Receptor Subunit

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Peter B. Crino - One of the best experts on this subject based on the ideXlab platform.

  • altered expression of neurotransmitter Receptor Subunit and uptake site mrnas in hemimegalencephaly
    Epilepsia, 2004
    Co-Authors: Marianna Baybis, Anita Patel, William J. Kupsky, Eleonora Aronica, Diane C Chugani, David A Lynch, Guy M Mckhann, Peter B. Crino
    Abstract:

    PURPOSE: Hemimegalencephaly (HMEG) is characterized by unilateral hemispheric enlargement and severe cytoarchitectural abnormalities that are highly associated with intractable epilepsy. No studies have defined alterations in neurotransmitter-Receptor Subunit gene expression in HMEG. We hypothesize that a differential expression of excitatory amino acid and gamma-aminobutyric acid (GABA)A-Receptor Subunit messenger RNAs (mRNAs) exists in HMEG. METHODS: The expression of mRNAs encoding 20 neurotransmitter-Receptor Subunits, synthetic enzymes, and uptake sites as well as select additional candidate genes was defined in HMEG samples (n=8) compared with homotopic control cortex specimens by using targeted complementary DNA (cDNA) arrays. Expression of GLT-1 (a glial glutamate transporter), EAAC-1 (neuronal glutamate transporter), and NMDA2B was corroborated by immunohistochemical, Western, and ligand-binding assays. RESULTS: Differential expression of 11 neurotransmitter-related mRNAs was demonstrated in HMEG compared with control cortex. For example, expression of GLT-1 and GluR6 mRNAs was enhanced, whereas diminished expression of the neuronal glutamate transporter EAAC-1, GABAAalpha2, GABAAgamma2, GABAAgamma3, NMDA2B, GluR1, GluR2, GluR4, and GluR5 Subunits occurred. Reduced NMDA2B Subunit mRNA expression in HMEG was confirmed by Receptor ligand-binding assays by using the NMDA2B-Receptor antagonist ifenprodil, which revealed barely detectable levels of NMDA2B binding compared with that in control cortex. CONCLUSIONS: Selective alterations occur in distinct neurotransmitter-Receptor and -uptake sites in HMEG. Differential expression of neurotransmitter-Receptor and -uptake sites in HMEG may contribute to epileptogenesis in HMEG

  • Altered expression of neurotransmitter-Receptor Subunit and uptake site mRNAs in hemimegalencephaly.
    Epilepsia, 2004
    Co-Authors: Marianna Baybis, Anita Patel, William J. Kupsky, Eleonora Aronica, Diane C Chugani, David A Lynch, Guy M Mckhann, Allana Lee, Peter B. Crino
    Abstract:

    Hemimegalencephaly (HMEG) is characterized by unilateral hemispheric enlargement and severe cytoarchitectural abnormalities that are highly associated with intractable epilepsy. No studies have defined alterations in neurotransmitter-Receptor Subunit gene expression in HMEG. We hypothesize that a differential expression of excitatory amino acid and gamma-aminobutyric acid (GABA)A-Receptor Subunit messenger RNAs (mRNAs) exists in HMEG. The expression of mRNAs encoding 20 neurotransmitter-Receptor Subunits, synthetic enzymes, and uptake sites as well as select additional candidate genes was defined in HMEG samples (n=8) compared with homotopic control cortex specimens by using targeted complementary DNA (cDNA) arrays. Expression of GLT-1 (a glial glutamate transporter), EAAC-1 (neuronal glutamate transporter), and NMDA2B was corroborated by immunohistochemical, Western, and ligand-binding assays. Differential expression of 11 neurotransmitter-related mRNAs was demonstrated in HMEG compared with control cortex. For example, expression of GLT-1 and GluR6 mRNAs was enhanced, whereas diminished expression of the neuronal glutamate transporter EAAC-1, GABAAalpha2, GABAAgamma2, GABAAgamma3, NMDA2B, GluR1, GluR2, GluR4, and GluR5 Subunits occurred. Reduced NMDA2B Subunit mRNA expression in HMEG was confirmed by Receptor ligand-binding assays by using the NMDA2B-Receptor antagonist ifenprodil, which revealed barely detectable levels of NMDA2B binding compared with that in control cortex. Selective alterations occur in distinct neurotransmitter-Receptor and -uptake sites in HMEG. Differential expression of neurotransmitter-Receptor and -uptake sites in HMEG may contribute to epileptogenesis in HMEG.

D Ball - One of the best experts on this subject based on the ideXlab platform.

  • Association analysis of the GABA A Receptor Subunit genes cluster on 5q33–34 and alcohol dependence in a Japanese population
    Molecular psychiatry, 2000
    Co-Authors: E.w. Loh, S Higuchi, S Matsushita, C-k Chen, Robin M. Murray, D Ball
    Abstract:

    Recent investigations suggest that genetic susceptibility to alcohol dependence may be conferred by GABA(A) Receptor Subunit genes. In this study, three RFLPs at the GABA(A)beta2, GABAAalpha6, GABA(A)alpha1 and two at the GABA(A)gamma2 Receptor Subunit genes, were examined for association with alcohol dependence in 189 subjects meeting DSM-III-R criteria for this disorder and 152 unrelated controls from a Japanese population. The results demonstrated no association between the AlwNI RFLP at the GABA(A)alpha6 Receptor Subunit gene and alcohol dependence (P = 0.059). However, the NciI RFLP at the GABA(A)gamma2 Receptor Subunit gene was associated with alcohol dependence comorbid with antisocial personality disorder (P = 0.021). This supports a recent finding reporting an association between the GABA(A)gamma2 Receptor Subunit gene and alcohol dependence with criminal record in a Finnish population. Taking into account the effects of multiple comparisons, this result should be interpreted with caution pending replication.

  • Association analysis of the GABA_A Receptor Subunit genes cluster on 5q33–34 and alcohol dependence in a Japanese population
    Molecular Psychiatry, 2000
    Co-Authors: S Higuchi, S Matsushita, R Murray, C-k Chen, D Ball
    Abstract:

    Recent investigations suggest that genetic susceptibility to alcohol dependence may be conferred by GABA_A Receptor Subunit genes. In this study, three RFLPs at the GABA_Aβ2, GABA_Aα6, GABA_Aα1 and two at the GABA_Aγ2 Receptor Subunit genes, were examined for association with alcohol dependence in 189 subjects meeting DSM-III-R criteria for this disorder and 152 unrelated controls from a Japanese population. The results demonstrated no association between the Alw NI RFLP at the GABA_Aα6 Receptor Subunit gene and alcohol dependence ( P  = 0.059). However, the Nci I RFLP at the GABA_Aγ2 Receptor Subunit gene was associated with alcohol dependence comorbid with antisocial personality disorder ( P  = 0.021). This supports a recent finding reporting an association between the GABA_Aγ2 Receptor Subunit gene and alcohol dependence with criminal record in a Finnish population. Taking into account the effects of multiple comparisons, this result should be interpreted with caution pending replication.

Cheryl M. Heesch - One of the best experts on this subject based on the ideXlab platform.

  • GABA(A) alpha1 and alpha2 Receptor Subunit expression in rostral ventrolateral medulla in nonpregnant and pregnant rats.
    Brain research, 2003
    Co-Authors: C. Michael Foley, Jeffery J. Stanton, Elmer M. Price, J. Thomas Cunningham, Eileen M. Hasser, Cheryl M. Heesch
    Abstract:

    Pregnancy results in attenuated baroreflex mediated sympathoexcitatory responses which may be due to potentiation of gamma-aminobutyric acid (GABA) inhibition in the rostral ventrolateral medulla (RVLM). The major metabolite of progesterone, 3alpha-hydroxy-dihydroprogesterone (3alpha-OH-DHP), which is elevated in pregnancy, is a potent neurosteroid positive modulator of GABA(A) Receptors, and sensitivity of GABA(A) Receptors to 3alpha-OH-DHP is dependent on the Receptor Subunit composition. The purpose of this study was to evaluate the GABA(A) alpha(1) and alpha(2) Receptor Subunit mRNA and protein expression in the RVLM of nonpregnant and late term pregnant rats. Micropunches of RVLM were collected from nonpregnant and late term pregnant rats and the expression levels of GABA(A) alpha(1) and alpha(2) Receptor Subunits were analyzed using quantitative competitive reverse transcriptase polymerase chain reaction (RT-PCR) and immunoblot techniques. The competitive RT-PCR analysis allows comparison of expression levels between different mRNA, and the mRNA expression level of GABA(A) alpha(1) was several hundred fold greater than GABA(A) alpha(2) in both groups. However, this relative distribution of GABA(A) alpha(1) and alpha(2) Receptor Subunits protein or mRNA expression was not altered in late term pregnant compared to nonpregnant rats. These data demonstrate, that within the RVLM of both nonpregnant and late term pregnant rats, the relative expression levels of GABA(A) alpha(1,2) Receptor Subunits favor GABA(A) Receptors susceptible to positive modulation by progesterone metabolites.

  • GABAA α1 and α2 Receptor Subunit expression in rostral ventrolateral medulla in nonpregnant and pregnant rats
    Brain Research, 2003
    Co-Authors: C. Michael Foley, Jeffery J. Stanton, Elmer M. Price, J. Thomas Cunningham, Eileen M. Hasser, Cheryl M. Heesch
    Abstract:

    Abstract Pregnancy results in attenuated baroreflex mediated sympathoexcitatory responses which may be due to potentiation of γ-aminobutyric acid (GABA) inhibition in the rostral ventrolateral medulla (RVLM). The major metabolite of progesterone, 3α-hydroxy-dihydroprogesterone (3α-OH-DHP), which is elevated in pregnancy, is a potent neurosteroid positive modulator of GABA A Receptors, and sensitivity of GABA A Receptors to 3α-OH-DHP is dependent on the Receptor Subunit composition. The purpose of this study was to evaluate the GABA A α 1 and α 2 Receptor Subunit mRNA and protein expression in the RVLM of nonpregnant and late term pregnant rats. Micropunches of RVLM were collected from nonpregnant and late term pregnant rats and the expression levels of GABA A α 1 and α 2 Receptor Subunits were analyzed using quantitative competitive reverse transcriptase polymerase chain reaction (RT-PCR) and immunoblot techniques. The competitive RT-PCR analysis allows comparison of expression levels between different mRNA, and the mRNA expression level of GABA A α 1 was several hundred fold greater than GABA A α 2 in both groups. However, this relative distribution of GABA A α 1 and α 2 Receptor Subunits protein or mRNA expression was not altered in late term pregnant compared to nonpregnant rats. These data demonstrate, that within the RVLM of both nonpregnant and late term pregnant rats, the relative expression levels of GABA A α 1,2 Receptor Subunits favor GABA A Receptors susceptible to positive modulation by progesterone metabolites.

David A Lynch - One of the best experts on this subject based on the ideXlab platform.

  • altered expression of neurotransmitter Receptor Subunit and uptake site mrnas in hemimegalencephaly
    Epilepsia, 2004
    Co-Authors: Marianna Baybis, Anita Patel, William J. Kupsky, Eleonora Aronica, Diane C Chugani, David A Lynch, Guy M Mckhann, Peter B. Crino
    Abstract:

    PURPOSE: Hemimegalencephaly (HMEG) is characterized by unilateral hemispheric enlargement and severe cytoarchitectural abnormalities that are highly associated with intractable epilepsy. No studies have defined alterations in neurotransmitter-Receptor Subunit gene expression in HMEG. We hypothesize that a differential expression of excitatory amino acid and gamma-aminobutyric acid (GABA)A-Receptor Subunit messenger RNAs (mRNAs) exists in HMEG. METHODS: The expression of mRNAs encoding 20 neurotransmitter-Receptor Subunits, synthetic enzymes, and uptake sites as well as select additional candidate genes was defined in HMEG samples (n=8) compared with homotopic control cortex specimens by using targeted complementary DNA (cDNA) arrays. Expression of GLT-1 (a glial glutamate transporter), EAAC-1 (neuronal glutamate transporter), and NMDA2B was corroborated by immunohistochemical, Western, and ligand-binding assays. RESULTS: Differential expression of 11 neurotransmitter-related mRNAs was demonstrated in HMEG compared with control cortex. For example, expression of GLT-1 and GluR6 mRNAs was enhanced, whereas diminished expression of the neuronal glutamate transporter EAAC-1, GABAAalpha2, GABAAgamma2, GABAAgamma3, NMDA2B, GluR1, GluR2, GluR4, and GluR5 Subunits occurred. Reduced NMDA2B Subunit mRNA expression in HMEG was confirmed by Receptor ligand-binding assays by using the NMDA2B-Receptor antagonist ifenprodil, which revealed barely detectable levels of NMDA2B binding compared with that in control cortex. CONCLUSIONS: Selective alterations occur in distinct neurotransmitter-Receptor and -uptake sites in HMEG. Differential expression of neurotransmitter-Receptor and -uptake sites in HMEG may contribute to epileptogenesis in HMEG

  • Altered expression of neurotransmitter-Receptor Subunit and uptake site mRNAs in hemimegalencephaly.
    Epilepsia, 2004
    Co-Authors: Marianna Baybis, Anita Patel, William J. Kupsky, Eleonora Aronica, Diane C Chugani, David A Lynch, Guy M Mckhann, Allana Lee, Peter B. Crino
    Abstract:

    Hemimegalencephaly (HMEG) is characterized by unilateral hemispheric enlargement and severe cytoarchitectural abnormalities that are highly associated with intractable epilepsy. No studies have defined alterations in neurotransmitter-Receptor Subunit gene expression in HMEG. We hypothesize that a differential expression of excitatory amino acid and gamma-aminobutyric acid (GABA)A-Receptor Subunit messenger RNAs (mRNAs) exists in HMEG. The expression of mRNAs encoding 20 neurotransmitter-Receptor Subunits, synthetic enzymes, and uptake sites as well as select additional candidate genes was defined in HMEG samples (n=8) compared with homotopic control cortex specimens by using targeted complementary DNA (cDNA) arrays. Expression of GLT-1 (a glial glutamate transporter), EAAC-1 (neuronal glutamate transporter), and NMDA2B was corroborated by immunohistochemical, Western, and ligand-binding assays. Differential expression of 11 neurotransmitter-related mRNAs was demonstrated in HMEG compared with control cortex. For example, expression of GLT-1 and GluR6 mRNAs was enhanced, whereas diminished expression of the neuronal glutamate transporter EAAC-1, GABAAalpha2, GABAAgamma2, GABAAgamma3, NMDA2B, GluR1, GluR2, GluR4, and GluR5 Subunits occurred. Reduced NMDA2B Subunit mRNA expression in HMEG was confirmed by Receptor ligand-binding assays by using the NMDA2B-Receptor antagonist ifenprodil, which revealed barely detectable levels of NMDA2B binding compared with that in control cortex. Selective alterations occur in distinct neurotransmitter-Receptor and -uptake sites in HMEG. Differential expression of neurotransmitter-Receptor and -uptake sites in HMEG may contribute to epileptogenesis in HMEG.

Marianna Baybis - One of the best experts on this subject based on the ideXlab platform.

  • altered expression of neurotransmitter Receptor Subunit and uptake site mrnas in hemimegalencephaly
    Epilepsia, 2004
    Co-Authors: Marianna Baybis, Anita Patel, William J. Kupsky, Eleonora Aronica, Diane C Chugani, David A Lynch, Guy M Mckhann, Peter B. Crino
    Abstract:

    PURPOSE: Hemimegalencephaly (HMEG) is characterized by unilateral hemispheric enlargement and severe cytoarchitectural abnormalities that are highly associated with intractable epilepsy. No studies have defined alterations in neurotransmitter-Receptor Subunit gene expression in HMEG. We hypothesize that a differential expression of excitatory amino acid and gamma-aminobutyric acid (GABA)A-Receptor Subunit messenger RNAs (mRNAs) exists in HMEG. METHODS: The expression of mRNAs encoding 20 neurotransmitter-Receptor Subunits, synthetic enzymes, and uptake sites as well as select additional candidate genes was defined in HMEG samples (n=8) compared with homotopic control cortex specimens by using targeted complementary DNA (cDNA) arrays. Expression of GLT-1 (a glial glutamate transporter), EAAC-1 (neuronal glutamate transporter), and NMDA2B was corroborated by immunohistochemical, Western, and ligand-binding assays. RESULTS: Differential expression of 11 neurotransmitter-related mRNAs was demonstrated in HMEG compared with control cortex. For example, expression of GLT-1 and GluR6 mRNAs was enhanced, whereas diminished expression of the neuronal glutamate transporter EAAC-1, GABAAalpha2, GABAAgamma2, GABAAgamma3, NMDA2B, GluR1, GluR2, GluR4, and GluR5 Subunits occurred. Reduced NMDA2B Subunit mRNA expression in HMEG was confirmed by Receptor ligand-binding assays by using the NMDA2B-Receptor antagonist ifenprodil, which revealed barely detectable levels of NMDA2B binding compared with that in control cortex. CONCLUSIONS: Selective alterations occur in distinct neurotransmitter-Receptor and -uptake sites in HMEG. Differential expression of neurotransmitter-Receptor and -uptake sites in HMEG may contribute to epileptogenesis in HMEG

  • Altered expression of neurotransmitter-Receptor Subunit and uptake site mRNAs in hemimegalencephaly.
    Epilepsia, 2004
    Co-Authors: Marianna Baybis, Anita Patel, William J. Kupsky, Eleonora Aronica, Diane C Chugani, David A Lynch, Guy M Mckhann, Allana Lee, Peter B. Crino
    Abstract:

    Hemimegalencephaly (HMEG) is characterized by unilateral hemispheric enlargement and severe cytoarchitectural abnormalities that are highly associated with intractable epilepsy. No studies have defined alterations in neurotransmitter-Receptor Subunit gene expression in HMEG. We hypothesize that a differential expression of excitatory amino acid and gamma-aminobutyric acid (GABA)A-Receptor Subunit messenger RNAs (mRNAs) exists in HMEG. The expression of mRNAs encoding 20 neurotransmitter-Receptor Subunits, synthetic enzymes, and uptake sites as well as select additional candidate genes was defined in HMEG samples (n=8) compared with homotopic control cortex specimens by using targeted complementary DNA (cDNA) arrays. Expression of GLT-1 (a glial glutamate transporter), EAAC-1 (neuronal glutamate transporter), and NMDA2B was corroborated by immunohistochemical, Western, and ligand-binding assays. Differential expression of 11 neurotransmitter-related mRNAs was demonstrated in HMEG compared with control cortex. For example, expression of GLT-1 and GluR6 mRNAs was enhanced, whereas diminished expression of the neuronal glutamate transporter EAAC-1, GABAAalpha2, GABAAgamma2, GABAAgamma3, NMDA2B, GluR1, GluR2, GluR4, and GluR5 Subunits occurred. Reduced NMDA2B Subunit mRNA expression in HMEG was confirmed by Receptor ligand-binding assays by using the NMDA2B-Receptor antagonist ifenprodil, which revealed barely detectable levels of NMDA2B binding compared with that in control cortex. Selective alterations occur in distinct neurotransmitter-Receptor and -uptake sites in HMEG. Differential expression of neurotransmitter-Receptor and -uptake sites in HMEG may contribute to epileptogenesis in HMEG.