Displaying publications 1 - 20 of 27 in total

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  1. A device to facilitate preparation of high-density neural cell cultures in MEAs
    Mok SY, Lim YM, Goh SY
    J Neurosci Methods, 2009 May 15;179(2):284-91.
    PMID: 19428539 DOI: 10.1016/j.jneumeth.2009.02.009
    A device to facilitate high-density seeding of dissociated neural cells on planar multi-electrode arrays (MEAs) is presented in this paper. The device comprises a metal cover with two concentric cylinders-the outer cylinder fits tightly on to the external diameter of a MEA to hold it in place and an inner cylinder holds a central glass tube for introducing a cell suspension over the electrode area of the MEA. An O-ring is placed at the bottom of the inner cylinder and the glass tube to provide a fluid-tight seal between the glass tube and the MEA electrode surface. The volume of cell suspension in the glass tube is varied according to the desired plating density. After plating, the device can be lifted from the MEA without leaving any residue on the contact surface. The device has enabled us to increase and control the plating density of neural cell suspension with low viability, and to prepare successful primary cultures from cryopreserved neurons and glia. The cultures of cryopreserved dissociated cortical neurons that we have grown in this manner remained spontaneously active over months, exhibited stable development and similar network characteristics as reported by other researchers.
    Matched MeSH terms: Neurons/physiology*
  2. Associable representations as field of influence for dynamic cognitive processes
    Cacha LA, Poznanski RR
    J Integr Neurosci, 2011 Dec;10(4):423-37.
    PMID: 22262534
    In earlier models, synaptic plasticity forms the basis for cellular signaling underlying learning and memory. However, synaptic computation of learning and memory in the brain remains controversial. In this paper, we discuss ways in which synaptic plasticity remodels subcellular networks by deflecting trajectories in neuronal state-space as regulating patterns for the synthesis of dynamic continuity that form cognitive networks of associable representations through endogenous dendritic coding to consolidate memory.
    Matched MeSH terms: Neurons/physiology*
  3. Fulltext Catecholaminergic neurons in the comissural region of the nucleus of the solitary tract modulate hyperosmolality-induced responses
    Freiria-Oliveira AH, Blanch GT, Pedrino GR, Cravo SL, Murphy D, Menani JV, et al.
    Am J Physiol Regul Integr Comp Physiol, 2015 Nov 01;309(9):R1082-91.
    PMID: 26333788 DOI: 10.1152/ajpregu.00432.2014
    Noradrenergic A2 neurons of the nucleus of the solitary tract (NTS) have been suggested to contribute to body fluid homeostasis and cardiovascular regulation. In the present study, we investigated the effects of lesions of A2 neurons of the commissural NTS (cNTS) on the c-Fos expression in neurons of the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei, arterial pressure, water intake, and urinary excretion in rats with plasma hyperosmolality produced by intragastric 2 M NaCl (2 ml/rat). Male Holtzman rats (280-320 g) received an injection of anti-dopamine-β-hydroxylase-saporin (12.6 ng/60 nl; cNTS/A2-lesion, n = 28) or immunoglobulin G (IgG)-saporin (12.6 ng/60 nl; sham, n = 24) into the cNTS. The cNTS/A2 lesions increased the number of neurons expressing c-Fos in the magnocellular PVN in rats treated with hypertonic NaCl (90 ± 13, vs. sham: 47 ± 20; n = 4), without changing the number of neurons expressing c-Fos in the parvocellular PVN or in the SON. Contrary to sham rats, intragastric 2 M NaCl also increased arterial pressure in cNTS/A2-lesioned rats (16 ± 3, vs. sham: 2 ± 2 mmHg 60 min after the intragastric load; n = 9), an effect blocked by the pretreatment with the vasopressin antagonist Manning compound (0 ± 3 mmHg; n = 10). In addition, cNTS/A2 lesions enhanced hyperosmolality-induced water intake (10.5 ± 1.4, vs. sham: 7.7 ± 0.8 ml/60 min; n = 8-10), without changing renal responses to hyperosmolality. The results suggest that inhibitory mechanisms dependent on cNTS/A2 neurons reduce water intake and vasopressin-dependent pressor response to an acute increase in plasma osmolality.
    Matched MeSH terms: Adrenergic Neurons/physiology*
  4. Current Perspectives of Healthy Mitochondrial Function for Healthy Neurons
    Arunachalam M, Ramesh M, Thiagarajan V, Singla SK, Mudhol S, Muthukumar SP
    Curr Drug Targets, 2021;22(14):1688-1703.
    PMID: 33618645 DOI: 10.2174/1389450122666210222163528
    The neuron is high-energy utilizing tissue. The rate of neuronal cell respiration is higher than in other cells. Cellular respiration occurs with mitochondria. The healthy production and functions of mitochondria play a key role in the maintenance of healthy neurons. In pathological conditions such as neurodegenerative diseases, healthy mitochondria help to alleviate pathological events in neuronal cells. Conversely, mitochondrial dysfunction promotes the acceleration of the neurodegenerative process. Furthermore, glial-derived mitochondria contribute to multiple roles in the regulation of healthy neuron functions. It also supports releasing of the neurotransmitters; generation of the impulses, regulation of the membrane potential and molecular dynamics; controlling of the axonal transport; controlling of the mitochondrial fission and fusion functions in the peripheral as well as the central nervous system. Moreover, it plays a key role in the regeneration process of neuronal cells. Therefore, healthy mitochondria can provide a healthy environment for neuronal cell function and can treat neurodegenerative disorders. In this review, we explore the current view of healthy mitochondria and their role in healthy neuronal functions.
    Matched MeSH terms: Neurons/physiology*
  5. Cytoprotective Effect of Tocotrienol-Rich Fraction and α-Tocopherol Vitamin E Isoforms Against Glutamate-Induced Cell Death in Neuronal Cells
    Rati Selvaraju T, Khaza'ai H, Vidyadaran S, Sokhini Abd Mutalib M, Ramachandran V, Hamdan Y
    Int J Vitam Nutr Res, 2014;84(3-4):140-51.
    PMID: 26098478 DOI: 10.1024/0300-9831/a000201
    Glutamate is the major mediator of excitatory signals in the mammalian central nervous system. Extreme amounts of glutamate in the extracellular spaces can lead to numerous neurodegenerative diseases. We aimed to clarify the potential of the following vitamin E isomers, tocotrienol-rich fraction (TRF) and α-tocopherol (α-TCP), as potent neuroprotective agents against glutamate-induced injury in neuronal SK-N-SH cells. Cells were treated before and after glutamate injury (pre- and post-treatment, respectively) with 100-300 ng/ml TRF/α-TCP. Exposure to 120 mM glutamate significantly reduced cell viability to 76% and 79% in the pre- and post-treatment studies, respectively; however, pre- and post-treatment with TRF/α-TCP attenuated the cytotoxic effect of glutamate. Compared to the positive control (glutamate-injured cells not treated with TRF/α-TCP), pre-treatment with 100, 200, and 300 ng/ml TRF significantly improved cell viability following glutamate injury to 95.2%, 95.0%, and 95.6%, respectively (p<0.05).The isomers not only conferred neuroprotection by enhancing mitochondrial activity and depleting free radical production, but also increased cell viability and recovery upon glutamate insult. Our results suggest that vitamin E has potent antioxidant potential for protecting against glutamate injury and recovering glutamate-injured neuronal cells. Our findings also indicate that both TRF and α-TCP could play key roles as anti-apoptotic agents with neuroprotective properties.
    Matched MeSH terms: Neurons/physiology
  6. Fulltext Development and Differentiation of Midbrain Dopaminergic Neuron: From Bench to Bedside
    Wang M, Ling KH, Tan JJ, Lu CB
    Cells, 2020 06 18;9(6).
    PMID: 32570916 DOI: 10.3390/cells9061489
    Parkinson's Disease (PD) is a neurodegenerative disorder affecting the motor system. It is primarily due to substantial loss of midbrain dopamine (mDA) neurons in the substantia nigra pars compacta and to decreased innervation to the striatum. Although existing drug therapy available can relieve the symptoms in early-stage PD patients, it cannot reverse the pathogenic progression of PD. Thus, regenerating functional mDA neurons in PD patients may be a cure to the disease. The proof-of-principle clinical trials showed that human fetal graft-derived mDA neurons could restore the release of dopamine neurotransmitters, could reinnervate the striatum, and could alleviate clinical symptoms in PD patients. The invention of human-induced pluripotent stem cells (hiPSCs), autologous source of neural progenitors with less ethical consideration, and risk of graft rejection can now be generated in vitro. This advancement also prompts extensive research to decipher important developmental signaling in differentiation, which is key to successful in vitro production of functional mDA neurons and the enabler of mass manufacturing of the cells required for clinical applications. In this review, we summarize the biology and signaling involved in the development of mDA neurons and the current progress and methodology in driving efficient mDA neuron differentiation from pluripotent stem cells.
    Matched MeSH terms: Dopaminergic Neurons/physiology*
  7. Differentiation of stem cells derived from carious teeth into dopaminergic-like cells
    Gnanasegaran N, Govindasamy V, Abu Kasim NH
    Int Endod J, 2016 Oct;49(10):937-49.
    PMID: 26354006 DOI: 10.1111/iej.12545
    AIM: To investigate whether dental pulp stem cells from carious teeth (DPSCs-CT) can differentiate into functional dopaminergic-like (DAergic) cells and provide an alternative cell source in regenerative medicine.

    METHODOLOGY: Dental pulp stem cells from healthy (DPSCs) and carious teeth (DPSCs-CT) were isolated from young donors. Both cell lines were expanded in identical culture conditions and subsequently differentiated towards DAergic-like cells using pre-defined dopaminergic cocktails. The dopaminergic efficiencies were evaluated both at gene and protein as well as at secretome levels.

    RESULTS: The efficiency of DPSCs-CT to differentiate into DAergic-like cells was not equivalent to that of DPSCs. This was further reflected in both gene and protein generation whereby key neuronal markers such as nestin, NURR1 and beta-III-tubulin were expressed significantly lower as compared to differentiated DPSCs (P 

    Matched MeSH terms: Dopaminergic Neurons/physiology*
  8. Fulltext Effect of tualang honey against KA-induced oxidative stress and neurodegeneration in the cortex of rats
    Mohd Sairazi NS, K N S S, Asari MA, Mummedy S, Muzaimi M, Sulaiman SA
    BMC Complement Altern Med, 2017 Jan 09;17(1):31.
    PMID: 28068984 DOI: 10.1186/s12906-016-1534-x
    Administration of KA on rodents has resulted in seizures, behavioral changes, oxidative stress, and neuronal degeneration on selective population of neurons in the brain. The present study was undertaken to investigate the extent of neuroprotective effect conferred by Malaysian Tualang Honey (TH), an antioxidant agent, in the cerebral cortex of rats against KA-induced oxidative stress and neurodegeneration in an animal model of KA-induced excitotoxicity.
    Matched MeSH terms: Neurons/physiology
  9. Effects of action observation on corticospinal excitability: Muscle specificity, direction, and timing of the mirror response
    Naish KR, Houston-Price C, Bremner AJ, Holmes NP
    Neuropsychologia, 2014 11;64:331-48.
    PMID: 25281883 DOI: 10.1016/j.neuropsychologia.2014.09.034
    Many human behaviours and pathologies have been attributed to the putative mirror neuron system, a neural system that is active during both the observation and execution of actions. While there are now a very large number of papers on the mirror neuron system, variations in the methods and analyses employed by researchers mean that the basic characteristics of the mirror response are not clear. This review focuses on three important aspects of the mirror response, as measured by modulations in corticospinal excitability: (1) muscle specificity; (2) direction; and (3) timing of modulation. We focus mainly on electromyographic (EMG) data gathered following single-pulse transcranial magnetic stimulation (TMS), because this method provides precise information regarding these three aspects of the response. Data from paired-pulse TMS paradigms and peripheral nerve stimulation (PNS) are also considered when we discuss the possible mechanisms underlying the mirror response. In this systematic review of the literature, we examine the findings of 85 TMS and PNS studies of the human mirror response, and consider the limitations and advantages of the different methodological approaches these have adopted in relation to discrepancies between their findings. We conclude by proposing a testable model of how action observation modulates corticospinal excitability in humans. Specifically, we propose that action observation elicits an early, non-specific facilitation of corticospinal excitability (at around 90ms from action onset), followed by a later modulation of activity specific to the muscles involved in the observed action (from around 200ms). Testing this model will greatly advance our understanding of the mirror mechanism and provide a more stable grounding on which to base inferences about its role in human behaviour.
    Matched MeSH terms: Mirror Neurons/physiology*
  10. Fulltext Fezf2-positive fork cell-like neurons in the mouse insular cortex
    Taniguchi M, Iwahashi M, Oka Y, Tiong SYX, Sato M
    PLoS One, 2022;17(9):e0274170.
    PMID: 36067159 DOI: 10.1371/journal.pone.0274170
    The fork cell and von Economo neuron, which are found in the insular cortex and/or the anterior cingulate cortex, are defined by their unique morphologies. Their shapes are not pyramidal; the fork cell has two primary apical dendrites and the von Economo neurons are spindle-shaped (bipolar). Presence of such neurons are reported only in the higher animals, especially in human and great ape, indicating that they are specific for most evolved species. Although it is likely that these neurons are involved in higher brain function, lack of results with experimental animals makes further investigation difficult. We here ask whether equivalent neurons exist in the mouse insular cortex. In human, Fezf2 has been reported to be highly expressed in these morphologically distinctive neurons and thus, we examined the detailed morphology of Fezf2-positive neurons in the mouse brain. Although von Economo-like neurons were not identified, Fezf2-positive fork cell-like neurons with two characteristic apical dendrites, were discovered. Examination with electron microscope indicated that these neurons did not embrace capillaries, rather they held another cell. We here term such neurons as holding neurons. We further observed several molecules, including neuromedin B (NMB) and gastrin releasing peptide (GRP) that are known to be localized in the fork cells and/or von Economo cells in human, were localized in the mouse insular cortex. Based on these observations, it is likely that an equivalent of the fork cell is present in the mouse.
    Matched MeSH terms: Neurons/physiology
  11. Functional Neuroproteomics: An Imperative Approach for Unravelling Protein Implicated Complexities of Brain
    Husain I, Ahmad W, Ali A, Anwar L, Nuruddin SM, Ashraf K, et al.
    CNS Neurol Disord Drug Targets, 2021;20(7):613-624.
    PMID: 33530918 DOI: 10.2174/1871527320666210202121624
    A proteome is defined as a comprehensive protein set either of an organ or an organism at a given time and under specific physiological conditions. Accordingly, the study of the nervous system's proteomes is called neuroproteomics. In the neuroproteomics process, various pieces of the nervous system are "fragmented" to understand the dynamics of each given sub-proteome in a much better way. Functional proteomics addresses the organisation of proteins into complexes and the formation of organelles from these multiprotein complexes that control various physiological processes. Current functional studies of neuroproteomics mainly talk about the synapse structure and its organisation, the major building site of the neuronal communication channel. The proteomes of synaptic vesicle, presynaptic terminal, and postsynaptic density, have been examined by various proteomics techniques. The objectives of functional neuroproteomics are: to solve the proteome of single neurons or astrocytes grown in cell cultures or from the primary brain cells isolated from tissues under various conditions, to identify the set of proteins that characterize specific pathogenesis, or to determine the group of proteins making up postsynaptic or presynaptic densities. It is usual to solve a particular sub-proteome like the heat-shock response proteome or the proteome responding to inflammation. Post-translational protein modifications alter their functions and interactions. The techniques to detect synapse phosphoproteome are available. However, techniques for the analysis of ubiquitination and sumoylation are under development.
    Matched MeSH terms: Neurons/physiology
  12. Genomic instantiation of consciousness in neurons through a biophoton field theory
    Cacha LA, Poznanski RR
    J Integr Neurosci, 2014 Jun;13(2):253-92.
    PMID: 25012712 DOI: 10.1142/S0219635214400081
    A theoretical framework is developed based on the premise that brains evolved into sufficiently complex adaptive systems capable of instantiating genomic consciousness through self-awareness and complex interactions that recognize qualitatively the controlling factors of biological processes. Furthermore, our hypothesis assumes that the collective interactions in neurons yield macroergic effects, which can produce sufficiently strong electric energy fields for electronic excitations to take place on the surface of endogenous structures via alpha-helical integral proteins as electro-solitons. Specifically the process of radiative relaxation of the electro-solitons allows for the transfer of energy via interactions with deoxyribonucleic acid (DNA) molecules to induce conformational changes in DNA molecules producing an ultra weak non-thermal spontaneous emission of coherent biophotons through a quantum effect. The instantiation of coherent biophotons confined in spaces of DNA molecules guides the biophoton field to be instantaneously conducted along the axonal and neuronal arbors and in-between neurons and throughout the cerebral cortex (cortico-thalamic system) and subcortical areas (e.g., midbrain and hindbrain). Thus providing an informational character of the electric coherence of the brain - referred to as quantum coherence. The biophoton field is realized as a conscious field upon the re-absorption of biophotons by exciplex states of DNA molecules. Such quantum phenomenon brings about self-awareness and enables objectivity to have access to subjectivity in the unconscious. As such, subjective experiences can be recalled to consciousness as subjective conscious experiences or qualia through co-operative interactions between exciplex states of DNA molecules and biophotons leading to metabolic activity and energy transfer across proteins as a result of protein-ligand binding during protein-protein communication. The biophoton field as a conscious field is attributable to the resultant effect of specifying qualia from the metabolic energy field that is transported in macromolecular proteins throughout specific networks of neurons that are constantly transforming into more stable associable representations as molecular solitons. The metastability of subjective experiences based on resonant dynamics occurs when bottom-up patterns of neocortical excitatory activity are matched with top-down expectations as adaptive dynamic pressures. These dynamics of on-going activity patterns influenced by the environment and selected as the preferred subjective experience in terms of a functional field through functional interactions and biological laws are realized as subjectivity and actualized through functional integration as qualia. It is concluded that interactionism and not information processing is the key in understanding how consciousness bridges the explanatory gap between subjective experiences and their neural correlates in the transcendental brain.
    Matched MeSH terms: Neurons/physiology*
  13. Housing under the pyramid reduces susceptibility of hippocampal CA3 pyramidal neurons to prenatal stress in the developing rat offspring
    Murthy KD, George MC, Ramasamy P, Mustapha ZA
    Indian J Exp Biol, 2013 Dec;51(12):1070-8.
    PMID: 24579372
    Mother-offspring interaction begins before birth. The foetus is particularly vulnerable to environmental insults and stress. The body responds by releasing excess of the stress hormone cortisol, which acts on glucocorticoid receptors. Hippocampus in the brain is rich in glucocorticoid receptors and therefore susceptible to stress. The stress effects are reduced when the animals are placed under a model wooden pyramid. The present study was to first explore the effects of prenatal restraint-stress on the plasma corticosterone levels and the dendritic arborisation of CA3 pyramidal neurons in the hippocampus of the offspring. Further, to test whether the pyramid environment would alter these effects, as housing under a pyramid is known to reduce the stress effects, pregnant Sprague Dawley rats were restrained for 9 h per day from gestation day 7 until parturition in a wire-mesh restrainer. Plasma corticosterone levels were found to be significantly increased. In addition, there was a significant reduction in the apical and the basal total dendritic branching points and intersections of the CA3 hippocampal pyramidal neurons. The results thus suggest that, housing in the pyramid dramatically reduces prenatal stress effects in rats.
    Matched MeSH terms: Neurons/physiology
  14. Fulltext IGF-1 enhances cell proliferation and survival during early differentiation of mesenchymal stem cells to neural progenitor-like cells
    Huat TJ, Khan AA, Pati S, Mustafa Z, Abdullah JM, Jaafar H
    BMC Neurosci, 2014;15:91.
    PMID: 25047045 DOI: 10.1186/1471-2202-15-91
    There has been increasing interest recently in the plasticity of mesenchymal stem cells (MSCs) and their potential to differentiate into neural lineages. To unravel the roles and effects of different growth factors in the differentiation of MSCs into neural lineages, we have differentiated MSCs into neural lineages using different combinations of growth factors. Based on previous studies of the roles of insulin-like growth factor 1 (IGF-1) in neural stem cell isolation in the laboratory, we hypothesized that IGF-1 can enhance proliferation and reduce apoptosis in neural progenitor-like cells (NPCs) during differentiation of MSCs into NCPs.We induced MSCs differentiation under four different combinations of growth factors: (A) EGF + bFGF, (B) EGF + bFGF + IGF-1, (C) EGF + bFGF + LIF, (D) EGF + bFGF + BDNF, and (E) without growth factors, as a negative control. The neurospheres formed were characterized by immunofluorescence staining against nestin, and the expression was measured by flow cytometry. Cell proliferation and apoptosis were also studied by MTS and Annexin V assay, respectively, at three different time intervals (24 hr, 3 days, and 5 days). The neurospheres formed in the four groups were then terminally differentiated into neuron and glial cells.
    Matched MeSH terms: Neurons/physiology
  15. Fulltext Induced mitochondrial membrane potential for modeling solitonic conduction of electrotonic signals
    Poznanski RR, Cacha LA, Ali J, Rizvi ZH, Yupapin P, Salleh SH, et al.
    PLoS One, 2017;12(9):e0183677.
    PMID: 28880876 DOI: 10.1371/journal.pone.0183677
    A cable model that includes polarization-induced capacitive current is derived for modeling the solitonic conduction of electrotonic potentials in neuronal branchlets with microstructure containing endoplasmic membranes. A solution of the nonlinear cable equation modified for fissured intracellular medium with a source term representing charge 'soakage' is used to show how intracellular capacitive effects of bound electrical charges within mitochondrial membranes can influence electrotonic signals expressed as solitary waves. The elastic collision resulting from a head-on collision of two solitary waves results in localized and non-dispersing electrical solitons created by the nonlinearity of the source term. It has been shown that solitons in neurons with mitochondrial membrane and quasi-electrostatic interactions of charges held by the microstructure (i.e., charge 'soakage') have a slower velocity of propagation compared with solitons in neurons with microstructure, but without endoplasmic membranes. When the equilibrium potential is a small deviation from rest, the nonohmic conductance acts as a leaky channel and the solitons are small compared when the equilibrium potential is large and the outer mitochondrial membrane acts as an amplifier, boosting the amplitude of the endogenously generated solitons. These findings demonstrate a functional role of quasi-electrostatic interactions of bound electrical charges held by microstructure for sustaining solitons with robust self-regulation in their amplitude through changes in the mitochondrial membrane equilibrium potential. The implication of our results indicate that a phenomenological description of ionic current can be successfully modeled with displacement current in Maxwell's equations as a conduction process involving quasi-electrostatic interactions without the inclusion of diffusive current. This is the first study in which solitonic conduction of electrotonic potentials are generated by polarization-induced capacitive current in microstructure and nonohmic mitochondrial membrane current.
    Matched MeSH terms: Neurons/physiology*
  16. Fulltext Inhibitory action of gonadotropin-inhibitory hormone on the signaling pathways induced by kisspeptin and vasoactive intestinal polypeptide in GnRH neuronal cell line, GT1-7
    Son YL, Ubuka T, Soga T, Yamamoto K, Bentley GE, Tsutsui K
    FASEB J, 2016 06;30(6):2198-210.
    PMID: 26929433 DOI: 10.1096/fj.201500055
    Gonadotropin-inhibitory hormone (GnIH) acts as a negative regulator of reproduction by acting on gonadotropes and gonadotropin-releasing hormone (GnRH) neurons. Despite its functional significance, the molecular mechanism of GnIH action in the target cells has not been fully elucidated. To expand our previous study on GnIH actions in gonadotropes, we investigated the potential signal transduction pathway that conveys the inhibitory action of GnIH in GnRH neurons by using the GnRH neuronal cell line, GT1-7. We examined whether GnIH inhibits the action of kisspeptin and vasoactive intestinal polypeptide (VIP), positive regulators of GnRH neurons. Although GnIH significantly suppressed the stimulatory effect of kisspeptin on GnRH release in hypothalamic culture, GnIH had no inhibitory effect on kisspeptin stimulation of serum response element and nuclear factor of activated T-cell response element activities and ERK phosphorylation, indicating that GnIH may not directly inhibit kisspeptin signaling in GnRH neurons. On the contrary, GnIH effectively eliminated the stimulatory effect of VIP on p38 and ERK phosphorylation, c-Fos mRNA expression, and GnRH release. The use of pharmacological modulators strongly demonstrated the specific inhibitory action of GnIH on the adenylate cyclase/cAMP/protein kinase A pathway, suggesting a common inhibitory mechanism of GnIH action in GnRH neurons and gonadotropes.-Son, Y. L., Ubuka, T., Soga, T., Yamamoto, K., Bentley, G. E., Tsutsui, K. Inhibitory action of gonadotropin-inhibitory hormone on the signaling pathways induced by kisspeptin and vasoactive intestinal polypeptide in GnRH neuronal cell line, GT1-7.
    Matched MeSH terms: Neurons/physiology
  17. Fulltext Interactions of noncanonical motifs with hnRNP A2 promote activity-dependent RNA transport in neurons
    Muslimov IA, Tuzhilin A, Tang TH, Wong RK, Bianchi R, Tiedge H
    J. Cell Biol., 2014 May 26;205(4):493-510.
    PMID: 24841565 DOI: 10.1083/jcb.201310045
    A key determinant of neuronal functionality and plasticity is the targeted delivery of select ribonucleic acids (RNAs) to synaptodendritic sites of protein synthesis. In this paper, we ask how dendritic RNA transport can be regulated in a manner that is informed by the cell's activity status. We describe a molecular mechanism in which inducible interactions of noncanonical RNA motif structures with targeting factor heterogeneous nuclear ribonucleoprotein (hnRNP) A2 form the basis for activity-dependent dendritic RNA targeting. High-affinity interactions between hnRNP A2 and conditional GA-type RNA targeting motifs are critically dependent on elevated Ca(2+) levels in a narrow concentration range. Dendritic transport of messenger RNAs that carry such GA motifs is inducible by influx of Ca(2+) through voltage-dependent calcium channels upon β-adrenergic receptor activation. The combined data establish a functional correspondence between Ca(2+)-dependent RNA-protein interactions and activity-inducible RNA transport in dendrites. They also indicate a role of genomic retroposition in the phylogenetic development of RNA targeting competence.
    Matched MeSH terms: Neurons/physiology*
  18. Lingzhi or Reishi Medicinal Mushroom, Ganoderma lucidum (Agaricomycetes), Ameliorates Nonspatial Learning and Memory Deficits in Rats with Hypercholesterolemia and Alzheimer's Disease
    Rahman MA, Hossain S, Abdullah N, Aminudin N
    Int J Med Mushrooms, 2020;22(11):1067-1078.
    PMID: 33426838 DOI: 10.1615/IntJMedMushrooms.2020036354
    Alzheimer's disease (AD) is the leading neurodegenerative disorder affecting memory and learning of aged people. Hypercholesterolemia had been implicated as one of the stark hallmarks of AD. Recent AD control guidelines have suggested lifestyle modification to slow down the progression of AD. In this regard, medicinal mushroom Ganoderma lucidum seems apt. In the present study, hot water extract of G. lucidum (200 mg/kg body weight) was fed to the hypercholesterolemic and AD model rats for 8 weeks. Nonspatial memory and learning abilities of the model animals was assessed using novel object recognition (NOR) test, rotarod test, and locomotor/open-field test. Then, the animals were sacrificed and transmission electron micrograph (TEM) view of the hippocampal neurons was assessed. In all the nonspatial memory and learning tests, the G. lucidum HWE fed rats performed better indicating improved memory and learning abilities. TEM view showed regular arrangement of the neurons in the G. lucidum HWE fed rats compared with those of the deranged arrangement of the AD rats. G. lucidum might have aided in restoring the memory and learning abilities of the AD model animals through maintaining neuronal structure and function. Thus, G. lucidum could be suggested as a medicotherapeutic agent against AD.
    Matched MeSH terms: Neurons/physiology
  19. Localization of the motor neuron somata of geniohyoid muscle in rat: A horseradish peroxidase study
    Razlan ANB, Ullah M, Kapitonova MY, Liaqat Ali Khan NB, Fuad SBSA
    Anat Histol Embryol, 2018 Oct;47(5):410-416.
    PMID: 29888399 DOI: 10.1111/ahe.12372
    The aim of the study was to investigate the location of motor neuron somata of geniohyoid muscle in rat. Nine Sprague-Dawley rats were used in this study. Operations were performed under general anaesthesia. Nembutal sodium, 40 mg per kg intraperitoneally was used for anaesthesia. 0.02 to 0.05 ml of 30% horseradish peroxidase (Sigma Type VI) solution in normal saline was injected into the exposed right geniohyoid muscle. After 48 hr, the animals were fixed by perfusion through left ventricle of heart, first by 100 ml normal saline and then with 500 ml of 1.25% glutaraldehyde and 1% paraformaldehyde in 0.1 M phosphate buffer, pH 7.4, at room temperature, and finally with 500 ml of 10% sucrose in the same buffer at 4°C. The medulla oblongata and first cervical segment of spinal cord were removed, kept in 10% sucrose in above phosphate buffer at 4°C for 24 hr. Thereafter, their serial transverse sections were cut in a cryostat at a thickness of 60 μm. The sections were treated according to tetramethyl benzidine (TMB)-horseradish peroxidase (HRP) method. HRP-labelled neuron somata were observed at the following sites: (a) In ventral part of right main hypoglossal nucleus in upper two-thirds of the closed part of medulla oblongata. (b) In ventrolateral subnucleus of hypoglossal nucleus in lower third of closed part of medulla oblongata. (c) At spinomedullary junction, they were located in dorsomedial part of right ventral grey column; a few were also seen here scattered on right side of central canal and among corticospinal fibres.
    Matched MeSH terms: Motor Neurons/physiology*
  20. Fulltext Osmoregulation requires brain expression of the renal Na-K-2Cl cotransporter NKCC2
    Konopacka A, Qiu J, Yao ST, Greenwood MP, Greenwood M, Lancaster T, et al.
    J Neurosci, 2015 Apr 01;35(13):5144-55.
    PMID: 25834041 DOI: 10.1523/JNEUROSCI.4121-14.2015
    The Na-K-2Cl cotransporter 2 (NKCC2) was thought to be kidney specific. Here we show expression in the brain hypothalamo-neurohypophyseal system (HNS), wherein upregulation follows osmotic stress. The HNS controls osmotic stability through the synthesis and release of the neuropeptide hormone, arginine vasopressin (AVP). AVP travels through the bloodstream to the kidney, where it promotes water conservation. Knockdown of HNS NKCC2 elicited profound effects on fluid balance following ingestion of a high-salt solution-rats produced significantly more urine, concomitant with increases in fluid intake and plasma osmolality. Since NKCC2 is the molecular target of the loop diuretics bumetanide and furosemide, we asked about their effects on HNS function following disturbed water balance. Dehydration-evoked GABA-mediated excitation of AVP neurons was reversed by bumetanide, and furosemide blocked AVP release, both in vivo and in hypothalamic explants. Thus, NKCC2-dependent brain mechanisms that regulate osmotic stability are disrupted by loop diuretics in rats.
    Matched MeSH terms: Neurons/physiology
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