E.G. Jones

Journal Article CONNEXIONS OF THE SOMATIC SENSORY CORTEX OF THE RHESUS MONKEY: I.—IPSILATERAL CORTICAL CONNEXIONS Get access E. G. JONES, E. G. JONES Department of Human AnatomyOxford Search for other works by this author on: Oxford Academic PubMed Google Scholar T. P. S. POWELL T. P. S. POWELL Department of Human AnatomyOxford Search for other works by this author on: Oxford Academic PubMed Google Scholar Brain, Volume 92, Issue 3, March 1969, Pages 477–502, https://doi.org/10.1093/brain/92.3.477 Published: 01 March 1969 Article history Received: 03 January 1969 Published: 01 March 1969

The number and proportion of neurons displaying GABA immunoreactivity were determined for 50-micron-wide columns through the thickness of 10 areas of monkey cerebral cortex, including the precentral motor area (area 4), 3 cytoarchitectonic fields of the first somatic sensory area (areas 3b, 1, and 2), 2 areas of parietal association cortex (areas 5 and 7), the first and second visual areas (areas 17 and 18), area 21 of the temporal lobe, and areas of the orbital and lateral frontal cortex. Methods of fixation and immunocytochemical processing were designed to maximize the number of stained cells in 15-micron-thick frozen sections and 1-micron-thick plastic sections. In 8 of the 10 areas the number and proportion of GABA-immunoreactive neurons per 50-micron-wide column were found to be the same (34-43 cells/column; 25% of the total neuronal population). Areas 17 and 3b differed. Area 17 contained 50% more GABA-immunoreactive neurons (52-66 cells/column) but more than twice the total number of neurons, so that the GABA cells made up less than 20% of the total. In 3 monkeys, the number and proportion of GABA-positive neurons per 50-micron-wide column in area 3b were smaller than in adjacent areas of sensorimotor cortex (26-42 cells/column; 19-22%). In 2 other monkeys, the number and proportion (34-43 cells/column; 24-26%) were the same as in adjacent areas. Despite the similarity among most areas of monkey cortex, within some areas, the number of GABA-positive neurons per 50-micron-wide column varied as much as 30%. These variations form a significant, repeating pattern only in area 18, where narrow bands (150-200 micron wide) of relatively few stained cells alternated with either narrow or wide bands (600-700 micron wide) in which columns contained more cells. The GABA-immunoreactive neurons were unevenly distributed across layers, with every area containing large numbers and proportions of stained cells in layer II, and every area but area 4 displaying a second concentration in the principal thalamocortical recipient layers. In area 4, the number of GABA-positive neurons declined sharply from layer II to layer III and remained low through layer VI. For areas displaying the greatest intra-areal variability, only 1 or 2 layers contributed significantly to that variability (layer IV in area 3b, layers III and V in area 18, and layers II and III in area 17).(ABSTRACT TRUNCATED AT 400 WORDS)

Anatomical methods which depend upon the anterograde axonal transport of isotopically labeled neuronal proteins or the retrograde axonal transport of the enzyme, horseradish peroxidase, have been used to elucidate the relationships between the reticular complex and the dorsal thalamus and cerebral cortex. Injections of tritiated amino acids in the dorsal thalamus or cerebral cortex in rats, cats and monkeys, show that as the bundles of thalamo-cortical and cortico-thalamic fibers joining a particular dorsal thalamic nucleus to its associated area of the cerebral cortex traverse the reticular complex, they each give rise to a dense zone of terminals occupying a sector of the reticular complex which is relatively constant for that dorsal thalamic nucleus and cortical area. However, because of the wide extent of the dendritic fields of the reticular cells and the degree of overlap between the sectors of the complex subtended by adjacent dorsal thalamic nuclei and adjacent cortical areas, it is likely that the reticular complex samples thalamo-cortical and cortico-thalamic activity in a somewhat unspecific manner. Fibers passing to the reticular complex from the intralaminar nuclei of the thalamus appear to be associated with the projection from the intralaminar nuclei to the striatum. Injections of tritiated amino acids in the reticular complex itself and injections of horseradish peroxidase in various other parts of the brain show that the only efferent pathway from the reticular complex terminates in the nuclei of the dorsal thalamus. The reticular complex does not appear to send fibers to other components of the ventral thalamus nor to the cerebral cortex.

Abstract Autoradiographic, axonal degeneration, and horseradish peroxidase fiber tracing methods were employed to investigate the organization, development and potential plasticity of the thalamocortical projection to the somatic sensory cortex of the rat. In the adult animal, thalamocortical terminals are concentrated primarily in layers I and IV and in the upper part of layer VI. Fibers terminating in layers IV and VI arise from a different thalamic region than those terminating in layer I. Discrete clusters of fibers and terminals 250–450 μm wide are distributed only to the parts of the SI cortex containing dense aggregates of layer IV granule cells and not to the intervening, less granular and commissurally connected zones. At birth, thalamocortical fibers have invaded the deep part of the developing SI cortex and are concentrated in the upper part of layer VI. Between the age of two and three days, an additional concentration of fibers appears in the part of the cortical plate which will become layer IV. Layer IV is clearly recognizable by three days of age and the dense granule cell aggregates appear in it no more than one day later. The ingrowth of commissural fibers (Wise and Jones, '76) lags behind that of thalamic fibers. The mature commissural fiber pattern is not established until the age of seven days. After removal of the developing thalamocortical system by thalamotomy in newborn rats, subsequent investigation of the commissural system in the adult showed that no commissural fibers or terminals had invaded either laminae or zones of the cortex deprived of thalamic input. Similarly, commissurotomy at birth was not followed by sprouting of thalamic fibers into zones or laminae deprived of commissural connections. The connectional specificity observed in these neocortical fiber systems contrasts markedly with the plasticity of connections reported in allocortical systems. Removal of thalamocortical afferents before they attain their definitive distribution does not radically effect the overall development of the dense granule cell aggregates in layer IV. Within the aggregates, however, subsidiary features such as the “barrels” fail to appear. This finding suggests that certain elements of cortical architecture such as the dense granule cell aggregates are independent of thalamic afferents while others, such as the barrels, result from the interaction of the developing thalamocortical fibers and/or terminals with maturing neurons.

NMDA receptor antagonists can induce a schizophrenia-like psychosis, but the role of NMDA receptors in the pathophysiology of schizophrenia remains unclear. Expression patterns of mRNAs for five NMDA receptor subunits (NR1/NR2A-D) were determined by in situ hybridization in prefrontal, parieto-temporal, and cerebellar cortex of brains from schizophrenics and from neuroleptic-treated and nonmedicated controls. In the cerebral cortex of both schizophrenics and controls, mRNAs for NR1, NR2A, NR2B, and NR2D subunits were preferentially expressed in layers II/III, Va, and VIa, with much higher levels in the prefrontal than in the parieto-temporal cortex. Levels of mRNA for the NR2C subunit were very low overall. By contrast, the cerebellar cortex of both schizophrenics and controls contained very high levels of NR2C subunit mRNA, whereas levels for the other subunit mRNAs were very low, except NR1, for which levels were moderate. Significant alterations in the schizophrenic cohort were confined to the prefrontal cortex. Here there was a shift in the relative proportions of mRNAs for the NR2 subunit family, with a 53% relative increase in expression of the NR2D subunit mRNA. No comparable changes were found in neuroleptic-treated or untreated controls. These findings indicate regional heterogeneity of NMDA receptor subunit expression in human cerebral and cerebellar cortex. In schizophrenics, the alterations in expression of NR2 subunit mRNA in prefrontal cortex are potential indicators of deficits in NMDA receptor-mediated neurotransmission accompanying functional hypoactivity of the frontal lobes.