Modeling the Nonlinear Dynamic Interactions of Afferent Pathways in the Dentate Gyrus of the Hippocampus

Dimoka, Angelika; Courellis, Spiros H.; Marmarelis, Vasilis Z.; Berger, Theodore W.

doi:10.1007/s10439-008-9463-6

Cited by 5 publications

(3 citation statements)

References 56 publications

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“…The fact that we only found an effect in the molecular layer of the dentate gyrus and not in other regions of the hippocampus or in the cortex could indicate that mice at this age are at an early stage of the disease. The molecular layer of the dentate gyrus of the hippocampus receives a direct input from the entorhinal cortex via the perforant pathway [ 41 , 42 ]. Degeneration of these areas is an early event in both AD and cardiovascular disease [ 39 , 43 , 44 ].…”

Section: Discussionmentioning

confidence: 99%

Sex Differences in Presynaptic Density and Neurogenesis in Middle-Aged ApoE4 and ApoE Knockout Mice

Rijpma

Jansen

Arnoldussen

et al. 2013

Journal of Neurodegenerative Diseases

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Atherosclerosis and apolipoprotein E ε4 (APOE4) genotype are risk factors for Alzheimer's disease (AD) and cardiovascular disease (CVD). Sex differences exist in prevalence and manifestation of both diseases. We investigated sex differences respective to aging, focusing on cognitive parameters in apoE4 and apoE knockout (ko) mouse models of AD and CVD. Presynaptic density and neurogenesis were investigated immunohistochemically in male and female apoE4, apoE ko, and wild-type mice. Middle-aged female apoE4 mice showed decreased presynaptic density in the inner molecular layer of the dentate gyrus of the hippocampus. Middle-aged female apoE ko mice showed a trend towards increased neurogenesis in the hippocampus compared with wild-type mice. No differences in these parameters could be observed in middle-aged male mice. Specific harmful interactions between apoE4 and estrogen could be responsible for decreased presynaptic density in female apoE4 mice. The trend of increased neurogenesis found in female apoE ko mice supports previous studies suggesting that temporarily increased amount of synaptic contacts and/or neurogenesis is a compensatory mechanism for synaptic failure. To our knowledge, no other studies investigating presynaptic density in aging female apoE4 or apoE ko mice are available. Sex-specific differences between APOE genotypes could account for some sex differences in AD and CVD.

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Section: Discussionmentioning

confidence: 99%

Sex Differences in Presynaptic Density and Neurogenesis in Middle-Aged ApoE4 and ApoE Knockout Mice

Rijpma

Jansen

Arnoldussen

et al. 2013

Journal of Neurodegenerative Diseases

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“…The first-order kernel describes the linear response, while higher-order kernels describe the nonlinear response. The Volterra-Wiener approach is a black-box approach in that it does not require specific knowledge of the internal system structure or properties (e.g., ion channel conductances), thus the methodology has been successfully applied to model neuronal systems [7][8][9] as well as other complex physiological systems such as the heart [10]. Once the kernels are identified, they can be eigen-decomposed into a set of component impulse responses, of which the most significant in terms of their relative contribution to the overall system response are the principal dynamic modes (PDMs) [11,12].…”

Section: Introductionmentioning

confidence: 99%

Transformation of neuronal modes associated with low-Mg2 + /high-K + conditions in an in vitro model of epilepsy

et al. 2009

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Nonparametric system modeling constitutes a robust method for the analysis of physiological systems as it can be used to identify nonlinear dynamic input-output relationships and facilitate their description. First-and second-order kernels of hippocampal CA3 pyramidal neurons in an in vitro slice preparation were computed using the Volterra-Wiener approach to investigate system changes associated with epileptogenic lowmagnesium/high-potassium (low-Mg 2+ /high-K + ) conditions. The principal dynamic modes (PDMs) of neurons were calculated from the first-and second-order kernel estimates in order to characterize changes in neural coding functionality. From our analysis, an increase in nonlinear properties was observed in kernels under low-Mg 2+ /high-K + . Furthermore, the PDMs revealed that the sampled hippocampal CA3 neurons were primarily of integrating character and that the contribution of a differentiating mode component was enhanced under low-Mg 2+ /high-K + .

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“…Furthermore, the LPP preferentially targets newly integrated adult-born granule cells (Woods et al, 2018). To reduce possible confounding influences resulting from the stimulation of both pathways, such as nonlinear interactions (Dimoka et al, 2008), it is preferred to stimulate either the MPP or the LPP. While most in vivo studies in rats stimulate the MPP and LPP separately, it is impossible to target just one pathway in the much smaller mouse brain .…”

Section: Limitationsmentioning

confidence: 99%

Roles of the autism candidate genes neuroligin-3, neuroligin-4, and neurobeachin in synaptic plasticity ande excitation-inhibition balance in the dentate gyrus

Muellerleile¹

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Autism spectrum disorder (ASD) is a common neurodevelopmental disorder with a multifarious clinical presentation. Even though many genetic risk factors have been identified and studied in mouse models, the neurophysiological mechanisms underlying the autistic phenotype are still unclear. Based on the high rates of comorbidity with epilepsy, it was hypothesized that the balance between excitation and inhibition in neural circuits may be disrupted in autistic individuals. In this dissertation, synaptic and network activity was measured in three different genetically modified mouse models that exhibit the characteristic behavioral abnormalities of the disorder: the Neurobeachin (Nbea) haploinsufficient mouse, the Neuroligin-3 (Nlgn3) knockout (KO) mouse, and the Neuroligin-4 (Nlgn4) KO mouse. Each of the affected proteins is involved in the formation and/or function of synapses in the central nervous system. Therefore, it was posited that the reduction or deletion of these proteins might alter the balance of excitatory to inhibitory synaptic transmission in individual neurons and in neural circuits. Extracellular recordings in the hippocampal dentate gyrus of anesthetized mice revealed that the excitation-inhibition (E-I) balance was reduced in Nbea haploinsufficient and Nlgn4 KO mice, but unchanged in Nlgn3 KO mice despite a reduction in excitatory synaptic transmission to dentate granule cells. Unexpectedly, the intrinsic excitability of dentate granule cells was altered in all three mouse models. These results imply that a homeostatic increase in the intrinsic excitability is able to compensate for the decreased excitatory transmission in Nlgn3 KO mice, whereas the decreased intrinsic excitability in the Nbea haploinsufficient and Nlgn4 KO mice leads to a reduction in the E-I balance. Taken together, these findings suggest that the influence of genetic factors on the E-I balance might be a potential common mechanism underlying the development of ASD.

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Modeling the Nonlinear Dynamic Interactions of Afferent Pathways in the Dentate Gyrus of the Hippocampus

Cited by 5 publications

References 56 publications

Sex Differences in Presynaptic Density and Neurogenesis in Middle-Aged ApoE4 and ApoE Knockout Mice

Sex Differences in Presynaptic Density and Neurogenesis in Middle-Aged ApoE4 and ApoE Knockout Mice

Transformation of neuronal modes associated with low-Mg2 + /high-K + conditions in an in vitro model of epilepsy

Roles of the autism candidate genes neuroligin-3, neuroligin-4, and neurobeachin in synaptic plasticity ande excitation-inhibition balance in the dentate gyrus

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