INT92017

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Context Info
Confidence 0.18
First Reported 2000
Last Reported 2009
Negated 0
Speculated 1
Reported most in Body
Documents 3
Total Number 5
Disease Relevance 1.69
Pain Relevance 3.75

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

plasma membrane (Flvcr2) transmembrane transport (Flvcr2)
Anatomy Link Frequency
frontal cortex 3
plasma 2
substantia nigra 2
neurons 2
hippocampus 1
Flvcr2 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Dopamine 146 100.00 Very High Very High Very High
gABA 40 100.00 Very High Very High Very High
Glutamate 21 100.00 Very High Very High Very High
monoamine 3 99.98 Very High Very High Very High
cocaine 16 99.84 Very High Very High Very High
Hippocampus 15 99.04 Very High Very High Very High
Ventral tegmentum 4 97.88 Very High Very High Very High
Substantia nigra 5 96.32 Very High Very High Very High
withdrawal 3 94.60 High High
Neurotransmitter 9 88.08 High High
Disease Link Frequency Relevance Heat
Schizophrenia 222 100.00 Very High Very High Very High
Urological Neuroanatomy 6 98.40 Very High Very High Very High
Targeted Disruption 1 91.04 High High
Recurrence 1 89.64 High High
Congenital Anomalies 51 87.24 High High
Convulsion 147 84.24 Quite High
Epilepsy 65 81.72 Quite High
Absence Epilepsy 18 77.48 Quite High
Partial Seizures 70 48.96 Quite Low
Stress 14 45.52 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Monoamine transporter expression was differentially altered by cocaine; dopamine transporter mRNA levels in the ventral tegmental area, but not in the substantia nigra, were increased following withdrawal from cocaine, suggesting a role for the upregulated mesolimbic dopamine transporter in the mechanisms underlying relapse to cocaine taking.
Regulation (altered) of Gene_expression (expression) of transporter in substantia nigra associated with ventral tegmentum, dopamine, substantia nigra, withdrawal, recurrence, cocaine and monoamine
1) Confidence 0.18 Published 2000 Journal Brain Res. Mol. Brain Res. Section Abstract Doc Link 11072100 Disease Relevance 0.09 Pain Relevance 1.25
DAT is dynamically regulated at the plasma membrane by a number of intracellular signals [9,10,46,47], and recent data have also shown that transporter levels can be regulated by DA [48], pseudosubstrate stimulants such as AMPH [48,49], and inhibitors of DAT function such as cocaine [50].
Regulation (regulated) of Gene_expression (levels) of transporter in plasma associated with dopamine and cocaine
2) Confidence 0.04 Published 2007 Journal PLoS Biology Section Body Doc Link PMC2020502 Disease Relevance 0 Pain Relevance 0.19
Ueda et al (2003) showed that zonisamide could also increase extracellular GABA by the up-regulation of a neuronal glutamate transporter (ie, EAAC-1) and a decreased production of the GABA transporter (ie, GAT-1) in the rat hippocampus and frontal cortex.
Regulation (regulation) of Gene_expression (production) of transporter in frontal cortex associated with glutamate, gaba, urological neuroanatomy and hippocampus
3) Confidence 0.02 Published 2006 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2671817 Disease Relevance 0.34 Pain Relevance 0.93
There is a well-known association of enhanced DA D2 function in schizophrenia, and the D1A receptor function may also be abnormal in schizophrenia.165 The level of expression of DA transporter is possibly an illness trait in schizophrenia,166 and mouse models of schizophrenia have reduced expression of DA transporter.167 Increased transcription of TH in the substantia nigra is also found in schizophrenia,168 and transgenic mice used as animal models of schizophrenia have reduced density and numbers of TH neurons in the substantia nigra pars compacta.169
Spec (may) Regulation (abnormal) of Gene_expression (expression) of transporter in neurons associated with targeted disruption, dopamine, substantia nigra and schizophrenia
4) Confidence 0.01 Published 2009 Journal Schizophrenia Bulletin Section Body Doc Link PMC2643957 Disease Relevance 0.92 Pain Relevance 0.46
Ueda et al (2003) showed that zonisamide could also increase extracellular GABA by the up-regulation of a neuronal glutamate transporter (ie, EAAC-1) and a decreased production of the GABA transporter (ie, GAT-1) in the rat hippocampus and frontal cortex.
Regulation (regulation) of in hippocampus Gene_expression (production) of transporter in frontal cortex associated with glutamate, gaba, urological neuroanatomy and hippocampus
5) Confidence 0.01 Published 2006 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2671817 Disease Relevance 0.34 Pain Relevance 0.93

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