publication . Thesis

The role of schizophrenia susceptibility genes in associative learning

Clifton, Nicholas;
Open Access English
  • Country: United Kingdom
Abstract
Schizophrenia is highly heritable, indicating that a large proportion of one’s susceptibility to developing the disorder is attributable to genetics. Recent large-scale genomic studies have revealed that genetic variants in patients with schizophrenia affect genes involved in synaptic plasticity processes, which are required for learning and memory, including genes encoding protein complexes associated with the NMDA receptor and the postsynaptic density. Further evidence suggests that associative learning may be particularly affected, although it is unclear which components of this cognitive process are implicated in schizophrenia.\ud The present studies investi...
Subjects
free text keywords: RC0321, RM
Related Organizations
Funded by
NIH| MOLECULAR GENETICS OF SCHIZOPHRENIA
Project
  • Funder: National Institutes of Health (NIH)
  • Project Code: 5R01MH059588-04
  • Funding stream: NATIONAL INSTITUTE OF MENTAL HEALTH
,
NIH| Genetic Epidemiology of COPD
Project
  • Funder: National Institutes of Health (NIH)
  • Project Code: 5U01HL089897-02
  • Funding stream: NATIONAL HEART, LUNG, AND BLOOD INSTITUTE
,
NIH| Pathways from genotype and environment to melanoma
Project
  • Funder: National Institutes of Health (NIH)
  • Project Code: 1R01CA088363-01A1
  • Funding stream: NATIONAL CANCER INSTITUTE
,
NIH| Admixture Mapping for Breast Cancer in Latinas
Project
  • Funder: National Institutes of Health (NIH)
  • Project Code: 1R01CA120120-01A2
  • Funding stream: NATIONAL CANCER INSTITUTE
,
NIH| MOLECULAR GENETICS OF SCHIZOPHRENIA
Project
  • Funder: National Institutes of Health (NIH)
  • Project Code: 1R01MH059587-01A1
  • Funding stream: NATIONAL INSTITUTE OF MENTAL HEALTH
433 references, page 1 of 29

Table 3.1 The enrichment of extinction-related genes in schizophrenia patient CNVs exists in each cohort independently. ....................................................................78 Table 3.2 No learning-related gene sets were enriched in the CNVs of patients with melanoma. ............................................................................................................79 Table 3.3 Extinction learning-related genes within loci previously implicated in schizophrenia through CNV studies (deletions or duplications) and genome-wide association studies................................................................................................81 Table 5.1 Specific 45mer oligonucleotide probe sequences targeting Homer1 isoforms. ............................................................................................................................125 Table 7.1 Effects of systemic, hippocampal, infralimbic and amygdalar manipulations on the extinction of conditioned fear memory........................................................187 Barad M, Blouin AM, Cain CK (2004) Like extinction, latent inhibition of conditioned fear in mice is blocked by systemic inhibition of L-type voltage-gated calcium channels. Learn Mem 11:536-539.

Barch DM, Carter CS, MacDonald AW, Braver TS, Cohen JD (2003) Context-processing deficits in schizophrenia: diagnostic specificity, 4-week course, and relationships to clinical symptoms. J Abnorm Psychol 112:132- 143. [OpenAIRE]

Barnes P, Kirtley A, Thomas KL (2012) Quantitatively and qualitatively different cellular processes are engaged in CA1 during the consolidation and reconsolidation of contextual fear memory. Hippocampus 22:149- 171.

Barnes P, Thomas KL (2008) Proteolysis of proBDNF is a key regulator in the formation of memory. PLoS One 3:e3248.

Baruch I, Hemsley DR, Gray JA (1988) Differential performance of acute and chronic schizophrenics in a latent inhibition task. J Nerv Ment Dis 176:598-606.

Bassett AS, Chow EWC (2008) Schizophrenia and 22q11.2 deletion syndrome. Curr Psychiatry Rep 10:148-157.

Baude A, Nusser Z, Roberts JD, Mulvihill E, McIlhinney RA, Somogyi P (1993) The metabotropic glutamate receptor (mGluR1 alpha) is concentrated at perisynaptic membrane of neuronal subpopulations as detected by immunogold reaction. Neuron 11:771-787. [OpenAIRE]

Bauer EP, Schafe GE, LeDoux JE (2002) NMDA receptors and L-type voltage-gated calcium channels contribute to long-term potentiation and different components of fear memory formation in the lateral amygdala. J Neurosci 22:5239-5249. [OpenAIRE]

Baumeister A a, Francis JL (2002) Historical development of the dopamine hypothesis of schizophrenia. J Hist Neurosci 11:265-277.

Bazin N, Perruchet P (1996) Implicit and explicit associative memory in patients with schizophrenia. Schizophr Res 22:241-248.

Beasley CL, Reynolds GP (1997) Parvalbumin-immunoreactive neurons are reduced in the prefrontal cortex of schizophrenics. Schizophr Res 24:349-355.

Behar TN, Scott CA, Greene CL, Wen X, Smith S V., Maric D, Liu QY, Colton CA, Barker JL (1999) Glutamate acting at NMDA receptors stimulates embryonic cortical neuronal migration. J Neurosci Off J Soc Neurosci 19:4449-4461. [OpenAIRE]

Beneken J, Tu JC, Xiao B, Nuriya M, Yuan JP, Worley PF, Leahy DJ (2000) Structure of the Homer EVH1 domainpeptide complex reveals a new twist in polyproline recognition. Neuron 26:143-154. [OpenAIRE]

Benros ME, Mortensen PB, Eaton WW (2012) Autoimmune diseases and infections as risk factors for schizophrenia. Ann N Y Acad Sci 1262:56-66. [OpenAIRE]

Berke JD, Paletzki RF, Aronson GJ, Hyman SE, Gerfen CR (1998) A complex program of striatal gene expression induced by dopaminergic stimulation. J Neurosci Off J Soc Neurosci 18:5301-5310. [OpenAIRE]

433 references, page 1 of 29
Related research
Abstract
Schizophrenia is highly heritable, indicating that a large proportion of one’s susceptibility to developing the disorder is attributable to genetics. Recent large-scale genomic studies have revealed that genetic variants in patients with schizophrenia affect genes involved in synaptic plasticity processes, which are required for learning and memory, including genes encoding protein complexes associated with the NMDA receptor and the postsynaptic density. Further evidence suggests that associative learning may be particularly affected, although it is unclear which components of this cognitive process are implicated in schizophrenia.\ud The present studies investi...
Subjects
free text keywords: RC0321, RM
Related Organizations
Funded by
NIH| MOLECULAR GENETICS OF SCHIZOPHRENIA
Project
  • Funder: National Institutes of Health (NIH)
  • Project Code: 5R01MH059588-04
  • Funding stream: NATIONAL INSTITUTE OF MENTAL HEALTH
,
NIH| Genetic Epidemiology of COPD
Project
  • Funder: National Institutes of Health (NIH)
  • Project Code: 5U01HL089897-02
  • Funding stream: NATIONAL HEART, LUNG, AND BLOOD INSTITUTE
,
NIH| Pathways from genotype and environment to melanoma
Project
  • Funder: National Institutes of Health (NIH)
  • Project Code: 1R01CA088363-01A1
  • Funding stream: NATIONAL CANCER INSTITUTE
,
NIH| Admixture Mapping for Breast Cancer in Latinas
Project
  • Funder: National Institutes of Health (NIH)
  • Project Code: 1R01CA120120-01A2
  • Funding stream: NATIONAL CANCER INSTITUTE
,
NIH| MOLECULAR GENETICS OF SCHIZOPHRENIA
Project
  • Funder: National Institutes of Health (NIH)
  • Project Code: 1R01MH059587-01A1
  • Funding stream: NATIONAL INSTITUTE OF MENTAL HEALTH
433 references, page 1 of 29

Table 3.1 The enrichment of extinction-related genes in schizophrenia patient CNVs exists in each cohort independently. ....................................................................78 Table 3.2 No learning-related gene sets were enriched in the CNVs of patients with melanoma. ............................................................................................................79 Table 3.3 Extinction learning-related genes within loci previously implicated in schizophrenia through CNV studies (deletions or duplications) and genome-wide association studies................................................................................................81 Table 5.1 Specific 45mer oligonucleotide probe sequences targeting Homer1 isoforms. ............................................................................................................................125 Table 7.1 Effects of systemic, hippocampal, infralimbic and amygdalar manipulations on the extinction of conditioned fear memory........................................................187 Barad M, Blouin AM, Cain CK (2004) Like extinction, latent inhibition of conditioned fear in mice is blocked by systemic inhibition of L-type voltage-gated calcium channels. Learn Mem 11:536-539.

Barch DM, Carter CS, MacDonald AW, Braver TS, Cohen JD (2003) Context-processing deficits in schizophrenia: diagnostic specificity, 4-week course, and relationships to clinical symptoms. J Abnorm Psychol 112:132- 143. [OpenAIRE]

Barnes P, Kirtley A, Thomas KL (2012) Quantitatively and qualitatively different cellular processes are engaged in CA1 during the consolidation and reconsolidation of contextual fear memory. Hippocampus 22:149- 171.

Barnes P, Thomas KL (2008) Proteolysis of proBDNF is a key regulator in the formation of memory. PLoS One 3:e3248.

Baruch I, Hemsley DR, Gray JA (1988) Differential performance of acute and chronic schizophrenics in a latent inhibition task. J Nerv Ment Dis 176:598-606.

Bassett AS, Chow EWC (2008) Schizophrenia and 22q11.2 deletion syndrome. Curr Psychiatry Rep 10:148-157.

Baude A, Nusser Z, Roberts JD, Mulvihill E, McIlhinney RA, Somogyi P (1993) The metabotropic glutamate receptor (mGluR1 alpha) is concentrated at perisynaptic membrane of neuronal subpopulations as detected by immunogold reaction. Neuron 11:771-787. [OpenAIRE]

Bauer EP, Schafe GE, LeDoux JE (2002) NMDA receptors and L-type voltage-gated calcium channels contribute to long-term potentiation and different components of fear memory formation in the lateral amygdala. J Neurosci 22:5239-5249. [OpenAIRE]

Baumeister A a, Francis JL (2002) Historical development of the dopamine hypothesis of schizophrenia. J Hist Neurosci 11:265-277.

Bazin N, Perruchet P (1996) Implicit and explicit associative memory in patients with schizophrenia. Schizophr Res 22:241-248.

Beasley CL, Reynolds GP (1997) Parvalbumin-immunoreactive neurons are reduced in the prefrontal cortex of schizophrenics. Schizophr Res 24:349-355.

Behar TN, Scott CA, Greene CL, Wen X, Smith S V., Maric D, Liu QY, Colton CA, Barker JL (1999) Glutamate acting at NMDA receptors stimulates embryonic cortical neuronal migration. J Neurosci Off J Soc Neurosci 19:4449-4461. [OpenAIRE]

Beneken J, Tu JC, Xiao B, Nuriya M, Yuan JP, Worley PF, Leahy DJ (2000) Structure of the Homer EVH1 domainpeptide complex reveals a new twist in polyproline recognition. Neuron 26:143-154. [OpenAIRE]

Benros ME, Mortensen PB, Eaton WW (2012) Autoimmune diseases and infections as risk factors for schizophrenia. Ann N Y Acad Sci 1262:56-66. [OpenAIRE]

Berke JD, Paletzki RF, Aronson GJ, Hyman SE, Gerfen CR (1998) A complex program of striatal gene expression induced by dopaminergic stimulation. J Neurosci Off J Soc Neurosci 18:5301-5310. [OpenAIRE]

433 references, page 1 of 29
Related research
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