Updated neuronal scaling rules for the brains of Glires (rodents/lagomorphs).

Brain size scales as different functions of its number of neurons across mammalian orders such as rodents, primates, and insectivores. In rodents, we have previously shown that, across a sample of 6 species, from mouse to capybara, the cerebral cortex, cerebellum and the remaining brain structures increase in size faster than they gain neurons, with an accompanying decrease in neuronal density in these structures [Herculano-Houzel et al.: Proc Natl Acad Sci USA 2006;103:12138-12143]. Important remaining questions are whether such neuronal scaling rules within an order apply equally to all pertaining species, and whether they extend to closely related taxa. Here, we examine whether 4 other species of Rodentia, as well as the closely related rabbit (Lagomorpha), conform to the scaling rules identified previously for rodents. We report the updated neuronal scaling rules obtained for the average values of each species in a way that is directly comparable to the scaling rules that apply to primates [Gabi et al.: Brain Behav Evol 2010;76:32-44], and examine whether the scaling relationships are affected when phylogenetic relatedness in the dataset is accounted for. We have found that the brains of the spiny rat, squirrel, prairie dog and rabbit conform to the neuronal scaling rules that apply to the previous sample of rodents. The conformity to the previous rules of the new set of species, which includes the rabbit, suggests that the cellular scaling rules we have identified apply to rodents in general, and probably to Glires as a whole (rodents/lagomorphs), with one notable exception: the naked mole-rat brain is apparently an outlier, with only about half of the neurons expected from its brain size in its cerebral cortex and cerebellum.

Immunohistochemical study of six cases of Taylor's type focal cortical dysplasia: correlation with electroclinical data.

PURPOSE: Cortical specimens from six patients operated on for drug-resistant epilepsy diagnosed as Taylor's type focal cortical dysplasia were submitted to neuropathological and immunohistochemical studies. METHODS: All patients were submitted to presurgical investigations including clinical and neuropsychological evaluations, EEG/video telemetry of ictal and interictal events, magnetic resonance imaging, and ictal and interictal single-photon emission computed tomography (SPECT). Recordings from electrocorticography (ECoG) were obtained in four cases and from subdural electrode implantation in two. Postsurgical follow-up was assessed according to Engel's score. Immunohistochemistry (IHC) was processed for parvalbumin (PV), calbindin D28-K (CB), nonphosphorylated neurofilaments (SMI-311), glial fibrillary acidic protein (GFAP) in all cases. RESULTS: We found continuous/quasi-continuous spikes and sharp-wave patterns in three cases and frequent repetitive bursting of polyspikes and ECoG seizures in two cases. Every patient showed cortical dyslamination, abnormal and giant neurons, and balloon cells. GFAP immunoreactivity was found in astrocytes and some balloon cells that were less intensely stained. Nonphosphorylated neurofilaments SMI-311 immunoreactivity was found in normal and giant neurons and in some balloon cells, making visible thin neuropils. PV immunoreactivity was present in normal interneurons and in fibers in layers IV-V. PV-negative balloon cells were surrounded by abundant PV-positive fibers. CB immunoreactivity was found mostly in interneurons in layers II-III. CONCLUSIONS: Our research is inconclusive. More cases should be investigated, and we must draw more accurate anatomic correlations between the ECoG recordings and surgical specimens studied with IHC.