Pyramidal Cell Structure Research Articles

Cellular 3D-reconstruction and analysis in the human cerebral cortex using automatic serial sections

Techniques involving three-dimensional (3D) tissue structure reconstruction and analysis provide a better understanding of changes in molecules and function. We have developed AutoCUTS-LM, an automated system that allows the latest advances in 3D tissue reconstruction and cellular analysis developments using light microscopy on various tissues, including archived tissue. The workflow in this paper involved advanced tissue sampling methods of the human cerebral cortex, an automated serial section collection system, digital tissue library, cell detection using convolution neural network, 3D cell reconstruction, and advanced analysis. Our results demonstrated the detailed structure of pyramidal cells (number, volume, diameter, sphericity and orientation) and their 3D spatial organization are arranged in a columnar structure. The pipeline of these combined techniques provides a detailed analysis of tissues and cells in biology and pathology.

HIV-1 Tat and Morphine Differentially Disrupt Pyramidal Cell Structure and Function and Spatial Learning in Hippocampal Area CA1: Continuous versus Interrupted Morphine Exposure.

About half the people infected with human immunodeficiency virus (HIV) have neurocognitive deficits that often include memory impairment and hippocampal deficits, which can be exacerbated by opioid abuse. To explore the effects of opioids and HIV on hippocampal CA1 pyramidal neuron structure and function, we induced HIV-1 transactivator of transcription (Tat) expression in transgenic mice for 14 d and co-administered time-release morphine or vehicle subcutaneous implants during the final 5 d (days 9–14) to establish steady-state morphine levels. Morphine was withheld from some ex vivo slices during recordings to begin to assess the initial pharmacokinetic consequences of opioid withdrawal. Tat expression reduced hippocampal CA1 pyramidal neuronal excitability at lower stimulating currents. Pyramidal cell firing rates were unaffected by continuous morphine exposure. Behaviorally, exposure to Tat or high dosages of morphine impaired spatial memory Exposure to Tat and steady-state levels of morphine appeared to have largely independent effects on pyramidal neuron structure and function, a response that is distinct from other vulnerable brain regions such as the striatum. By contrast, acutely withholding morphine (from morphine-tolerant ex vivo slices) revealed unique and selective neuroadaptive shifts in CA1 pyramidal neuronal excitability and dendritic plasticity, including some interactions with Tat. Collectively, the results show that opioid-HIV interactions in hippocampal area CA1 are more nuanced than previously assumed, and appear to vary depending on the outcome assessed and on the pharmacokinetics of morphine exposure.

Variation in Pyramidal Cell Morphology Across the Human Anterior Temporal Lobe.

Pyramidal neurons are the most abundant and characteristic neuronal type in the cerebral cortex and their dendritic spines are the main postsynaptic elements of cortical excitatory synapses. Previous studies have shown that pyramidal cell structure differs across layers, cortical areas, and species. However, within the human cortex, the pyramidal dendritic morphology has been quantified in detail in relatively few cortical areas. In the present work, we performed intracellular injections of Lucifer Yellow at several distances from the temporal pole. We found regional differences in pyramidal cell morphology, which showed large inter-individual variability in most of the morphological variables measured. However, some values remained similar in all cases. The smallest and least complex cells in the most posterior temporal region showed the greatest dendritic spine density. Neurons in the temporal pole showed the greatest sizes with the highest number of spines. Layer V cells were larger, more complex, and had a greater number of dendritic spines than those in layer III. The present results suggest that, while some aspects of pyramidal structure are conserved, there are specific variations across cortical regions, and species.

A Role for Matrix Metalloproteases in Antidepressant Efficacy.

Major depressive disorder is a debilitating condition that affects approximately 15% of the United States population. Though the neurophysiological mechanisms that underlie this disorder are not completely understood, both human and rodent studies suggest that excitatory/inhibitory (E/I) balance is reduced with the depressive phenotype. In contrast, antidepressant efficacy in responsive individuals correlates with increased excitatory neurotransmission in select brain regions, suggesting that the restoration of E/I balance may improve mood. Enhanced excitatory transmission can occur through mechanisms including increased dendritic arborization and synapse formation in pyramidal neurons. Reduced activity of inhibitory neurons may also contribute to antidepressant efficacy. Consistent with this possibility, the fast-acting antidepressant ketamine may act by selective inhibition of glutamatergic input to GABA releasing parvalbumin (PV)-expressing interneurons. Recent work has also shown that a negative allosteric modulator of the GABA-A receptor α subunit can improve depression-related behavior. PV-expressing interneurons are thought to represent critical pacemakers for synchronous network events. These neurons also represent the predominant GABAergic neuronal population that is enveloped by the perineuronal net (PNN), a lattice-like structure that is thought to stabilize glutamatergic input to this cell type. Disruption of the PNN reduces PV excitability and increases pyramidal cell excitability. Various antidepressant medications increase the expression of matrix metalloproteinases (MMPs), enzymes that can increase pyramidal cell dendritic arborization and spine formation. MMPs can also cleave PNN proteins to reduce PV neuron-mediated inhibition. The present review will focus on mechanisms that may underlie antidepressant efficacy, with a focus on monoamines as facilitators of increased matrix metalloprotease (MMP) expression and activation. Discussion will include MMP-dependent effects on pyramidal cell structure and function, as well as MMP-dependent effects on PV expressing interneurons. We conclude with discussion of antidepressant use for those at risk for Alzheimer’s disease, and we also highlight areas for further study.

The Role of Dendritic Brain-Derived Neurotrophic Factor Transcripts on Altered Inhibitory Circuitry in Depression

BackgroundA parallel downregulation of brain-derived neurotrophic factor (BDNF) and somatostatin (SST), a marker of inhibitory gamma-aminobutyric acid interneurons that target pyramidal cell dendrites, has been reported in several brain areas of subjects with major depressive disorder (MDD). Rodent genetic studies suggest that they are linked and that both contribute to the illness. However, the mechanism by which they contribute to the pathophysiology of the illness has remained elusive. MethodsWith quantitative polymerase chain reaction, we determined the expression level of BDNF transcript variants and synaptic markers in the prefrontal cortex of patients with MDD and matched control subjects (n = 19/group) and of C57BL/6J mice exposed to chronic stress or control conditions (n = 12/group). We next suppressed Bdnf transcripts with long 3′ untranslated region (L-3′-UTR) using short hairpin RNA and investigated changes in cell morphology, gene expression, and behavior. ResultsL-3′-UTRs containing BDNF messenger RNAs, which migrate to distal dendrites of pyramidal neurons, are selectively reduced, and their expression was highly correlated with SST expression in the prefrontal cortex of subjects with MDD. A similar downregulation occurs in mice submitted to chronic stress. We next show that Bdnf L-3′-UTR knockdown is sufficient to induce 1) dendritic shrinkage in cortical neurons, 2) cell-specific MDD-like gene changes (including Sst downregulation), and 3) depressive- and anxiety-like behaviors. The translational validity of the Bdnf L-3′-UTR short hairpin RNA–treated mice was confirmed by significant cross-species correlation of changes in MDD-associated gene expression. ConclusionsThese findings provide evidence for a novel MDD-related pathological mechanism linking local neurotrophic support, pyramidal cell structure, dendritic inhibition, and mood regulation.

EFEK ASAM ALFA LIPOAT PADA KADAR MDA DAN HISTOLOGI OTAK DIABETES MELLITUS TIPE 1

Background. Diabetic neuropaty is a condition that can affect pyramidal cells and neuronal cells in the hippocampus. Alpha lipoic acid is effective in pathological conditions where ROS (Reactive Oxygen Species) have been implicated, include in brain. Objective. To investigate effects of ALA on oxidative stress in diabetic brain of male Wistar rats. Methods. True experimental design and Posttest Only Control Group are used in this study. Thirty male rats were randomly divided into 5 groups: normal rats without ALA (NTA), diabetic rats without ALA (DTA), diabetic rats with ALA 80 mg, ALA dose 200 mg, and ALA dose 500 mg/kg/day. ALA therapy in mice conducted orally once a day. Diabetes was induced in rats by single intraperitonial injection of streptozotocin (STZ) at 60 mg/kg body weight. The content of malondialdehyde (MDA) in the brain was measured by spectrophotometeric assays. Brain structure (pyramidal cell in hippocampus) was assessed by staining with hematoxylin and eosin. Results. MDA levels in the DTA, DA80 and DA200 is greater than the levels of MDA in the NTA group, but not statistically significant at the MDA values (p = 0,260). Test-Product Moment Pearson correlation showed a weak positive relationship and not significant (r = 0,327) between the groups of NTA, DA80 and DA200 with MDA. No differences pyramidal cell structure between NTA and DTA. Conclusion. The treatment for 4 weeks with ALA had not reduced oxidative stress in diabetic brain.

Sex differences in hippocampal area CA3 pyramidal cells.

Numerous studies have demonstrated differences between males and females in hippocampal structure, function, and plasticity. There also are many studies about the different predisposition of a males and females for disorders where the hippocampus plays an important role. Many of these reports focus on area CA1, but other subfields are also very important, and unlikely to be the same as area CA1 based on what is known. Here we review basic studies of male and female structure, function, and plasticity of area CA3 pyramidal cells of adult rats. The data suggest that the CA3 pyramidal cells of males and females are distinct in structure, function, and plasticity. These sex differences cannot be simply explained by the effects of circulating gonadal hormones. This view agrees with previous studies showing that there are substantial sex differences in the brain that cannot be normalized by removing the gonads and depleting peripheral gonadal hormones. Implications of these comparisons for understanding sex differences in hippocampal function and dysfunction are discussed. © 2016 Wiley Periodicals, Inc.

Phospho-Tau and Cognitive Decline in Alzheimer's Disease. Commentary: Tau in physiology and pathology.

In the brain, abnormal phosphorylation of tau leads to the formation of paired helical filaments, which are the main components of intraneuronal neurofibrillary tangles (NFT) (Grundke-Iqbal et al., 1986) that are characteristic of Alzheimer's disease (AD) and other tauopathies (Lee et al., 2001). There is an intense debate about the relationship of phospho-tau and the typical cognitive deficits in AD (Castellani et al., 2008) but, owing to the limited data that is available about synaptic circuits in the normal human brain and in that of the AD patient, the basic mechanism/s of cognitive deterioration are still a mystery. The article by Wang and Mandelkow (2016) presents a timely review of the roles of tau in physiology and disease. However, the role of hyperphosphorylation of tau in dendritic pathology is not fully addressed. Wang and Mandelkow concluded that NFT are probably unrelated to cognitive impairment, mainly based on studies using several lines of mice transgenic for wild-type or mutant human tau. However, in a previous study assessing the possible alterations to dendritic spines in pyramidal cells from AD patients (Merino-Serrais et al., 2013), we found a remarkable loss of dendritic spines from pyramidal cells containing NFT. Since pyramidal neurons represent the principal building blocks of the cerebral cortex and dendritic spines are the main postsynaptic elements of cortical excitatory synapses and are fundamental structures in memory, learning, and cognition (DeFelipe, 2015), these alterations constitute what we think is an important early event in the pathogenesis of AD. We used intracellular injections of Lucifer yellow (LY) in fixed brain tissue from AD patients to visualize and reconstruct dendritic arbors of pyramidal neurons—using high-resolution tile scan stacks of confocal microscopy images—to compare neurons that were free of signs of any neurofibrillary pathology with those showing either diffuse phospho-tau (putative pre-tangle state) or aggregated tau NFT. Following injection in the parahippocampal cortex and CA1, the sections were immunostained for LY and phospho-tau. In the so-called putative “pre-tangle” stage, the dendritic trees of pyramidal neurons were unchanged (pattern I; Figure 1, Panel 1). In the presence of well-developed NFT, however, dendritic spine loss was obvious (pattern IIb; Figure 1, Panel 2). In cases with an intermediate state of neurofibrillary pathology (pattern IIa), the loss of dendritic spines was more variable. Importantly, we compared neighboring cells with and without neurofibrillary pathology (see A, B in Figure 1, Panel 1) to avoid confounding factors such as: (1) morphological differences in the structure of pyramidal cells due to regional specializations (i.e., pyramidal cells in different cortical regions and layers may show morphological differences); (2) high inter-individual variability (sex, age, medical treatment, etc.,) factors that could affect brain structure; and (3) the highly variable course of AD, as the neuropathological changes are not homogenous among patients or in different regions of the brain of the same patient, giving rise to variation in the alterations to cortical circuits. Figure 1 Panel 1. Neurons and dendrites in the parahippocampal cortex of patient P9 injected with LY whose soma is free of phospho-tau PHF-tauAT8-ir (PHF-tauAT8-; A–D) or contains phospho-tau (PHF-tauAT8+ in the putative pre-tangle state (Pattern I; E–H) ... We concluded that the presence of phospho-tau in neurons does not necessarily mean that they suffer severe and irreversible effects as thought previously, but rather the characteristic cognitive impairment in AD is likely to depend on the relative number of neurons that have well-developed tangles. Certainly, these observations differ from those of studies on transgenic mouse brains, where human mutant tau was overexpressed. However, this discrepancy could be explained by the fact that transgenic mouse brains do not reproduce all features of AD found in humans. Furthermore, there are many molecular and structural differences between mouse and human brain. Thus, extrapolation of data obtained in mice and humans is rather difficult and possible mismatches between the two species should be taken into consideration when dealing with animal models of AD.

Dendritic branching angles of pyramidal cells across layers of the juvenile rat somatosensory cortex.

The characterization of the structural design of cortical microcircuits is essential for understanding how they contribute to function in both health and disease. Since pyramidal neurons represent the most abundant neuronal type and their dendritic spines constitute the major postsynaptic elements of cortical excitatory synapses, our understanding of the synaptic organization of the neocortex largely depends on the available knowledge regarding the structure of pyramidal cells. Previous studies have identified several apparently common rules in dendritic geometry. We study the dendritic branching angles of pyramidal cells across layers to further shed light on the principles that determine the geometric shapes of these cells. We find that the dendritic branching angles of pyramidal cells from layers II-VI of the juvenile rat somatosensory cortex suggest common design principles, despite the particular morphological and functional features that are characteristic of pyramidal cells in each cortical layer. J. Comp. Neurol. 524:2567-2576, 2016. © 2016 Wiley Periodicals, Inc.

Laminar Differences in Dendritic Structure of Pyramidal Neurons in the Juvenile Rat Somatosensory Cortex.

Pyramidal cell structure varies between different cortical areas and species, indicating that the cortical circuits that these cells participate in are likely to be characterized by different functional capabilities. Structural differences between cortical layers have been traditionally reported using either the Golgi method or intracellular labeling, but the structure of pyramidal cells has not previously been systematically analyzed across all cortical layers at a particular age. In the present study, we investigated the dendritic architecture of complete basal arbors of pyramidal neurons in layers II, III, IV, Va, Vb, and VI of the hindlimb somatosensory cortical region of postnatal day 14 rats. We found that the characteristics of basal dendritic morphologies are statistically different in each cortical layer. The variations in size and branching pattern that exist between pyramidal cells of different cortical layers probably reflect the particular functional properties that are characteristic of the cortical circuit in which they participate. This new set of complete basal dendritic arbors of 3D-reconstructed pyramidal cell morphologies across each cortical layer will provide new insights into interlaminar information processing in the cerebral cortex.

Branching angles of pyramidal cell dendrites follow common geometrical design principles in different cortical areas.

Unraveling pyramidal cell structure is crucial to understanding cortical circuit computations. Although it is well known that pyramidal cell branching structure differs in the various cortical areas, the principles that determine the geometric shapes of these cells are not fully understood. Here we analyzed and modeled with a von Mises distribution the branching angles in 3D reconstructed basal dendritic arbors of hundreds of intracellularly injected cortical pyramidal cells in seven different cortical regions of the frontal, parietal, and occipital cortex of the mouse. We found that, despite the differences in the structure of the pyramidal cells in these distinct functional and cytoarchitectonic cortical areas, there are common design principles that govern the geometry of dendritic branching angles of pyramidal cells in all cortical areas.

Pyramidal cells in V1 of African rodents are bigger, more branched and more spiny than those in primates

Pyramidal cells are characterized by markedly different sized dendritic trees, branching patterns, and spine density across the cortical mantle. Moreover, pyramidal cells have been shown to differ in structure among homologous cortical areas in different species; however, most of these studies have been conducted in primates. Whilst pyramidal cells have been quantified in a few cortical areas in some other species there are, as yet, no uniform comparative data on pyramidal cell structure in a homologous cortical area among species in different Orders. Here we studied layer III pyramidal cells in V1 of three species of rodents, the greater cane rat, highveld gerbil, and four-striped mouse, by the same methodology used to sample data from layer III pyramidal cells in primates. The data reveal markedly different trends between rodents and primates: there is an appreciable increase in the size, branching complexity, and number of spines in the dendritic trees of pyramidal cells with increasing size of V1 in the brain in rodents, whereas there is relatively little difference in primates. Moreover, pyramidal cells in rodents are larger, more branched and more spinous than those in primates. For example, the dendritic trees of pyramidal cells in V1 of the adult cane rat are nearly three times larger, and have more than 10 times the number of spines in their basal dendritic trees, than those in V1 of the adult macaque (7900 and 600, respectively), which has a V1 40 times the size that of the cane rat. It remains to be determined to what extent these differences may result from development or reflect evolutionary and/or processing specializations.

G-Protein-Associated Signal Transduction Processes Are Restored after Postweaning Environmental Enrichment in Ts65Dn, a Down Syndrome Mouse Model

Individuals with Down syndrome (DS) present cognitive deficits that can be improved by early implementation of special care programs. However, they showed limited and temporary cognitive effects. We previously demonstrated that postnatal environmental enrichment (EE) improved clearly, though temporarily, the execution of visuospatial memory tasks in Ts65Dn mice, a DS model bearing a partial trisomy of murine chromosome 16; but in contrast to wild-type littermates, there was a lack of structural plasticity in pyramidal cell structure in the trisomic cerebral cortex. In the present study, we have investigated the impact of EE on the function of adenylyl cyclase and phospholipase C as a possible mechanism underlying the time-limited improvements observed. Basal production of cyclic adenosine monophosphate (cAMP) was not affected, but responses to GTPγS, isoprenaline, noradrenaline, SKF 38393 and forskolin were depressed in the Ts65Dn hippocampus. In EE conditions, cAMP accumulation was not significantly modified in control animals with respect to nonenriched controls. However, EE had a marked effect in Ts65Dn mice, in which cAMP production was significantly increased. Similarly, EE increased phospholipase C activity in Ts65Dn mice, in response to carbachol and calcium. We conclude that EE restores the G-protein-associated signal transduction systems that are altered in Ts65Dn mice.

FGF-2 induces behavioral recovery after early adolescent injury to the motor cortex of rats

Motor cortex injuries in adulthood lead to poor performance in behavioral tasks sensitive to limb movements in the rat. We have shown previously that motor cortex injury on day 10 or day 55 allow significant spontaneous recovery but not injury in early adolescence (postnatal day 35 “P35”). Previous studies have indicated that injection of basic fibroblast growth factor (FGF-2) enhances behavioral recovery after neonatal cortical injury but such effect has not been studied following motor cortex lesions in early adolescence. The present study undertook to investigate the possibility of such behavioral recovery. Rats with unilateral motor cortex lesions were assigned to two groups in which they received FGF-2 or bovine serum albumin (BSA) and were tested in a number of behavioral tests (postural asymmetry, skilled reaching, sunflower seed manipulation, forepaw inhibition in swimming). Golgi–Cox analysis was used to examine the dendritic structure of pyramidal cells in the animals’ parietal (layer III) and forelimb (layer V) area of the cortex. The results indicated that rats injected with FGF-2 (but not BSA) showed significant behavioral recovery that was associated with increased dendritic length and spine density. The present study suggests a role for FGF-2 in the recovery of function following injury during early adolescence.

Pyramidal cells in prefrontal cortex of primates: marked differences in neuronal structure among species.

The most ubiquitous neuron in the cerebral cortex, the pyramidal cell, is characterized by markedly different dendritic structure among different cortical areas. The complex pyramidal cell phenotype in granular prefrontal cortex (gPFC) of higher primates endows specific biophysical properties and patterns of connectivity, which differ from those in other cortical regions. However, within the gPFC, data have been sampled from only a select few cortical areas. The gPFC of species such as human and macaque monkey includes more than 10 cortical areas. It remains unknown as to what degree pyramidal cell structure may vary among these cortical areas. Here we undertook a survey of pyramidal cells in the dorsolateral, medial, and orbital gPFC of cercopithecid primates. We found marked heterogeneity in pyramidal cell structure within and between these regions. Moreover, trends for gradients in neuronal complexity varied among species. As the structure of neurons determines their computational abilities, memory storage capacity and connectivity, we propose that these specializations in the pyramidal cell phenotype are an important determinant of species-specific executive cortical functions in primates.

Samarium–cobalt 2:17 magnets: Analysis of the coercive field of Sm 2(CoFeCuZr) 17 high-temperature permanent magnets

While there is no doubt that the large coercivity of 2:17-based permanent magnets is due to pinning of domain walls at the cell boundaries of the pyramidal cell structure, the process leading to the formation of the strong pinning barrier is controversial. It is shown that the experimental facts and micromagnetic analysis support the model according to which the cell walls transform into the high-anisotropy 1:5 structure during the cooling process from 800 to 400 °C.

Inhibition of protein kinase C signaling protects prefrontal cortex dendritic spines and cognition from the effects of chronic stress

The prefrontal cortex r regulates behavior, cognition, and emotion by using working memory. Prefrontal functions are impaired by stress exposure. Acute, stress-induced deficits arise from excessive protein kinase C (PKC) signaling, which diminishes prefrontal neuronal firing. Chronic stress additionally produces architectural changes, reducing dendritic complexity and spine density of cortico-cortical pyramidal neurons, thereby disrupting excitatory working memory networks. In vitro studies have found that sustained PKC activity leads to spine loss from hippocampal-cultured neurons, suggesting that PKC may contribute to spine loss during chronic stress exposure. The present study tested whether inhibition of PKC with chelerythrine before daily stress would protect prefrontal spines and working memory. We found that inhibition of PKC rescued working memory impairments and reversed distal apical dendritic spine loss in layer II/III pyramidal neurons of rat prelimbic cortex. Greater spine density predicted better cognitive performance, the first direct correlation between pyramidal cell structure and working memory abilities. These findings suggest that PKC inhibitors may be neuroprotective in disorders with dysregulated PKC signaling such as bipolar disorder, schizophrenia, post-traumatic stress disorder, and lead poisoning--conditions characterized by impoverished prefrontal structural and functional integrity.

Morphine self-administration effects on the structure of cortical pyramidal cells in addiction-resistant rats

Repeated administration of drugs of abuse is thought to induce a variety of persistent changes in both behavior and brain morphology, including modifications of neurons from the brain regions involved in addiction. We have studied the morphology of the basal dendritic arbor of cortical pyramidal neurons in addiction-resistant Fischer 344 strain rats that self-administered morphine. Pyramidal neurons in the prelimbic and motor cortex were intracellularly injected with Lucifer Yellow in fixed tissue and they were reconstructed in three dimensions using Neurolucida software. Morphine self-administration did not produce significant changes in the structure of the dendritic arbors or in the spine density of pyramidal neurons in either the prelimbic or motor cortex of F344 rats. Moreover, pyramidal cell morphology did not differ in these two cortical areas in saline self-administered animals. However, when the structure of these cortical pyramidal cells from Fischer 344 rats was compared with that previously reported in addiction-prone Lewis rats in the same cortical areas, significant morphological differences were found between both strains. Indeed, these differences were not only observed following morphine self-administration but also in saline self-administered control animals. We suggest that strain differences in the structure of pyramidal cells in certain cortical areas might represent an anatomical substrate for the distinct vulnerability to the reinforcing effects of morphine exhibited by Fischer 344 and Lewis rats in operant self-administration paradigms.

Effects of wild-type and mutant human amyloid precursor protein on cortical afferent network

Alzheimer's disease is characterized by severe neuronal disintegration supposed to be partly associated with amyloid pathology. Recently, we described morphological alterations of pyramidal cell structure in transgenic mice expressing wild-type or mutant human amyloid precursor protein (hAPP) (strains B6-Py8.9 and Tg2576), which are unrelated to direct plaque-associated changes. In this study, we focused on the pattern of cortical afferent connections in these transgenic mice. The quantity of cholinergic afferents is increased in both transgenic lines. Glutamatergic intra- and interhemispheric afferents are augmented in B6-Py8.9 mice but decreased in Tg2576 mice. Furthermore, perisomatic inhibition of pyramidal neurons was found to be reduced in Tg2576 mice. Findings suggest different effects of wild-type and mutant hAPP on neuronal connectivity.

Specialization of pyramidal cell structure in the visual areas V1, V2 and V3 of the South American rodent, Dasyprocta primnolopha

Marked phenotypic variation has been reported in pyramidal cells in the primate cerebral cortex. These extent and systematic nature of these specializations suggest that they are important for specialized aspects of cortical processing. However, it remains unknown as to whether regional variations in the pyramidal cell phenotype are unique to primates or if they are widespread amongst mammalian species. In the present study we determined the receptive fields of neurons in striate and extrastriate visual cortex, and quantified pyramidal cell structure in these cortical regions, in the diurnal, large-brained, South American rodent Dasyprocta primnolopha. We found evidence for a first, second and third visual area (V1, V2 and V3, respectively) forming a lateral progression from the occipital pole to the temporal pole. Pyramidal cell structure became increasingly more complex through these areas, suggesting that regional specialization in pyramidal cell phenotype is not restricted to primates. However, cells in V1, V2 and V3 of the agouti were considerably more spinous than their counterparts in primates, suggesting different evolutionary and developmental influences may act on cortical microcircuitry in rodents and primates.