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Molecular and Cellular Physiology of Neurons

31 Aug 1999-
TL;DR: Enhanced by more than two hundred illustrations, Molecular and Cellular Physiology of Neurons, Second Edition is intended for anyone who seeks to understand the fundamentals of nerve cell function, including undergraduate and graduate students in neuroscience, students of bioengineering and cognitive science, and practicing neuroscientists who want to deepen their knowledge of recent discoveries in molecular and cellular neurophysiology.
Abstract: Molecular and Cellular Physiology of Neurons, Second Edition "is a comprehensive, up-to-date introduction to essential concepts of cellular neuroscience. Emphasizing experimental approaches and recent discoveries, it provides an in-depth look at the structure and function of nerve cells, from protein receptors and synapses to the biochemical processes that drive the mammalian nervous system.Starting with the basics of electrical current flow across cell membranes, Gordon Fain covers voltage gating and receptor activation in the context of channel diversity, excitatory and inhibitory synaptic transmission, neuromodulation, and sensory transduction. Emphasizing long-term processes of synaptic potentiation and depression involved in memory, consciousness, and attention, he demonstrates how cells produce neural signals and regulate signal flow to enhance or impede cell-to-cell communication. Fain also addresses the relation of molecular and cellular mechanisms to evolving theories of neurological disease and addiction.Enhanced by more than two hundred illustrations, Molecular and Cellular Physiology of Neurons, Second Edition "is intended for anyone who seeks to understand the fundamentals of nerve cell function, including undergraduate and graduate students in neuroscience, students of bioengineering and cognitive science, and practicing neuroscientists who want to deepen their knowledge of recent discoveries in molecular and cellular neurophysiology.
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Journal ArticleDOI
TL;DR: There is increasing evidence that the second messenger responsible for the modulation of the transduction cascade during background adaptation is primarily, if not exclusively, Ca(2+), whose intracellular free concentration is decreased by illumination.
Abstract: When light is absorbed within the outer segment of a vertebrate photoreceptor, the conformation of the photopigment rhodopsin is altered to produce an activated photoproduct called metarhodopsin II...

527 citations

Journal ArticleDOI
TL;DR: This review focuses on the application of nanomaterials for neural interfacing, covering a variety of specific applications of nanoengineered devices, including drug delivery, imaging, topographic patterning, electrode design, nanoscale transistors for high‐resolution neural interfaced, and photoactivated interfaces.
Abstract: This review focuses on the application of nanomaterials for neural interfacing. The junction between nanotechnology and neural tissues can be particularly worthy of scientific attention for several reasons: (i) Neural cells are electroactive, and the electronic properties of nanostructures can be tailored to match the charge transport requirements of electrical cellular interfacing. (ii) The unique mechanical and chemical properties of nanomaterials are critical for integration with neural tissue as long-term implants. (iii) Solutions to many critical problems in neural biology/medicine are limited by the availability of specialized materials. (iv) Neuronal stimulation is needed for a variety of common and severe health problems. This confluence of need, accumulated expertise, and potential impact on the well-being of people suggests the potential of nanomaterials to revolutionize the field of neural interfacing. In this review, we begin with foundational topics, such as the current status of neural electrode (NE) technology, the key challenges facing the practical utilization of NEs, and the potential advantages of nanostructures as components of chronic implants. After that the detailed account of toxicology and biocompatibility of nanomaterials in respect to neural tissues is given. Next, we cover a variety of specific applications of nanoengineered devices, including drug delivery, imaging, topographic patterning, electrode design, nanoscale transistors for high-resolution neural interfacing, and photoactivated interfaces. We also critically evaluate the specific properties of particular nanomaterials—including nanoparticles, nanowires, and carbon nanotubes—that can be taken advantage of in neuroprosthetic devices. The most promising future areas of research and practical device engineering are discussed as a conclusion to the review.

471 citations

Journal ArticleDOI
TL;DR: Results indicate that passive and active membrane and synaptic properties of medium-sized spiny neurons are altered in the R6/2 transgenic, which will affect communication in the basal ganglia circuitry and suggest areas to target for pharmacotherapies to alleviate and reduce the symptoms of HD.
Abstract: We examined passive and active membrane properties and synaptic responses of medium-sized spiny striatal neurons in brain slices from presymptomatic (∼40 days of age) and symptomatic (∼90 days of a...

319 citations

Journal ArticleDOI
TL;DR: It is concluded that ketamine challenge is useful for studying the positive, negative, and cognitive symptoms, dopaminergic and GABAergic dysfunction, age of onset, functional dysconnectivity, and abnormal cortical oscillations observed in acute schizophrenia.
Abstract: The observation that antagonists of the N-methyl-D-aspartate glutamate receptor (NMDAR), such as phencyclidine (PCP) and ketamine, transiently induce symptoms of acute schizophrenia had led to a paradigm shift from dopaminergic to glutamatergic dysfunction in pharmacological models of schizophrenia. The glutamate hypothesis can explain negative and cognitive symptoms of schizophrenia better than the dopamine hypothesis, and has the potential to explain dopamine dysfunction itself. The pharmacological and psychomimetic effects of ketamine, which is safer for human subjects than phencyclidine, are herein reviewed. Ketamine binds to a variety of receptors, but principally acts at the NMDAR, and convergent genetic and molecular evidence point to NMDAR hypofunction in schizophrenia. Furthermore, NMDAR hypofunction can explain connectional and oscillatory abnormalities in schizophrenia in terms of both weakened excitation of inhibitory -aminobutyric acidergic (GABAergic) interneurons that synchronize cortical networks and disinhibition of principal cells. Individuals with prenatal aberrations of NMDAR might experience the onset of schizophrenia towards the completion of synaptic pruning in adolescence, when network connectivity drops below a critical value. We conclude that ketamine challenge is useful for studying the positive, negative, and cognitive symptoms, dopaminergic and GABAergic dysfunction, age of onset, functional dysconnectivity, and abnormal cortical oscillations observed in acute schizophrenia.

243 citations


Cites background from "Molecular and Cellular Physiology o..."

  • ...NMDARs are heteromeric, composed of an NR1 subunit and modulatory subunits of the NR2 (NR2A-D) family (Fain, 1999)....

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  • ...At most synapses, glutamate is the agonist released from the presynaptic terminal, while ambient, micromolar concentrations of glycine are thought to activate the glycine binding site (Fain, 1999)....

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  • ...Thus, the NMDAR is necessary for the induction of LTP, a comprehensive delineation of which is beyond the scope of this review (Fain, 1999)....

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  • ...NMDAR antagonists that block the glutamate or glycine binding sites are competitive antagonists, such as 2-amino7-phosphonoheptanoic acid (AP7) (Fain, 1999)....

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  • ...Glutamate, an amino acid, is the principal excitatory neurotransmitter of the central nervous system (Fain, 1999)....

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Journal ArticleDOI
TL;DR: In this paper, the responses of photosynthetic gas exchange, chlorophyll fluorescence, content of pigments, main osmolytes, and malondialdehyde (MDA) to water-withholding for 15 days and re-hydration in seedlings of two mango cultivars (Mangifera indica L. var. “Choke Anand” and var.
Abstract: The responses of photosynthetic gas exchange, chlorophyll fluorescence, content of pigments, main osmolytes, and malondialdehyde (MDA) to water-withholding for 15 days and re-hydration in seedlings of two mango cultivars (Mangifera indica L. var. “Choke Anand’ and var. “Khieo Sawoei”) under 50% sunlight and full sunlight were investigated. For both cultivars, the water-witholding resulted in progressively decreases in leaf relative water content, net photosynthesis (P n), stomatal conductance (g s), and increases in the conversion of xanthophyll cycle pigments estimated by an index of leaf spectral reflectance (ΔPRI), carotenoid to chlorophyll ratio, non-photochemical quenching (NPQ), the contents of malondialdehyde (MDA) and compatible solutes (total soluble sugar and proline). The effect of the water stress was more pronounced in full sunlight than 50% sunlight. The maximum photochemistry efficiency measured at dawn was fairly constant during the period of the treatment for both cultivars under both light regimes. The water stress caused less pronounced inhibition of photosynthesis in “Choke Anand” than in “Khieo Sawoei” cultivar under both light regimes. After re-hydration, the recovery was relatively quicker in “Choke Anand” than in “Khieo Sawoei” cultivar. Both cultivars in both 50% and full sunlight showed complete recovery in photochemistry after 5 days of re-watering but photosynthesis did not show a complete recovery as indicated by gas exchange rates. As the results of lower NPQ, ΔPRI and osmotic adjustment in the cultivar “Khieo Sawoei” compared to the cultivar “Choke Anand”, the former cultivar was less tolerant to drought than the latter. Our study further showed that partial shading (e.g., 50% of sunlight) significantly alleviated the harmful effect of drought stress on mango cultivars but in fact stomata of seedlings grown in partial shade was more responsive to water deficit than in full light.

162 citations