Interaction of glutamatergic and adrenergic inputs of cortical neurons during conditioning.
ABSTRACT Background and evoked activities of sensorimotor cortex neurons have been examined on learning cats with conditioned placing reaction before, during and after iontophoretic application of synaptically active drugs. It was shown that glutamate exerted not only a direct excitatory effect on the cortical neurons during its application, but also developed modulatory influences on background and evoked impulse activity after cessation of application in the subsequent 10-20 min. Adrenergic influences on the activity of neocortical neurons evoked by application of adrenomimetic drugs were complex and consisted of at least two different types. Noradrenaline depressed background and particularly evoked activity of many neurons through beta1-adrenoreceptors. At the same time, activation of beta2-adrenoreceptors was accompanied by facilitation of background and evoked activity during application and 10-20 min after its cessation, as was shown in experiments with alupent. Co-application of glutamate and alupent improved facilitation of impulse response evoked by conditioned stimuli. It was concluded that beta1- and beta2-adrenergic inputs to neocortical neurons are involved in plasticity changes of glutamate inputs of some cortical neurons.
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ABSTRACT: The glutamatergic pathway has been consistently involved in the physiopathology of depressive disorder. However a complete dissection and integration of its role in the context of other known mechanisms is lacking. We summarized and integrated the evidence of various levels of interaction between glutamatergic and monoaminergic pathways (see videos). We identified six molecular pathways, some of which with specific regional distribution within the brain. From the six pathways we identified the key proteins and their coding genes, we then provided a detailed list of possible candidates with practical suggestions for association studies planning.Progress in Neurobiology 06/2011; 94(4):418-60. · 9.04 Impact Factor
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ABSTRACT: Increases in firing rate induced in secondary vestibular neurons by microiontophoretic application of glutamate were studied during long-lasting applications of noradrenaline (NA) and/or its antagonists and agonists. Sixty-nine percent of the tested neurons, scattered through all nuclei of the vestibular complex, modified their responsiveness to glutamate in the presence of NA. The effects were depressive in a majority (40%) and enhancing in a minority (29%) of cases. NA application depressed responses to glutamate more often than it increased them in lateral, medial and superior vestibular nuclei, while the reverse was true for the spinal nucleus. The mean intensities of NA-evoked effects were comparable in the various nuclei. The enhancing effects of NA were antagonized by application of the alpha2 receptor antagonist yohimbine, and their depressive effects were enhanced by the beta receptor antagonist timolol. It is concluded that NA exerts a control on the processing of vestibular information and that this modulation is exerted by at least two mechanisms involving alpha2 and beta noradrenergic receptors.Neuroscience Letters 09/2009; 464(3):173-8. · 2.03 Impact Factor
Article: Reference center spina bifidaAnnals of Physical and Rehabilitation Medicine. 01/2011; 54.