Interaction of glutamatergic and adrenergic inputs of cortical neurons during conditioning
Department of Physiology of Higher Nervous Activity, Bogomoletz Institute of Physiology, Ukraine. Neuroscience
(Impact Factor: 3.36).
03/1997; 76(3):877-90. DOI: 10.1016/S0306-4522(96)00329-6
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.
Available from: Claudia Grasso
- "than neuromodulation, regarded as the most significant function of the amine. An influence of noradrenaline on glutamatergic transmission , consisting in the modulation of post-synaptic potentials and/or of glutamate release and uptake, has been found in vitro in numerous structures such as olfactory cortex , hippocampal formation and entorhinal cortex , amygdala , cerebellum  and in vivo in sensorimotor cortex , lateral reticular nucleus  and spinal cord . "
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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. DOI:10.1016/j.neulet.2009.08.035 · 2.03 Impact Factor
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ABSTRACT: Changes in impulse activity of sensorimotor cortex neurons associated with interaction of glutamate and dopamine during conditioned placing reaction were investigated in experiments on cats. Application of either glutamate or levodopa as a dopamine precursor increased background and evoked impulse activity in many of sensorimotor cortex neurons. It occurred occasionally that an increased impulse activity of cortical neurons produced by joint application of glutamate and levodopa could be much more intense than that produced by one of these substances. Amphetamine acted on cortical neurons in a similar way as levodopa. Haloperidol, a non-selective blocker of dopamine1 and dopamine2 receptors, increased or did not change background and evoked impulse activity in some cortical neurons. In contrast to application of glutamate alone, simultaneous application of glutamate and haloperidol to the neocortex depressed neuronal responses connected with conditioned movement. Thus, glutamate cannot exert its potentiating effect on evoked neuronal activity due to the depressing action of haloperidol. This means that glutamate potentiation is realized to a great extent through molecular mechanisms common for glutamate and dopamine, possibly through G-proteins which are common for glutamate metabotropic and dopamine receptors.
Neuroscience 08/1998; 85(2):347-59. DOI:10.1016/S0306-4522(97)00643-X · 3.36 Impact Factor
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ABSTRACT: Experiments were conducted on cats to study the effects of iontophoretic application of glutamate and a number of modulators on the spike activity of neurons in the sensorimotor cortex during a conditioned reflex. These studies showed that glutamate, as well as exerting a direct influence on neuron spike activity, also had a delayed facilitatory action lasting 10-20 min after iontophoresis was finished. Adrenomimetics were found to have a double modulatory effect on intracortical glutamate connections: inhibitory and facilitatory effects were mediated by beta1 and beta2 adrenoceptors respectively. Although dopamine, like glutamate, facilitated neuron spike activity during the period of application, the simultaneous facilitatory actions of glutamate and L-DOPA were accompanied by occlusion of spike activity, and simultaneous application of glutamate and haloperidol suppressed spike activity associated with the conditioned reflex response. Facilitation thus appears to show a significant level of dependence on metabotropic glutamate receptors which, like dopamine receptors, are linked to the intracellular medium via Gi proteins.
Neuroscience and Behavioral Physiology 01/2000; 30(6):635-44. DOI:10.1023/A:1026690531090
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