title: Evaluation of expression and function of the H+/myo-inositol transporter HMIT.
abstract: BACKGROUND
  The phosphoinositide (PIns) signalling pathway regulates a series of neuronal processes, such as neurotransmitter release, that are thought to be altered in mood disorders. Furthermore, mood-stabilising drugs have been shown to inhibit key enzymes that regulate PIns production and alter neuronal growth cone morphology in an inositol-reversible manner. Here, we describe analyses of expression and function of the recently identified H+/myo-inositol transporter (HMIT) investigated as a potential regulator of PIns signalling.
  
  
  RESULTS
  We show that HMIT is primarily a neuronal transporter widely expressed in the rat and human brain, with particularly high levels in the hippocampus and cortex, as shown by immunohistochemistry. The transporter is localised at the Golgi apparatus in primary cultured neurones. No HMIT-mediated electrophysiological responses were detected in rat brain neurones or slices; in addition, inositol transport and homeostasis were unaffected in HMIT targeted null-mutant mice.
  
  
  CONCLUSIONS
  Together, these data do not support a role for HMIT as a neuronal plasma membrane inositol transporter, as previously proposed. However, we observed that HMIT can transport inositol triphosphate, indicating unanticipated intracellular functions for this transporter that may be relevant to mood control.
authors.affiliation: Psychiatry Discovery Technology Group, GlaxoSmithKline, New Frontiers Science Park, Harlow, UK. Elena.2.DiDaniel@gsk.com
authors.forename: Elena
authors.initials: E
authors.lastname: Di Daniel
authors.forename: Man H S
authors.initials: MH
authors.lastname: Mok
authors.forename: Emma
authors.initials: E
authors.lastname: Mead
authors.forename: Chiara
authors.initials: C
authors.lastname: Mutinelli
authors.forename: Erika
authors.initials: E
authors.lastname: Zambello
authors.forename: Laura L
authors.initials: LL
authors.lastname: Caberlotto
authors.forename: Theresa J
authors.initials: TJ
authors.lastname: Pell
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Langmead
authors.forename: Ajit J
authors.initials: AJ
authors.lastname: Shah
authors.forename: Graham
authors.initials: G
authors.lastname: Duddy
authors.forename: James N C
authors.initials: JN
authors.lastname: Kew
authors.forename: Peter R
authors.initials: PR
authors.lastname: Maycox
mesh_terms: D000818:Animals; D001921:Brain / Q000166:cytology*; D002460:Cell Line; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000166:cytology; D017353:Gene Deletion; D051246:Glucose Transport Proteins, Facilitative / Q000032:analysis* / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D007294:Inositol / Q000378:metabolism*; D051379:Mice; D018345:Mice, Knockout; D009154:Mutation; D009474:Neurons / Q000166:cytology* / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D051246:Glucose Transport Proteins, Facilitative; C437315:SLC2A13 protein, human; C544447:SLC2A13 protein, mouse; C486673:Slc2a13 protein, rat; D007294:Inositol