Schizophrenia is a very complex mental disease. It is actually quite possible that various mechanisms may end up producing similar symptoms. Several neurotransmitter systems have been implicated: dopamine, glutamate and GABA. Most of the hypotheses focus on synapses and receptors activated by those neurotransmitters. Let us try to think differently and forget the receptors for the moment: what would happen if an important inactivating system – such as glutamate transport in glial cells – was altered? How would it affect glutamatergic neurotransmission? Could a specific alteration in the expression of a particular glutamate transporter explain signs and symptoms of schizophrenia? The publications listed below should provide necessary background and aIDitional references which should help to answer the above questions. Bellesi M, Melone M, Gubbini A, Battistacci S & Conti F (2009) GLT-1 upregulation impairs prepulse inhibition of the startle reflex in adult rats. Glia 57 703-713 Kondziella D, Brenner E, Eyjolfsson EM & Sonnewald U (2007) How do glial-neuronal interactions fit into current neurotransmitter hypotheses of schizophrenia? Neurochemistry International 50 291-301 Melone M, Bellesi M, Ducati A, Iacoangeli M, Conti F (2011) Cellular and synaptic localization of EAAT2a in human cerebral cortex. Frontiers in Neuroanatomy 4 10.3389/fnana.2010.00151.
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