Atlas of Neuroanatomy and Neurophysiology by MD Frank H. Netter

Atlas of Neuroanatomy and Neurophysiology by MD Frank H. Netter

By MD Frank H. Netter

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Psychiatry 27:675– 680. , and Rama, R. 2007. Iron, oxidative stress and early neurological deterioration in ischemic stroke. Curr. Med. 14:857–874. L. 1999. A glutamatergic deficiency model of schizophrenia. Br. J. Psychiatry 174(Suppl. 37):2–6. L. 2001. Interactions between monoamines, glutamate, and GABA in schizophrenia: new evidence. Annu. Rev. Pharmacol. Toxicol. 41:237–260. , and Carlsson, A. 1990. Interactions between glutaminergic and monoaminergic systems within the basal ganglia – implications for schizophrenia and Parkinson’s disease.

Mechanisms regulating GABAergic inhibitory transmission in the basolateral amygdala: implications for epilepsy and anxiety disorders. Amino Acids 32:305– 315. D. 2005. An integrative theory of coeruleu-norepinephrine function: adaptive gain and optimal performance. Annu. Rev. Neurosci. 28:403–450. S. 1982. The cholinergic hypothesis of geriatric memory dysfunction. Science 21:408–417. E. 2007. Emerging disease-modifying therapies for the treatment of motor neuron disease/amyotrophic lateral sclerosis.

2007). , 2006; Straub and Weinberger, 2006). Several of these target the NMDA receptor and control proteins that act to strengthen the synapse. Dysfunction of NMDA control proteins can result in hypofunction of the NMDA synapse: the NMDA receptor hypofunction hypothesis of schizophrenia (Stahl, 2007a). Weak synapses with AMPA receptors may be pruned, but this process takes time. In addition, synaptic pruning is very active during adolescence. This may explain why schizophrenia onset is associated with the adolescent period of life (Stahl, 2007b).

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