Neurotransmitter

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M. A. Kurian - One of the best experts on this subject based on the ideXlab platform.

  • Clinical Features and Pharmacotherapy of Childhood Monoamine Neurotransmitter Disorders
    Pediatric Drugs, 2014
    Co-Authors: J. Ng, S. J. R. Heales, M. A. Kurian
    Abstract:

    Childhood Neurotransmitter disorders are increasingly recognised as an expanding group of inherited neurometabolic syndromes. They are caused by disturbance in synthesis, metabolism, and homeostasis of the monoamine Neurotransmitters, including the catecholamines (dopamine, norepinephrine, and epinephrine) and serotonin. Disturbances in monoamine neurotransmission will lead to neurological symptoms that often overlap with clinical features of other childhood neurological disorders (such as hypoxic ischaemic encephalopathy, cerebral palsy, other movement disorders, and paroxysmal conditions); consequently, Neurotransmitter disorders are frequently misdiagnosed. The diagnosis of Neurotransmitter disorders is made through detailed clinical assessment, analysis of cerebrospinal fluid Neurotransmitters, and further supportive diagnostic investigations. Early and accurate diagnosis of Neurotransmitter disorders is important, as many are amenable to therapeutic intervention. The principles of treatment for monoamine Neurotransmitter disorders are mainly directly derived from understanding these metabolic pathways. In disorders characterized by enzyme deficiency, we aim to increase monoamine substrate availability, boost enzyme co-factor levels, reduce monoamine breakdown, and replace depleted levels of monoamines with pharmacological analogs as clinically indicated. Most monoamine Neurotransmitter disorders lead to reduced levels of central dopamine and/or serotonin. Complete amelioration of motor symptoms is achievable in some disorders, such as Segawa’s syndrome, and, in other conditions, significant improvement in quality of life can be attained with pharmacotherapy. In this review, we provide an overview of the clinical features and current treatment strategies for childhood monoamine Neurotransmitter disorders.

  • the monoamine Neurotransmitter disorders an expanding range of neurological syndromes
    Lancet Neurology, 2011
    Co-Authors: S. J. R. Heales, M. A. Kurian, Paul Gissen, Martin Smith, Peter E Clayton
    Abstract:

    Summary The monoamine Neurotransmitter disorders consist of a rapidly expanding heterogeneous group of neurological syndromes characterised by primary and secondary defects in the biosynthesis degradation, or transport of dopamine, norepinephrine, epinephrine, and serotonin. Disease onset can occur any time from infancy onwards. Clinical presentation depends on the pattern and severity of Neurotransmitter abnormalities, and is predominated by neurological features (encephalopathy, epilepsy, and pyramidal and extrapyramidal motor disorders) that are primarily attributed to deficiency of cerebral dopamine, serotonin, or both. Many Neurotransmitter disorders mimic the phenotype of other neurological disorders (eg, cerebral palsy, hypoxic ischaemic encephalopathy, paroxysmal disorders, inherited metabolic diseases, and genetic dystonic or parkinsonian syndromes) and are, therefore, frequently misdiagnosed. Early clinical suspicion and appropriate investigations, including analysis of Neurotransmitters in CSF, are essential for accurate clinical diagnosis. Treatment strategies focus on the correction of monoamine deficiency by replacement of monoamine precursors, the use of monoamine analogues, inhibition of monoamine degradation, and addition of enzyme cofactors to promote monoamine production.

Peter E Clayton - One of the best experts on this subject based on the ideXlab platform.

  • the monoamine Neurotransmitter disorders an expanding range of neurological syndromes
    Lancet Neurology, 2011
    Co-Authors: S. J. R. Heales, M. A. Kurian, Paul Gissen, Martin Smith, Peter E Clayton
    Abstract:

    Summary The monoamine Neurotransmitter disorders consist of a rapidly expanding heterogeneous group of neurological syndromes characterised by primary and secondary defects in the biosynthesis degradation, or transport of dopamine, norepinephrine, epinephrine, and serotonin. Disease onset can occur any time from infancy onwards. Clinical presentation depends on the pattern and severity of Neurotransmitter abnormalities, and is predominated by neurological features (encephalopathy, epilepsy, and pyramidal and extrapyramidal motor disorders) that are primarily attributed to deficiency of cerebral dopamine, serotonin, or both. Many Neurotransmitter disorders mimic the phenotype of other neurological disorders (eg, cerebral palsy, hypoxic ischaemic encephalopathy, paroxysmal disorders, inherited metabolic diseases, and genetic dystonic or parkinsonian syndromes) and are, therefore, frequently misdiagnosed. Early clinical suspicion and appropriate investigations, including analysis of Neurotransmitters in CSF, are essential for accurate clinical diagnosis. Treatment strategies focus on the correction of monoamine deficiency by replacement of monoamine precursors, the use of monoamine analogues, inhibition of monoamine degradation, and addition of enzyme cofactors to promote monoamine production.

Rakesh Katragadda - One of the best experts on this subject based on the ideXlab platform.

  • Microfluidic neurotransmiter-based neural interfaces for retinal prosthesis
    2009 Annual International Conference of the IEEE Engineering in Medicine and Biology Society, 2009
    Co-Authors: Raymond Iezzi, Paul Finlayson, Yong Xu, Rakesh Katragadda
    Abstract:

    Natural inter-neuronal communication is mediated primarily via Neurotransmitter-gated ion channels. While most of the methods for neural interfacing have been based upon electrical stimulation, Neurotransmitter-based approaches for the spatially and temporally controlled delivery of Neurotransmitters are relatively new. Methods of Neurotransmitter stimulation retinal prosthesis may provide new ways to control neural excitation. Experimental results for retinal ganglion cell stimulation demonstrate the feasibility of a Neurotransmitter-based retinal prosthesis.

S. J. R. Heales - One of the best experts on this subject based on the ideXlab platform.

  • Clinical Features and Pharmacotherapy of Childhood Monoamine Neurotransmitter Disorders
    Pediatric Drugs, 2014
    Co-Authors: J. Ng, S. J. R. Heales, M. A. Kurian
    Abstract:

    Childhood Neurotransmitter disorders are increasingly recognised as an expanding group of inherited neurometabolic syndromes. They are caused by disturbance in synthesis, metabolism, and homeostasis of the monoamine Neurotransmitters, including the catecholamines (dopamine, norepinephrine, and epinephrine) and serotonin. Disturbances in monoamine neurotransmission will lead to neurological symptoms that often overlap with clinical features of other childhood neurological disorders (such as hypoxic ischaemic encephalopathy, cerebral palsy, other movement disorders, and paroxysmal conditions); consequently, Neurotransmitter disorders are frequently misdiagnosed. The diagnosis of Neurotransmitter disorders is made through detailed clinical assessment, analysis of cerebrospinal fluid Neurotransmitters, and further supportive diagnostic investigations. Early and accurate diagnosis of Neurotransmitter disorders is important, as many are amenable to therapeutic intervention. The principles of treatment for monoamine Neurotransmitter disorders are mainly directly derived from understanding these metabolic pathways. In disorders characterized by enzyme deficiency, we aim to increase monoamine substrate availability, boost enzyme co-factor levels, reduce monoamine breakdown, and replace depleted levels of monoamines with pharmacological analogs as clinically indicated. Most monoamine Neurotransmitter disorders lead to reduced levels of central dopamine and/or serotonin. Complete amelioration of motor symptoms is achievable in some disorders, such as Segawa’s syndrome, and, in other conditions, significant improvement in quality of life can be attained with pharmacotherapy. In this review, we provide an overview of the clinical features and current treatment strategies for childhood monoamine Neurotransmitter disorders.

  • the monoamine Neurotransmitter disorders an expanding range of neurological syndromes
    Lancet Neurology, 2011
    Co-Authors: S. J. R. Heales, M. A. Kurian, Paul Gissen, Martin Smith, Peter E Clayton
    Abstract:

    Summary The monoamine Neurotransmitter disorders consist of a rapidly expanding heterogeneous group of neurological syndromes characterised by primary and secondary defects in the biosynthesis degradation, or transport of dopamine, norepinephrine, epinephrine, and serotonin. Disease onset can occur any time from infancy onwards. Clinical presentation depends on the pattern and severity of Neurotransmitter abnormalities, and is predominated by neurological features (encephalopathy, epilepsy, and pyramidal and extrapyramidal motor disorders) that are primarily attributed to deficiency of cerebral dopamine, serotonin, or both. Many Neurotransmitter disorders mimic the phenotype of other neurological disorders (eg, cerebral palsy, hypoxic ischaemic encephalopathy, paroxysmal disorders, inherited metabolic diseases, and genetic dystonic or parkinsonian syndromes) and are, therefore, frequently misdiagnosed. Early clinical suspicion and appropriate investigations, including analysis of Neurotransmitters in CSF, are essential for accurate clinical diagnosis. Treatment strategies focus on the correction of monoamine deficiency by replacement of monoamine precursors, the use of monoamine analogues, inhibition of monoamine degradation, and addition of enzyme cofactors to promote monoamine production.

Baruch I Kanner - One of the best experts on this subject based on the ideXlab platform.

  • glutamate transporters from brain a novel Neurotransmitter transporter family
    FEBS Letters, 1993
    Co-Authors: Baruch I Kanner
    Abstract:

    The removal of Neurotransmitters by their transporters in presynaptic nerve terminals and glial cells plays an important role in the termination of synaptic transmission. Many Neurotransmitter transporters, which are sodium- and chloride-coupled, have been cloned and shown to constitute a large superfamily. Glutamate is the major excitatory Neurotransmitter in the central nervous system. If not efficiently removed, it causes death of neuronal cells. Its transporter couples the flow of glutamate to that of sodium and potassium. Recently three different but related glutamate transporters have been cloned, which have no significant homology to the members of the superfamily.