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: Cortical neuromodulatory transmitter systems refer to those classical neurotransmitters such as acetylcholine and monoamines, which share a number of common features. For instance, their centers are located in subcortical regions and send long projection axons to innervate the cortex. The same transmitter can either excite or inhibit cortical neurons depending on the composition of postsynaptic transmitter receptor subtypes. The overall functions of these transmitters are believed to serve as chemical bases of arousal, attention and motivation. The anatomy and physiology of neuromodulatory transmitter systems and their innervations in the cerebral cortex have been well characterized. In addition, ample evidence is available indicating that neuromodulatory transmitters also play roles in development and plasticity of the cortex. In this article, the anatomical organization and physiological function of each of the following neuromodulatory transmitters, acetylcholine, noradrenaline, serotonin, dopamine, and histamine, in the cortex will be described. The involvement of these transmitters in cortical plasticity will then be discussed. Available data suggest that neuromodulatory transmitters can modulate the excitability of cortical neurons, enhance the signal-to-noise ratio of cortical responses, and modify the threshold for activity-dependent synaptic modifications. Synaptic transmissions of these neuromodulatory transmitters are mediated via numerous subtype receptors, which are linked to multiple signal transduction mechanisms. Among the neuromodulatory transmitter receptor subtypes, cholinergic M(1), noradrenergic beta(1) and serotonergic 5-HT(2C) receptors appear to be more important than other receptor subtypes for cortical plasticity. In general, the contribution of neuromodulatory transmitter systems to cortical plasticity may be made through a facilitation of NMDA receptor-gated processes.Neuroscience 02/2002; 111(4):815-35. · 3.12 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.