Association cortex

Araneda, R. Andrade, R. (1991). 5-Hydroxytryptamine2 and 5-hydroxytryptamineiA receptors mediate opposing responses on membrane excitability in rat association cortex. Neuroscience 40, 399-412. 

Haj-Dahmane S, Andrade R 1996 Muscarinic activation of a voltage-dependent cation nonselective current in rat association cortex. J Neurosci 16 3848-3861 Hardie RC, Minke B 1993 Novel Ca2+ channels underlying transduction in Drosophila photoreceptors implications for phosphoinositide-mediated Ca2+ mobilization. Trends Neurosci 16 371-376... 

Yamaguchi, H., SugUiara, S., Ogawa, A., Oshima, N., lhara, Y. (2001) Alzheimer beta amyloid deposition enhanced by APOE epsUon 4 gene precedes neurofibritlary pathology in the frontal association cortex of non-demented senior subjects. J. Neuropathol. Exp. Neurol, 60,731-739. 

Figure 2. A. Distribution of the serotonin receptor, 5-HT2 subtype which binds the indoleamine hallucinogens, in human temporal cortex as indicated by the binding of radiolabelled ketanserin. While the receptor is relatively sparse in the hippocampal area and entorhinal cortex on the top right, it is concentrated in the temporal association cortex including the area concerned with visual association.

The thalamus is the gateway to cortical processing of all incoming sensory information, represented in Figure 2.1 by the three major systems somatosensory (S), auditory (A), and visual (V). Primary sensory cortices (SI, Al, VI) receive information from the appropriate input modules (sensory organ -I- thalamus). The association cortex integrates information from primary cortices, from subcortical structures, and from brain areas affiliated with memory to create an internal representation of the sensory information. The medial temporal lobe (i.e., hippocampus, amygdala) serves two major... 

Serotonin s effects include classical neuronal inhibition, as well as modulation. The study of dreaming teaches us that disinhibition is likely the cause of positive signs of hallucination, emotional intensification, and confabulation, whereas demodulation more likely causes the negative signs such as memory loss, disorientation, and bizarreness. Serotonin blockade induced disinhibition is one of the mechanisms by which the very same set of aspects of model psychoses is generated the visual distortion and hallucination could result from visual system disinhibition the emotional intensification could result from limbic system disinhibition and confabulation could result from associative cortex disinhibition. 

Goldman-Rakic PS. 1988. Topography of cognition Parallel distributed networks in primate association cortex. Ann Rev Neurosci 11 137-156. 

Buchanan RW, Francis A, Arango C, Miller K, Lefkowitz DM, et al. 2004. Morphometric assessment of the heteromodal association cortex in schizophrenia. Am J Psychiatry... 

Chance SA, Casanova MF, Switala AE, Crow TJ, Esiri MM. 2006b. Minicolumn thinning in temporal lobe association cortex but not primary auditory cortex in normal human ageing. Acta Neuropathol (Berl) 111(5) 459-464. 

Foxe JJ, Wylie GR, Martinez A, Schroeder CE, Javitt DC, et al. 2002. Auditory-somatosensory multisensory processing in auditory association cortex An fMRI study. J Neurophysiol 88(1) 540-543. 

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