Neuronal Glucose Transporter Isoform 3 Deficient Mice Demonstrate Features of Autism Spectrum Disorders View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2009-06-09

AUTHORS

Yuanzi Zhao, Camille Fung, Don Shin, Bo-Chul Shin, Shanthie Thamotharan, Raman Sankar, Dan Ehninger, Alcino Silva, Sherin U. Devaskar

ABSTRACT

Neuronal glucose transporter (GLUT) isoform 3 deficiency in null heterozygous mice led to abnormal spatial learning and working memory but normal acquisition and retrieval during contextual conditioning, abnormal cognitive flexibility with intact gross motor ability, electroencephalographic seizures, perturbed social behavior with reduced vocalization and stereotypies at low frequency. This phenotypic expression is unique as it combines the neurobehavioral with the epileptiform characteristics of autism spectrum disorders. This clinical presentation occurred despite metabolic adaptations consisting of an increase in microvascular/glial GLUT1, neuronal GLUT8 and monocarboxylate transporter isoform 2 concentrations, with minimal to no change in brain glucose uptake but an increase in lactate uptake. Neuron-specific glucose deficiency has a negative impact on neurodevelopment interfering with functional competence. This is the first description of GLUT3 deficiency that forms a possible novel genetic mechanism for pervasive developmental disorders, such as the neuropsychiatric autism spectrum disorders, requiring further investigation in humans. More... »

PAGES

286-299

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/mp.2009.51

DOI

http://dx.doi.org/10.1038/mp.2009.51

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1025154005

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/19506559


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37 schema:description Neuronal glucose transporter (GLUT) isoform 3 deficiency in null heterozygous mice led to abnormal spatial learning and working memory but normal acquisition and retrieval during contextual conditioning, abnormal cognitive flexibility with intact gross motor ability, electroencephalographic seizures, perturbed social behavior with reduced vocalization and stereotypies at low frequency. This phenotypic expression is unique as it combines the neurobehavioral with the epileptiform characteristics of autism spectrum disorders. This clinical presentation occurred despite metabolic adaptations consisting of an increase in microvascular/glial GLUT1, neuronal GLUT8 and monocarboxylate transporter isoform 2 concentrations, with minimal to no change in brain glucose uptake but an increase in lactate uptake. Neuron-specific glucose deficiency has a negative impact on neurodevelopment interfering with functional competence. This is the first description of GLUT3 deficiency that forms a possible novel genetic mechanism for pervasive developmental disorders, such as the neuropsychiatric autism spectrum disorders, requiring further investigation in humans.
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44 schema:keywords Deficient Mice Demonstrate Features
45 GLUT1
46 GLUT3 deficiency
47 GLUT8
48 Glucose Transporter Isoform 3 Deficient Mice Demonstrate Features
49 Isoform 3 Deficient Mice Demonstrate Features
50 Mice Demonstrate Features
51 Neuron-specific glucose deficiency
52 Neuronal Glucose Transporter Isoform 3 Deficient Mice Demonstrate Features
53 Neuronal glucose transporter (GLUT) isoform 3 deficiency
54 Transporter Isoform 3 Deficient Mice Demonstrate Features
55 ability
56 abnormal cognitive flexibility
57 abnormal spatial learning
58 acquisition
59 adaptation
60 autism spectrum disorder
61 behavior
62 brain glucose uptake
63 changes
64 characteristics
65 clinical presentation
66 cognitive flexibility
67 competence
68 concentration
69 conditioning
70 contextual conditioning
71 deficiency
72 demonstrate features
73 description
74 developmental disorders
75 disorders
76 electroencephalographic seizures
77 epileptiform characteristics
78 expression
79 features
80 first description
81 flexibility
82 frequency
83 functional competence
84 further investigation
85 genetic mechanisms
86 glial GLUT1
87 glucose deficiency
88 glucose transporter (GLUT) isoform 3 deficiency
89 glucose uptake
90 gross motor abilities
91 heterozygous mice
92 humans
93 impact
94 increase
95 intact gross motor ability
96 investigation
97 isoform 2 concentrations
98 isoform 3 deficiency
99 lactate uptake
100 learning
101 low frequency
102 mechanism
103 memory
104 metabolic adaptation
105 mice
106 microvascular/glial GLUT1
107 monocarboxylate transporter isoform 2 concentrations
108 motor abilities
109 negative impact
110 neurodevelopment
111 neuronal GLUT8
112 neuropsychiatric autism spectrum disorders
113 normal acquisition
114 novel genetic mechanism
115 null heterozygous mice
116 pervasive developmental disorder
117 phenotypic expression
118 possible novel genetic mechanism
119 presentation
120 reduced vocalizations
121 retrieval
122 seizures
123 social behavior
124 spatial learning
125 spectrum disorder
126 stereotypy
127 transporter (GLUT) isoform 3 deficiency
128 transporter isoform 2 concentrations
129 uptake
130 vocalizations
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