Properties of Doublecortin Expressing Neurons in the Adult Mouse Dentate Gyrus

Spampanato, Jay; Sullivan, Rodney N.; Turpin, Fabrice; Bartlett, Perry F.; Sah, Pankaj

doi:10.1371/journal.pone.0041029

Cited by 54 publications

(48 citation statements)

References 49 publications

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“…Synapse integrity was also intact in the DG of PS19 mice, with no significant differences measured from immunostaining (Figure 4c). This is consistent with the fact that there is a continuous turnover of neurons in the DG region compared to the other regions of the mouse brain (24), (25), (26). In the DG of AD patients (27) and a mouse model of AD (26), there is evidence that neurogenesis is increased.…”

Section: Discussionsupporting

confidence: 88%

In vivo measurement of glutamate loss is associated with synapse loss in a mouse model of tauopathy

et al. 2014

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Glutamate is the primary excitatory neurotransmitter in the brain, and is implicated in neurodegenerative diseases such as Alzheimer’s disease (AD) and several other tauopathies. The current method for measuring glutamate in vivo is using proton magnetic resonance spectroscopy (1H MRS), although it has poor spatial resolution and weak sensitivity to glutamate changes. In this study, we sought to measure the effect of tau pathology on glutamate levels throughout the brain of a mouse model of tauopathy using a novel magnetic resonance imaging (MRI) technique. We employed glutamate chemical exchange saturation transfer (GluCEST) imaging, which has been previously validated as a complimentary method for measuring glutamate levels with several important advantages over conventional 1H MRS. We hypothesized that the regional changes in glutamate levels would correlate with histological measurements of pathology including pathological tau, synapse and neuron loss. Imaging and spectroscopy were carried out on tau transgenic mice with the P301S mutation (PS19, n=9) and their wild-type littermates (WT, n=8), followed by immunohistochemistry of their brain tissue. GluCEST imaging resolution allowed for sub-hippocampal analysis of glutamate. Glutamate was significantly decreased by 29% in the CA sub-region of the PS19 hippocampus, and by 15% in the thalamus, where synapse loss was also measured. Glutamate levels and synapse density remained high in the dentate gyrus sub-region of the hippocampus, where neurogenesis is known to occur. The further development of GluCEST imaging for preclinical applications will be valuable, as therapies are being tested in mouse models of tauopathy.

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Section: Discussionsupporting

confidence: 88%

In vivo measurement of glutamate loss is associated with synapse loss in a mouse model of tauopathy

et al. 2014

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“…Positive and negative control tissues for the anti-NKCC1 and anti-KCC2 antibodies were used to confirm the labeling accuracy of these antibodies. The anti-NKCC1 antibody effectively labeled olfactory sensory neurons (not shown), and adult newborn granule cells (Spampanato et al 2012), but as expected, failed to label kidney. Similarly, the anti-KCC2 antibody labeled pyramidal cells in the hippocampus and cortex, but again, as expected, did not label kidney tissue (data not shown).…”

Section: Mechanism Of Feedback Excitationsupporting

confidence: 66%

Development and physiology of GABAergic feedback excitation in parvalbumin expressing interneurons of the mouse basolateral amygdala

et al. 2016

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We have previously shown that in the basolateral amygdala (BLA), action potentials in one type of parvalbumin (PV)‐expressing GABAergic interneuron can evoke a disynaptic feedback excitatory postsynaptic potential (fbEPSP) onto the same presynaptic interneuron. Here, using whole‐cell recordings from PV‐expressing interneurons in acute brain slices we expand on this finding to show that this response is first detectable at 2‐week postnatal, and is most prevalent in animals beyond 3 weeks of age (>P21). This circuit has a very high fidelity, and single action potential evoked fbEPSPs display few failures. Reconstruction of filled neurons, and electron microscopy show that interneurons that receive feedback excitation make symmetrical synapses on both the axon initial segments (AIS), as well as the soma and proximal dendrites of local pyramidal neurons, suggesting fbEPSP interneurons are morphologically distinct from the highly specialized chandelier neurons that selectively target the axon initial segment of pyramidal neurons. Single PV interneurons could trigger very large (~ 1 nA) feedback excitatory postsynaptic currents (fbEPSCs) suggesting that these neurons are heavily reciprocally connected to local glutamatergic principal cells. We conclude that in the BLA, a subpopulation of PV interneurons forms a distinct neural circuit in which a single action potential can recruit multiple pyramidal neurons to discharge near simultaneously and feed back onto the presynaptic interneuron.

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“…Though a microtubule-associated protein, it regulates filamentous actin structure in developing neurones [122] and also regulates the microtubules of axonal growth cones [123]. In the dentate gyrus of the developing hippocampus, Dcx is expressed with initial dendritic growth, but diminishes before maturity [124]. It also promotes the migration of human progenitor cell-derived neurones in the dentate gyrus [125].…”

Section: Immunocytochemical Markersmentioning

confidence: 99%

Clinical neuropathology practice guide 5-2013: markers of neuronal maturation

Sarnat¹

2013

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This review surveys immunocytochemical and histochemical markers of neuronal lineage for application to tissue sections of fetal and neonatal brain. They determine maturation of individual nerve cells as the tissue progresses to mature architecture. From a developmental perspective, neuronal markers are all about timing. These diverse cellular labels may be classified in two ways: 1) time of onset of expression (early; intermediate; late); 2) labeling of subcellular structures or metabolic functions (nucleoproteins; synaptic vesicle proteins; enolases; cytoskeletal elements; calcium-binding; nucleic acids; mitochondria). Apart from these positive markers of maturation, other negative markers are expressed in primitive neuroepithelial cells and early stages of neuroblast maturation, but no longer are demonstrated after initial stages of maturation. These examinations are relevant for studies of normal neuroembryology at the cellular level. In fetal and perinatal neuropathology they provide control criteria for application to malformations of the brain, inborn metabolic disorders and acquired fetal insults in which neuroblastic maturation may be altered. Disorders, in which cells differentiate abnormally, as in tuberous sclerosis and hemimegalencephaly, pose another yet aspect of mixed cellular lineage. The measurement in living patients, especially neonates, of serum and CSF levels of enolases, chromogranins and S-100 proteins as biomarkers of brain damage may potentially be correlated with their corresponding tissue markers at autopsy in infants who do not survive. The neuropathological markers here described can be performed in ordinary hospital laboratories, not just research facilities, and offer another dimension of diagnostic precision in interpreting abnormally developed fetal and postnatal brains.

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Properties of Doublecortin Expressing Neurons in the Adult Mouse Dentate Gyrus

Cited by 54 publications

References 49 publications

In vivo measurement of glutamate loss is associated with synapse loss in a mouse model of tauopathy

In vivo measurement of glutamate loss is associated with synapse loss in a mouse model of tauopathy

Development and physiology of GABAergic feedback excitation in parvalbumin expressing interneurons of the mouse basolateral amygdala

Clinical neuropathology practice guide 5-2013: markers of neuronal maturation

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