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1.
Handb Clin Neurol ; 150: 181-196, 2018.
Article in English | MEDLINE | ID: mdl-29496141

ABSTRACT

Postmortem studies on the human brain reside at the core of investigations on neurologic and psychiatric disorders. Ground-breaking advances continue to be made on the pathologic basis of many of these disorders, at molecular, cellular, and neural connectivity levels. In parallel, there is increasing emphasis on improving methods to extract relevant demographic and clinical information about brain donors and, importantly, translate it into measures that can reliably and effectively be incorporated in the design and data analysis of postmortem human investigations. Here, we review the main source of information typically available to brain banks and provide examples on how this information can be processed. In particular, we discuss approaches to establish primary and secondary diagnoses, estimate exposure to therapeutic treatment and substance abuse, assess agonal status, and use time of death as a proxy in investigations on circadian rhythms. Although far from exhaustive, these considerations are intended as a contribution to ongoing efforts from tissue banks and investigators aimed at establishing robust, well-validated methods for collecting and standardizing information about brain donors, further strengthening the scientific rigor of human postmortem studies.


Subject(s)
Brain/pathology , Diagnosis , Mental Disorders/diagnosis , Nervous System Diseases/diagnosis , Research Design , Tissue Banks , Humans , Tissue Donors
2.
Schizophr Bull ; 44(2): 317-327, 2018 02 15.
Article in English | MEDLINE | ID: mdl-29462456

ABSTRACT

Biomarker-guided treatments are needed in psychiatry, and previous data suggest oxidative stress may be a target in schizophrenia. A previous add-on trial with the antioxidant N-acetylcysteine (NAC) led to negative symptom reductions in chronic patients. We aim to study NAC's impact on symptoms and neurocognition in early psychosis (EP) and to explore whether glutathione (GSH)/redox markers could represent valid biomarkers to guide treatment. In a double-blind, randomized, placebo-controlled trial in 63 EP patients, we assessed the effect of NAC supplementation (2700 mg/day, 6 months) on PANSS, neurocognition, and redox markers (brain GSH [GSHmPFC], blood cells GSH levels [GSHBC], GSH peroxidase activity [GPxBC]). No changes in negative or positive symptoms or functional outcome were observed with NAC, but significant improvements were found in favor of NAC on neurocognition (processing speed). NAC also led to increases of GSHmPFC by 23% (P = .005) and GSHBC by 19% (P = .05). In patients with high-baseline GPxBC compared to low-baseline GPxBC, subgroup explorations revealed a link between changes of positive symptoms and changes of redox status with NAC. In conclusion, NAC supplementation in a limited sample of EP patients did not improve negative symptoms, which were at modest baseline levels. However, NAC led to some neurocognitive improvements and an increase in brain GSH levels, indicating good target engagement. Blood GPx activity, a redox peripheral index associated with brain GSH levels, could help identify a subgroup of patients who improve their positive symptoms with NAC. Thus, future trials with antioxidants in EP should consider biomarker-guided treatment.


Subject(s)
Acetylcysteine/pharmacology , Antioxidants/pharmacology , Biomarkers , Cognitive Dysfunction/drug therapy , Glutathione/drug effects , Outcome Assessment, Health Care , Prefrontal Cortex/drug effects , Psychotic Disorders/drug therapy , Schizophrenia/drug therapy , Acetylcysteine/administration & dosage , Adolescent , Adult , Antioxidants/administration & dosage , Cognitive Dysfunction/etiology , Cognitive Dysfunction/metabolism , Cognitive Dysfunction/physiopathology , Double-Blind Method , Female , Glutathione Peroxidase , Humans , Magnetic Resonance Spectroscopy , Male , Oxidation-Reduction , Prefrontal Cortex/metabolism , Psychotic Disorders/complications , Psychotic Disorders/metabolism , Psychotic Disorders/physiopathology , Schizophrenia/complications , Schizophrenia/metabolism , Schizophrenia/physiopathology , Young Adult
3.
Transl Psychiatry ; 4: e346, 2014 Jan 14.
Article in English | MEDLINE | ID: mdl-24424392

ABSTRACT

Several genes have recently been identified as risk factors for schizophrenia (SZ) by genome-wide association studies (GWAS), including ZNF804A which is thought to function in transcriptional regulation. However, the downstream pathophysiological changes that these genes confer remain to be elucidated. In 143 subjects (68 clinical high risk, first episode or chronic cases; 75 controls), we examined the association between 21 genetic markers previously identified by SZ GWAS or associated with putative intermediate phenotypes of SZ against three event-related potential (ERP) measures: mismatch negativity (MMN), amplitude of P300 during an auditory oddball task, and P300 amplitude during an auditory novelty oddball task. Controlling for age and sex, significant genetic association surpassing Bonferroni correction was detected between ZNF804A marker rs1344706 and P300 amplitude elicited by novel sounds (beta=4.38, P=1.03 × 10(-4)), which is thought to index orienting of attention to unexpected, salient stimuli. Subsequent analyses revealed that the association was driven by the control subjects (beta=6.35, P=9.08 × 10(-5)), and that the risk allele was correlated with higher novel P300b amplitude, in contrast to the significantly lower amplitude observed in cases compared to controls. Novel P300b amplitude was significantly correlated with a neurocognitive measure of auditory attention under interference conditions, suggesting a relationship between novel P300b amplitude and higher-order attentional processes. Our results suggest pleiotropic effects of ZNF804A on risk for SZ and neural mechanisms that are indexed by the novel P300b ERP component.


Subject(s)
Attention/physiology , Event-Related Potentials, P300/genetics , Evoked Potentials, Auditory/genetics , Kruppel-Like Transcription Factors/genetics , Schizophrenia/genetics , Adolescent , Adult , Biomarkers , Electroencephalography , Event-Related Potentials, P300/physiology , Evoked Potentials, Auditory/physiology , Female , Genetic Predisposition to Disease/genetics , Humans , Male , Schizophrenia/physiopathology , Young Adult
4.
BMC Psychiatry ; 9: 71, 2009 Nov 16.
Article in English | MEDLINE | ID: mdl-19917116

ABSTRACT

BACKGROUND: We have previously reported that the expression of the messenger ribonucleic acid (mRNA) for the NR2A subunit of the N-methyl-D-aspartate (NMDA) class of glutamate receptor was decreased in a subset of inhibitory interneurons in the cerebral cortex in schizophrenia. In this study, we sought to determine whether a deficit in the expression of NR2A mRNA was present in the subset of interneurons that contain the calcium buffer parvalbumin (PV) and whether this deficit was associated with a reduction in glutamatergic inputs in the prefrontal cortex (PFC) in schizophrenia. METHODS: We examined the expression of NR2A mRNA, labeled with a 35S-tagged riboprobe, in neurons that expressed PV mRNA, visualized with a digoxigenin-labeled riboprobe via an immunoperoxidase reaction, in twenty schizophrenia and twenty matched normal control subjects. We also immunohistochemically labeled the glutamatergic axon terminals with an antibody against vGluT1. RESULTS: The density of the PV neurons that expressed NR2A mRNA was significantly decreased by 48-50% in layers 3 and 4 in the subjects with schizophrenia, but the cellular expression of NR2A mRNA in the PV neurons that exhibited a detectable level of this transcript was unchanged. In addition, the density of vGluT1-immunoreactive boutons was significantly decreased by 79% in layer 3, but was unchanged in layer 5 of the PFC in schizophrenia. CONCLUSION: These findings suggest that glutamatergic neurotransmission via NR2A-containing NMDA receptors on PV neurons in the PFC may be deficient in schizophrenia. This may disinhibit the postsynaptic excitatory circuits, contributing to neuronal injury, aberrant information flow and PFC functional deficits in schizophrenia.


Subject(s)
Neurons/metabolism , Parvalbumins/metabolism , Prefrontal Cortex/metabolism , Schizophrenia/genetics , Schizophrenia/metabolism , Cell Count/statistics & numerical data , Digoxigenin/metabolism , Gene Expression , Gene Expression Profiling , Humans , Immunohistochemistry , Interneurons/metabolism , Neural Inhibition/genetics , Neural Inhibition/physiology , Oligonucleotide Array Sequence Analysis , Parvalbumins/genetics , Prefrontal Cortex/physiopathology , RNA, Messenger/metabolism , Receptors, N-Methyl-D-Aspartate/genetics , Receptors, N-Methyl-D-Aspartate/metabolism , Schizophrenia/physiopathology , Synaptic Transmission/genetics , Synaptic Transmission/physiology
5.
Schizophr Res ; 73(2-3): 193-207, 2005 Mar 01.
Article in English | MEDLINE | ID: mdl-15653262

ABSTRACT

Many of the functions that are mediated by the prefrontal cortex (PFC) are severely impaired in schizophrenia. The maturation of these functions takes place during late adolescence and early adulthood, which coincides with the period of time when overt symptomatology of schizophrenia most commonly emerges. Two developmental processes occurring during the periadolescence period appear to mediate the functional maturation of the PFC: pruning of exuberant synapses and myelination of axons. It has long been speculated in the literature that disturbances of these processes may result in dysfunction of the PFC and thereby trigger the emergence of symptoms and deficits of schizophrenia. Alternatively, but not mutually exclusively, it has also been suggested that these late developmental processes may not be aberrant but they "unmask" preexisting deficits in the PFC, resulting in the onset of symptoms. The important implication of both of these scenarios is that in either case the emergence of PFC functional disturbances and the onset of symptoms and deficits of schizophrenia would in theory be preventable by pharmacologic manipulation of the synaptic pruning and/or axonal myelination processes. Thus, better understanding of the cellular and molecular mechanisms that mediate these processes will provide truly novel insight into the therapeutics and prevention of schizophrenia.


Subject(s)
Myelin Sheath/metabolism , Prefrontal Cortex/metabolism , Prefrontal Cortex/physiopathology , Schizophrenia/metabolism , Schizophrenia/physiopathology , Synapses/metabolism , gamma-Aminobutyric Acid/metabolism , Humans , Nerve Net/physiopathology
6.
Am J Psychiatry ; 156(11): 1709-19, 1999 Nov.
Article in English | MEDLINE | ID: mdl-10553733

ABSTRACT

OBJECTIVE: Abnormalities in prefrontal cortical gamma-aminobutyric acid (GABA) neurotransmission may contribute to cognitive dysfunction in schizophrenia. The density of chandelier neuron axon terminals (cartridges) immunoreactive for the GABA membrane transporter (GAT-1) has been reported to be reduced in the dorsolateral prefrontal cortex of schizophrenic subjects. Because cartridges regulate the output of pyramidal cells, this study analyzed the laminar distribution of GAT-1-immunoreactive cartridges to determine whether certain subpopulations of pyramidal cells are preferentially affected. METHOD: Measurements were made of the density of GAT-1 -immunoreactive cartridges in layers 2-3a, 3b-4, and 6 of dorsolateral prefrontal cortex area 46 in 30 subjects with schizophrenia, each of whom was matched to one normal and one psychiatric comparison subject. GAT-1-immunoreactive cartridge density was also examined in monkeys chronically treated with haloperidol. RESULTS: Relative to both comparison groups, the schizophrenic subjects had significantly lower GAT-1-immunoreactive cartridge density in layers 2-3a and 3b-4. The decrease was most common and most marked in layers 3b-4, where 80% of the schizophrenic subjects exhibited an average 50.1% decrease in cartridge density in comparison with the matched normal subjects. In contrast, GAT-1-immunoreactive cartridge density was unchanged in the haloperidol-treated monkeys. CONCLUSIONS: These findings demonstrate that the density of GAT-1-immunoreactive cartridges is reduced in the majority of schizophrenic subjects and that this alteration may most prominently affect the function of pyramidal cells located in the middle cortical layers. This abnormality may reflect a number of underlying deficits, including a primary defect in dorsolateral prefrontal cortex circuitry or a secondary response to altered thalamic input to this region.


Subject(s)
Axons/chemistry , Carrier Proteins/analysis , Membrane Proteins/analysis , Membrane Transport Proteins , Nerve Tissue Proteins/analysis , Neurons/chemistry , Organic Anion Transporters , Prefrontal Cortex/chemistry , Schizophrenia/physiopathology , Animals , Antipsychotic Agents/pharmacology , Antipsychotic Agents/therapeutic use , Axons/drug effects , Axons/metabolism , Axons/ultrastructure , Carrier Proteins/metabolism , Carrier Proteins/physiology , Female , GABA Plasma Membrane Transport Proteins , Haloperidol/pharmacology , Humans , Immunohistochemistry , Macaca fascicularis , Male , Membrane Proteins/metabolism , Membrane Proteins/physiology , Middle Aged , Nerve Tissue Proteins/metabolism , Nerve Tissue Proteins/physiology , Neural Pathways/drug effects , Neural Pathways/metabolism , Neurons/metabolism , Neurons/ultrastructure , Prefrontal Cortex/physiopathology , Presynaptic Terminals/chemistry , Presynaptic Terminals/metabolism , Pyramidal Cells/chemistry , Pyramidal Cells/metabolism , Pyramidal Cells/ultrastructure , Schizophrenia/drug therapy , Schizophrenia/metabolism , Schizophrenic Psychology , Thalamus/drug effects , Thalamus/metabolism
7.
Biol Psychiatry ; 46(5): 616-26, 1999 Sep 01.
Article in English | MEDLINE | ID: mdl-10472415

ABSTRACT

Dysfunction of the dorsolateral prefrontal cortex appears to be a central feature of the pathophysiology of schizophrenia, and this dysfunction may be related to alterations in gamma aminobutyric acid (GABA) neurotransmission. Determining the causes and consequences of altered GABA neurotransmission in schizophrenia, and the relationship of these changes to other abnormalities in prefrontal cortical circuitry, requires an understanding of which of the multiple subpopulations of cortical GABA neurons are affected. The chandelier class of GABA neurons, especially those located in the middle layers of the prefrontal cortex (PFC), have been hypothesized to be preferentially involved in schizophrenia because they 1) receive direct synaptic input from dopamine axons, 2) exert powerful inhibitory control over the excitatory output of layer 3 pyramidal neurons, and 3) undergo substantial developmental changes during late adolescence, the typical age of onset of schizophrenia. Consistent with this hypothesis, the axon terminals of chandelier neurons, as revealed by immunoreactivity for the GABA membrane transporter, are reduced substantially in the middle layers of the PFC in schizophrenic subjects. This alteration appears to be selective for the chandelier class of GABA neurons and for the disease process of schizophrenia. These findings provide insight into the pathophysiologic mechanisms underlying prefrontal cortical dysfunction in schizophrenia, and they reveal new targets for therapeutic intervention in this illness.


Subject(s)
Prefrontal Cortex/metabolism , Prefrontal Cortex/physiopathology , Schizophrenia/metabolism , Schizophrenia/physiopathology , Synaptic Transmission/physiology , gamma-Aminobutyric Acid/metabolism , Adolescent , Animals , Axons/metabolism , Child , Child, Preschool , Humans , Infant , Memory/physiology , Neurons/physiology
8.
Proc Natl Acad Sci U S A ; 95(9): 5341-6, 1998 Apr 28.
Article in English | MEDLINE | ID: mdl-9560277

ABSTRACT

In the primate cerebral cortex, morphologically and functionally diverse classes of local circuit neurons containing the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) differentially regulate the activity of pyramidal cells, the principal type of excitatory output neurons. In schizophrenia, GABA neurotransmission in the prefrontal cortex (PFC) appears to be disturbed but whether specific populations of GABA neurons are affected is not known. The chandelier class of GABA neurons are of particular interest because their axon terminals, which form distinctive arrays termed "cartridges," provide inhibitory input exclusively to the axon initial segment of pyramidal cells. Thus, chandelier cells are positioned to powerfully regulate the excitatory output of pyramidal neurons and, consequently, to substantially affect the patterns of neuronal activity within the PFC. In this study, an antibody directed against the GABA membrane transporter GAT-1 was used to label GABA axon terminals in postmortem human brains. The relative density of GAT-1-immunoreactive axon cartridges furnished by chandelier neurons was decreased by 40% in the PFC of schizophrenic subjects compared with matched groups of normal control and nonschizophrenic psychiatric subjects. In contrast, markers of the axon terminals of other populations of GABA neurons were not altered in the schizophrenic subjects. Furthermore, the density of GAT-1-immunoreactive axon cartridges was not altered in psychiatric subjects who had been treated with antipsychotic medications. The changes in GAT-1-immunoreactive axon cartridges of chandelier neurons in schizophrenia are likely to reflect altered information processing within the PFC and in its output connections to other brain regions and could contribute to the cognitive impairments seen in this disorder.


Subject(s)
Carrier Proteins/metabolism , Membrane Proteins/metabolism , Membrane Transport Proteins , Organic Anion Transporters , Prefrontal Cortex/physiopathology , Schizophrenia/physiopathology , gamma-Aminobutyric Acid/physiology , Autopsy , Axons/metabolism , Female , GABA Plasma Membrane Transport Proteins , Humans , Male , Middle Aged , Nerve Endings/metabolism , Prefrontal Cortex/pathology , Synaptic Transmission
9.
Neuroscience ; 80(4): 1149-58, 1997 Oct.
Article in English | MEDLINE | ID: mdl-9284067

ABSTRACT

The peripubertal elimination of axospinous synapses and dendritic spines in monkey prefrontal cortex suggests that this region undergoes substantial reorganization during late postnatal development. Understanding the functional impact of these maturational refinements requires knowledge of the specific presynaptic elements involved in these changes. Two potential sources of these presynaptic terminals are the intrinsic axon collaterals furnished by pyramidal cells within a region and the associational axons that arise from pyramidal neurons in other cortical regions in the same hemisphere. In the adult, both of these types of axon terminals form synapses predominantly with dendritic spines on other pyramidal neurons, and thus they may be preferentially involved in the peripubertal pruning of axospinous synapses and dendritic spines. In order to test this hypothesis, iontophoretic injections of the anterograde tracer biotinylated dextran amine were made into the superficial layers of areas 9 or 46 of the prefrontal cortex of four prepubertal juvenile (14.9-21.5 months old) and three young adult macaque monkeys. Tangential reconstructions revealed a stripe-like pattern of labeled terminals for intrinsic and associational projections in both juvenile and adult animals. During puberty, the intrinsic circuitry underwent extensive topographic refinement, as demonstrated by a 42.7% decrease in stripe area and a 28.0% increase in gap distance between stripes. Furthermore, the mediolateral tangential spread of labeled stripes around the injection site decreased by 27.0%. In contrast, topographic refinement was not evident in the associational circuitry. In both layers 1 and 3, the densities of varicosities and branch points on labeled axons decreased by about 50% in intrinsic stripes during puberty, but only by approximately 30% in associational stripes. These findings suggest that the spatial form and magnitude of peripubertal refinements in prefrontal cortical connectivity may be specific for certain neural elements.


Subject(s)
Aging/physiology , Prefrontal Cortex/physiology , Sexual Maturation/physiology , Synapses/physiology , Animals , Axonal Transport , Axons/physiology , Axons/ultrastructure , Dendrites/physiology , Dendrites/ultrastructure , Macaca fascicularis , Macaca mulatta , Male , Prefrontal Cortex/cytology , Pyramidal Cells/cytology , Pyramidal Cells/physiology , Synapses/ultrastructure
10.
Am J Psychiatry ; 154(7): 1013-5, 1997 Jul.
Article in English | MEDLINE | ID: mdl-9210755

ABSTRACT

OBJECTIVE: The purpose of this study was to test the hypothesis that abnormalities in the parvalbumin-containing subclass of local circuit neurons contribute to altered gamma-aminobutyric acid (GABA) neurotransmission in the prefrontal cortex of schizophrenic subjects. METHOD: Profile counts and somal size measures were made of parvalbumin-immunoreactive neurons in areas 9, 46, and 17 from 15 matched pairs of schizophrenic and normal comparison subjects. RESULTS: No differences in relative density, laminar distribution, or somal size of labeled neurons were found in any region. CONCLUSIONS: These findings suggest that altered GABA neurotransmission in schizophrenia is due to either abnormalities in other sub-populations of prefrontal cortical GABA neurons or abnormalities in the parvalbumin-containing subclass that could not be detected in the present study.


Subject(s)
Parvalbumins/analysis , Prefrontal Cortex/chemistry , Schizophrenia/diagnosis , Cell Count , Humans , Male , Middle Aged , Neurons/chemistry , Neurons/cytology , Parvalbumins/immunology , Prefrontal Cortex/cytology , Prefrontal Cortex/physiopathology , Schizophrenia/physiopathology , Synaptic Transmission/physiology , gamma-Aminobutyric Acid/physiology
11.
Cereb Cortex ; 6(3): 446-56, 1996.
Article in English | MEDLINE | ID: mdl-8670670

ABSTRACT

The dependence of the developing dorsal lateral geniculate nucleus (LGd) on visual cortex for survival has been well documented. Complete removal of visual cortex during early postnatal development results in degeneration of the LGd. To further explore the nature of this trophic relationship, we depleted variable proportions of the principal targets of geniculocortical axons, layer IV neurons, and also variable proportions of the supragranular neurons by intraperitoneal injections of different dosages of a mitotic inhibitor MAM (methylazoxymethanol acetate) into pregnant hamsters at the time when these neurons were being generated in the ventricular zone. We demonstrate that after more than 75% loss of layer IV there is no reduction in cell number in the LGd. HRP (horseradish peroxidase) injections into the LGd in adult animals reveal an essentially normal pattern of termination without evidence of rerouting of geniculocortical axons to other cortical areas, nor compensatory increase in arborization in layer VI and VIb (subplate). Geniculocortical axons terminate principally in the middle stratum of the depleted cortex above layer V, with obvious reduction in both the extent and density of arborization. After higher dosages of MAM treatment resulting in more severe cell loss in layers II-IV with the apparent loss of layer IV, the extent and density of geniculocortical arborization are further reduced. Reduction in size as well as total number of geniculate neurons become detectable. Above depletions of 75% of layer IV neurons, the number of surviving LGd neurons is linearly related to the total number of remaining layer II-IV neurons in the cortex. These findings are discussed in light of the possible trophic mechanisms that match cell populations in number during development.


Subject(s)
Cerebral Cortex/physiology , Geniculate Bodies/physiology , Animals , Bromodeoxyuridine , Cell Count , Cerebral Cortex/anatomy & histology , Cerebral Cortex/growth & development , Cricetinae , Female , Geniculate Bodies/anatomy & histology , Geniculate Bodies/growth & development , Horseradish Peroxidase , Immunohistochemistry , Mesocricetus , Methylazoxymethanol Acetate/toxicity , Neural Pathways/anatomy & histology , Neural Pathways/growth & development , Neural Pathways/physiology , Pregnancy , Teratogens/toxicity
12.
Cereb Cortex ; 6(3): 457-69, 1996.
Article in English | MEDLINE | ID: mdl-8670671

ABSTRACT

During the early development of the neocortex, thalamocortical axons arrive potentially in time to instruct migrating cortical neurons in several aspects of local differentiation, such as number of layer IV neurons and efferent connectivity. Migration of layer IV neurons into the cortical plate just precedes thalamocortical invasion, suggesting that these neurons could cue or tropically direct thalamic ingrowth. To explore the interactions of layer IV neurons and their thalamocortical input, we administered a mitotic inhibitor methylazoxymethanol acetate (MAM) intraperitoneally to time d pregnant hamsters on E14 when layer IV neurons are normally being generated in striate cortex. Reduced numbers of cortical neurons overall, the absence of small diameter granule neurons, and the absence of the zone of reduced density of callosally projecting neurons suggest that neither the depletion of layer IV cells in the ventricular zone nor thalamic afferents in the subplate or cortical plate respecify the later generated cohort of neurons (presumptive layer II/III neurons) to acquire morphological and connectional properties of layer IV. Dil injections into the dorsal lateral geniculate nucleus (LGd) of animals from embryonic (E15) and postnatal (P7) ages show that the final position of thalamic axons with respect to layer V is not affected by the absence of E14 neurons. In the normal visual cortex, geniculocortical axons have begun their arborization in their presumptive target layer in the upper cortex immediately below the undifferentiated cortical plate on P4, while in MAM animals, this process occurs 1 d later. The extent and density of arborization is much reduced in the thinner cortex of the MAM animals. We thus find no evidence for instruction of migrating neurons by thalamocortical axons to assume the layer IV phenotype; if instruction does occur, it must take place in a very restricted time window. Thalamic axons can also find their laminar position in the absence of cells of this phenotype.


Subject(s)
Axons/physiology , Cerebral Cortex/growth & development , Geniculate Bodies/growth & development , Animals , Animals, Newborn , Carbocyanines , Cerebral Cortex/anatomy & histology , Cerebral Cortex/physiology , Corpus Callosum/anatomy & histology , Corpus Callosum/growth & development , Corpus Callosum/physiology , Cricetinae , Female , Fluorescent Dyes , Geniculate Bodies/anatomy & histology , Geniculate Bodies/physiology , Mesocricetus , Methylazoxymethanol Acetate/pharmacology , Neural Pathways/anatomy & histology , Neural Pathways/growth & development , Neural Pathways/physiology , Neurons, Afferent/physiology , Pregnancy , Teratogens/pharmacology
13.
Cereb Cortex ; 1(5): 433-43, 1991.
Article in English | MEDLINE | ID: mdl-1822751

ABSTRACT

While subplate neurons are lost in the development of the cerebral cortex of other mammalian species that have so far been investigated, in rodents the subplate (alternately termed layer VIb or VII) persists to adulthood, at least in part. We traced the developmental course of the subplate in the golden hamster, using two methods. We first used tritiated thymidine labeling to trace relative changes in the numbers of identified cohorts of cells in the subplate, layer VI, and the LGN. We also estimated the total number of cells in the subplate versus layer VI of the cortex from early in development to adulthood. These methods showed a high rate of cell loss in the subplate, between 50% and 80%, but with the clear retention of a substantial fraction of this early-generated population as a recognizable layer in adulthood. Species variations in the timing of cortical neurogenesis and the relative amount of cell loss in the subplate can be used to better describe the developmental function of this region.


Subject(s)
Cerebral Cortex/physiology , Neurons/physiology , Animals , Autoradiography , Cerebral Cortex/cytology , Cricetinae , Female , Geniculate Bodies/anatomy & histology , Geniculate Bodies/cytology , Mesocricetus , Pregnancy , Thymidine/metabolism
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