Neurons In Infragranular Layers Research Articles

Sensory-driven and spontaneous gamma oscillations engage distinct cortical circuitry.

Gamma oscillations are a robust component of sensory responses but are also part of the background spontaneous activity of the brain. To determine whether the properties of gamma oscillations in cortex are specific to their mechanism of generation, we compared in mouse visual cortex in vivo the laminar geometry and single-neuron rhythmicity of oscillations produced during sensory representation with those occurring spontaneously in the absence of stimulation. In mouse visual cortex under anesthesia (isoflurane and xylazine), visual stimulation triggered oscillations mainly between 20 and 50 Hz, which, because of their similar functional significance to gamma oscillations in higher mammals, we define here as gamma range. Sensory representation in visual cortex specifically increased gamma oscillation amplitude in the supragranular (L2/3) and granular (L4) layers and strongly entrained putative excitatory and inhibitory neurons in infragranular layers, while spontaneous gamma oscillations were distributed evenly through the cortical depth and primarily entrained putative inhibitory neurons in the infragranular (L5/6) cortical layers. The difference in laminar distribution of gamma oscillations during the two different conditions may result from differences in the source of excitatory input to the cortex. In addition, modulation of superficial gamma oscillation amplitude did not result in a corresponding change in deep-layer oscillations, suggesting that superficial and deep layers of cortex may utilize independent but related networks for gamma generation. These results demonstrate that stimulus-driven gamma oscillations engage cortical circuitry in a manner distinct from spontaneous oscillations and suggest multiple networks for the generation of gamma oscillations in cortex.

Improper activation of D1 and D2 receptors leads to excess noise in prefrontal cortex.

The dopaminergic system has been shown to control the amount of noise in the prefrontal cortex (PFC) and likely plays an important role in working memory and the pathophysiology of schizophrenia. We developed a model that takes into account the known receptor distributions of D1 and D2 receptors, the changes these receptors have on neuron response properties, as well as identified circuitry involved in working memory. Our model suggests that D1 receptor under-stimulation in supragranular layers gates internal noise into the PFC leading to cognitive symptoms as has been proposed in attention disorders, while D2 over-stimulation gates noise into the PFC by over-activation of cortico-striatal projecting neurons in infragranular layers. We apply this model in the context of a memory-guided saccade paradigm and show deficits similar to those observed in schizophrenic patients. We also show set-shifting impairments similar to those observed in rodents with D1 and D2 receptor manipulations. We discuss how the introduction of noise through changes in D1 and D2 receptor activation may account for many of the symptoms of schizophrenia depending on where this dysfunction occurs in the PFC.

Physiology and morphology of inverted pyramidal neurons in the rodent neocortex

An increasing number of studies indicate that there exists greater diversity of cortical neurons than previously appreciated. In the present report, we use a combination of physiological and morphological methods to characterize cortical neurons in infragranular layers with apical dendrites pointing toward the white-matter compared to those neurons with apical dendrites pointing toward the pia in both mouse and rat neocortex. Several features of the dendritic morphology and intrinsic and synaptic physiology of these “inverted” neurons revealed numerous differences among this cell type between species. We also found differences between the different cell types within the same species. These data reveal that similar cell types in the rat and mouse may not always share similar physiological and morphological properties. These data are relevant to models of information processing through micro- and larger neocortical circuits and indicate that different cell types found within similar lamina can have different functional properties.

Differential distribution of NADPH-diaphorase histochemistry in human cerebral cortex

β−Nicotinamidedinucleotide phosphate diaphorase (NADPH-d) colocalizes with NOS in the central nervous system. Two types of NADPH-d-positive neurons are present in the primate cerebral cortex: type 1, intensely and Golgi-like labeled neurons, a subset of GABAergic interneurons; type 2, lightly labeled neurons (divided into two subclasses, a first one having a lightly stained cell body bearing only one short process, and a second one showing intense NADPH-d staining with short processes extending radially). We have analyzed the distribution of NADPH-d activity in human frontal, temporal, and occipital cortical areas, finding remarkable laminar and interareal differences in cell size and distribution of the different cell types. There was a clear bias for type 1 neurons in infragranular layers in all areas considered; both in supra- and infragranular layers, their density was highest in frontal, and lowest in temporal cortex. The density of type 2 neurons was lower supragranularly in temporal cortex and infragranularly in occipital cortex. The overall density of type 2 cells was remarkably higher in occipital cortex than in the temporal and frontal ones. Type 1 neurons were significantly larger than type 2, and were smaller in the supragranular than in the infragranular subzone in occipital and temporal cortex. Type 1 cells were significantly larger in frontal cortex than in occipital and temporal cortex, and type 2 cells were significantly smaller in occipital than in temporal and frontal cortex. These area-related differences might reflect differences between heterotypic and homotypic cortex in the regulation of cortical blood flow.

Effects of neonatal freeze lesions on expression of parvalbumin in rat neocortex.

Neonatal freeze lesions to the cortical plate result in focal malformations of the cerebral cortex that resemble four-layered microgyria. These malformations have been associated with local and distant changes in neuronal architecture, and have been implicated in the neocortical epileptiform discharges that can spread up to 4 mm away from the malformation itself. In an effort to assess potential changes in the development of one population of inhibitory interneurons in this malformation, we measured the density of parvalbumin-immunoreactive (ParvIR) neurons in microgyric and control cerebral cortex on postnatal days 13, 15, 21 and 64. In comparison to controls, microgyric animals exhibited a transient decrease in the expression of parvalbumin immunoreactivity in supragranular neurons, both within the malformation itself and in normal six-layered cortex up to 2 mm adjacent to it. This difference disappeared by P21. In addition, there was a permanent diminution of the density of ParvIR neurons in infragranular layers both within and immediately adjacent to the microgyrus. These results indicate that early injury to the cortical plate gives rise to both focal and more widespread changes in cortical architecture.

Mapping to Mouse Chromosome 3 of the Gene Encoding Latexin (Lxn) Expressed in Neocortical Neurons in a Region-Specific Manner

Latexin was first found as a 29-kDa antigen expressed in a subset of neurons in infragranular layers of lateral, but not dorsal, neocortical areas in the rat using a monoclonal antibody PC3.1. It was found that the vast majority of latexin-expressing neurons in both layers V and VI within the lateral neocortex were generated concurrently at Embryonic Day 15, demonstrating a strict correlation between the molecular identity of neurons and the time of their generation. Since neurons expressing latexin are located in the restricted part of the neocortex, latexin has been used as a useful molecular marker to elucidate the mechanism underlying cortical regional specification. The latexin cDNA isolated from a cDNA library of the rat cerebral cortex encodes a protein composed of 223-amino-acid residues containing two potential Ca{sup 2+}/calmodulin-dependent protein kinase sites and one cGMP-dependent protein kinase phosphorylation site. The absence of any signal peptide or potential transmembrane domain is consistent with the apparent cytosolic localization of latexin in the rat brain. The transcripts of latexin were expressed in not only neutral but also nonneural tissues (e.g., lung, spleen, kidney, heart, and digestive tracts). Recently, it has been demonstrated that latexin purified from the rat brain has inhibitory activitymore » against carboxypeptidase A1, carboxypeptidase A2, and mast cell carboxypeptidase A, with less carboxypeptidase B-inhibiting activity. The amino acid sequence deduced from the rat latexin cDNA has no strict homology to any sequences so far known. Genomic Southern blot analysis using a cDNA probe of rat latexin suggested that the gene encoding latexin in the rat has homologues in other mammalian species and in the chicken, but not in the nematode, fly, or frog. 9 refs., 1 fig.« less