RÉSUMÉ
The aim of the present work was to study the potentiation of the AMPA and NMDA components of minimal excitatory postsynaptic currents (EPSC) evoked by activation of restricted numbers of synapses. EPSC of neurons in field CA1 in hippocampal slices were recorded in whole-call patch-clamp conditions selected such that both (AMPA and NMDA) components were present, and these were measured in parallel using computational methods in combination with pharmacological receptor blockade. There was a quite strong correlation between the amplitudes of the AMPA and NMDA components and this was regarded as evidence that they were generated by the same synapses. In cases producing this correlation, both components showed essentially equal long-term potentiation lasting from 5 min to 2 h after afferent tetanization. The data did not support the postsynaptic hypothesis and were in better agreement with the concept that the major mechanism for the persistence of the initial phase of long-term potentiation (up to 1-2 h) is based on increases in the quantity of transmitter released presynaptically.
Sujet(s)
Agonistes des acides aminés excitateurs/pharmacologie , Potentiels post-synaptiques excitateurs/effets des médicaments et des substances chimiques , Hippocampe/effets des médicaments et des substances chimiques , Potentialisation à long terme/effets des médicaments et des substances chimiques , N-Méthyl-aspartate/pharmacologie , AMPA/pharmacologie , Amino-2 phosphono-5 valérate/pharmacologie , Animaux , Antagonistes des acides aminés excitateurs/pharmacologie , Hippocampe/physiologie , Techniques in vitro , Techniques de patch-clamp , Rats , Rat Wistar , Facteurs tempsRÉSUMÉ
Excitatory postsynaptic currents (EPSC) were recorded from pyramidal neurons of the rat hippocampal slices as well as the AMPA and NMDA components. A strong enough correlation between the amplitudes of the components provided a reliable evidence of their generation by the same synapse. Both components revealed similar LTP following afferent tetanisation. The data obtained do not support postsynaptic mechanisms of the LTP maintenance but suggest that increased presynaptic release represents a basic mechanism of the early LTP maintenance.
Sujet(s)
Hippocampe/physiologie , Potentialisation à long terme/physiologie , Récepteur de l'AMPA/physiologie , Récepteurs du N-méthyl-D-aspartate/physiologie , Synapses/physiologie , Animaux , Stimulation électrique , Antagonistes des acides aminés excitateurs/pharmacologie , Techniques in vitro , Techniques de patch-clamp , Rats , Rat Wistar , Récepteur de l'AMPA/antagonistes et inhibiteurs , Récepteurs du N-méthyl-D-aspartate/antagonistes et inhibiteursRÉSUMÉ
Studies of the protective actions of three doses of delta-sleep-inducing peptide (DSIP) given at different times before barochamber compression of animals to an oxygen tension of 0.7 MPa showed that the optimum DSIP dose is 12 micrograms/100 g. Intraperitoneal administration of this dose of DSIP delayed the onset of generalized convulsive activity by a factor of 2-2.5 in animals exposed to an oxygen tension of 0.7 MPa and promoted normalization of the sleep-walking cycle within 24 h after exposure to hyperbaric oxygen (HBO), by creating an optimal balance between excitatory and inhibitory amino acid neuromediators.
Sujet(s)
Anticonvulsivants/pharmacologie , Peptide inducteur du sommeil lent/pharmacologie , Oxygénation hyperbare/effets indésirables , Crises épileptiques/prévention et contrôle , Animaux , Chambres d'exposition à l'atmosphère , Cortex cérébral/effets des médicaments et des substances chimiques , Cortex cérébral/métabolisme , Cortex cérébral/physiopathologie , Électroencéphalographie , Mâle , Agents neuromédiateurs/métabolisme , Rats , Crises épileptiques/étiologie , Crises épileptiques/métabolisme , Sommeil/effets des médicaments et des substances chimiques , Vigilance/effets des médicaments et des substances chimiquesRÉSUMÉ
Delta-sleep-inducing peptide (DSIP) exerted a protective effect against seizures, the effect depending on the DSIP ability to create an optimal ratio between inhibitory and excitatory amino acid neurotransmitters. Administration of the DSIP dramatically increased the contents of gamma-aminobutyric acid and homocarnosine while decreasing the glutamate and aspartate contents in the rat brain cortex.
Sujet(s)
Anticonvulsivants/pharmacologie , Peptide inducteur du sommeil lent/pharmacologie , Oxygénation hyperbare/effets indésirables , Animaux , Anticonvulsivants/administration et posologie , Chambres d'exposition à l'atmosphère , Chimie du cerveau/effets des médicaments et des substances chimiques , Cortex cérébral/effets des médicaments et des substances chimiques , Cortex cérébral/physiologie , Peptide inducteur du sommeil lent/administration et posologie , Relation dose-effet des médicaments , Électrodes implantées , Mâle , Rats , Crises épileptiques/étiologie , Crises épileptiques/prévention et contrôleRÉSUMÉ
The GABAergic system was adequate altered after simultaneous use of delta-sleeping peptide and piracetam in intact animals: gamma-butyric acid was accumulated unidirectionally by inhibiting brain glutamate decarboxylase activity. Administration of the peptide caused a slight decrease in the levels of aspartic acid, while piracetam contributed to a marked accumulation of the amino acid. The antistressor and adaptive effects of each drug were augmented if they were given simultaneously before acute emotional stress developed in the animals during one-hour hypokinesia; these effects were expressed as stabilized balance of inhibitory and excitatory neurotransmitter amino acids.