mossy fibres is therefore likely to be mediated by GK(ATP) channels situated on granule cell axons or terminals rather than on the cell bodies.

Animals↗

PubMed1989

Distribution of GABAergic neurons in late fetal and early postnatal rat hippocampus.

The ontogenesis of GABAergic neurons in the rat hippocampus was studied using an anti-GABA serum. GABA immunoreactivity appeared at the 18th day of gestation. At this stage, GABA-immunoreactive (GABA-IR) cells are grouped in two layers, one located deeply in the intermediate zone near the ventricular zone, and the other found superficially in the marginal zone near the hippocampal fissure. During the late embryonic and early postnatal life, GABA-IR neurons progressively disappeared from these two layers. The transient appearance of an abundant network of GABAergic neurons might be due to transient expression of GABA in some neurons or to cellular death. Later on, from the third postnatal day, the GABA-IR neurons appeared throughout the whole hippocampus according to a dorsoventral and lateromedial gradient. The setting of neuronal bodies preceded that of GABA-IR puncta (supposed to be mainly synaptic boutons) around the neuronal cell bodies and along the dendritic shafts. The puncta are only visible from the sixth day onwards and their number increased rapidly during the first 3 postnatal weeks. Our results indicate that GABA may have a role in neurotransmission in the hippocampus from a very early stage of development.

Aging↗

PubMed1989

Selective destruction of mossy fibers and granule cells with preservation of the GABAergic network in the inferior region of the rat hippocampus after colchicine treatment.

Lesions induced by colchicine injection into the rat hippocampus were investigated by means of electron microscopy and GABA immunocytochemistry. Granule cells were nearly completely destroyed 3 days after colchicine injection; since the necrosis of their axonal endings was delayed, an anterograde degeneration of the mossy fibers had probably taken place. The selectivity of the lesions was not limited to granule cells, for some pyramidal neurons in CA1 pyramidal layer were damaged. It was, however, striking to observe that throughout the hippocampal structure GABAergic neurons were spared from the effects of colchicine. For instance, GABAergic neurons were found in the vicinity of the completely destroyed granule cell layer. GABAergic neurons and terminals were also present in the CA3 region where the GABA-containing terminals formed a dense network of synapses with somata and dendrites of pyramidal cells. It was interesting to note that, consistent with previous studies, the GABAergic neurons in CA3 are innervated by mossy fibers. We conclude that after colchicine treatment the destruction of the granule cells was not associated with a lesion of the GABAergic network. This selective lesion provides a useful model with which to study the properties of CA3 neurons deprived of their major excitatory input but with an intact inhibitory network.

Animals↗

PubMed1989

Hippocampal plasticity in the kindling model of epilepsy in rats.

Histochemical and autoradiographic techniques were used to study mossy fiber sprouting which occurs in the hippocampus of kindled rats. In rats kindled by daily stimulation of amygdala or entorhinal cortex, the mossy fibers sprout to innervate the supragranular zone of fascia dentata; this synaptic reorganization was associated with a significant increase in the density of high-affinity kainic acid binding sites. Amygdala but not entorhinal kindling also induces sprouting of mossy fibers in the stratum infrapyramidale of CA3.

Amygdala↗