Connections of the cerebral cortex. I. The albino rat. A. Topography of the cortical areas

1946 ◽  
Vol 84 (2) ◽  
pp. 221-275 ◽  
Author(s):  
Wendell J. S. Krieg
1980 ◽  
Vol 17 (1-2) ◽  
pp. 79-83 ◽  
Author(s):  
R. Martinez-Rodriguez ◽  
M.A. Freire ◽  
R. Martinez-Murillo ◽  
A. Toledano ◽  
Esmeralda Cubillos

2002 ◽  
Vol 74 (1) ◽  
pp. 85-104 ◽  
Author(s):  
CARLOS LOPEZ-GARCIA ◽  
ASUNCION MOLOWNY ◽  
JUAN NACHER ◽  
XAVIER PONSODA ◽  
FRANCISCO SANCHO-BIELSA ◽  
...  

The medial cerebral cortex of lizards, an area homologous to the hippocampal fascia dentata, shows delayed postnatal neurogenesis, i.e., cells in the medial cortex ependyma proliferate and give rise to immature neurons, which migrate to the cell layer. There, recruited neurons differentiate and give rise to zinc containing axons directed to the rest of cortical areas, thus resulting in a continuous growth of the medial cortex and its zinc-enriched axonal projection. This happens along the lizard life span, even in adult lizards, thus allowing one of their most important characteristics: neuronal regeneration. Experiments in our laboratory have shown that chemical lesion of the medial cortex (affecting up to 95% of its neurons) results in a cascade of events: first, massive neuronal death and axonal-dendritic retraction and, secondly, triggered ependymal-neuroblast proliferation and subsequent neo-histogenesis and regeneration of an almost new medial cortex, indistinguishable from a normal undamaged one. This is the only case to our knowledge of the regeneration of an amniote central nervous centre by new neuron production and neo-histogenesis. Thus the lizard cerebral cortex is a good model to study neuronal regeneration and the complex factors that regulate its neurogenetic, migratory and neo-synaptogenetic events.


2006 ◽  
Vol 28 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Nathan B. Walters ◽  
Simon B. Eickhoff ◽  
Axel Schleicher ◽  
Karl Zilles ◽  
Katrin Amunts ◽  
...  

2000 ◽  
Vol 176 (3) ◽  
pp. 236-242 ◽  
Author(s):  
Sharon L. Eastwood ◽  
Nigel J. Cairns ◽  
Paul J. Harrison

BackgroundDecreased expression of proteins such as synaptophysin in the hippocampus and prefrontal cortex in schizophrenia is suggestive of synaptic pathology. However, the overall profile of changes is unclear.AimsTo investigate synaptophysin gene expression in the cerebral cortex in schizophrenia.MethodThe dorsolateral prefrontal (Brodmann area [BA] 9/46), anterior cingulate (BA 24), superior temporal (BA 22) and occipital (BA 17) cortex were studied in two series of brains, totalling 19 cases and 19 controls. Synaptophysin was measured by immunoautoradiography and immunoblotting. Synaptophysin messenger RNA (m RNA) was measured using in situ hybridisation.ResultsSynaptophysin was unchanged in schizophrenia, except for a reduction in BA 17 of one brain series. Synaptophysin mRNA was decreased in BA 17, and in BA 22 in the women with schizophrenia. No alterations were seen in BA 9/46.ConclusionsSynaptophysin expression is decreased in some cortical areas in schizophrenia. The alterations affect the mRNA more than the protein, and have an unexpected regional distribution. The characteristics of the implied synaptic pathology remain to be determined.


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