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Depersonalization disorder may be related to glutamate receptor activation imbalance.

Pikwer, Andreas LU (2011) In Medical Hypotheses 77. p.593-594
Abstract
Low-dose ketamine administration mimics, both clinically and on gross neuroimaging, depersonalization disorder. The perceptual effects of ketamine may be due to secondary stimulation of glutamate release and lamotrigine, possibly by inhibited glutamate release, may reduce some of ketamine's so-called dissociative effects. However, lamotrigine does not seem to be useful in the treatment of depersonalization disorder. Glutamate release in prefrontal cortex is increased by subanaesthetic doses of ketamine, resulting in increased inhibition, possibly via intercalated GABAerg cells, of projections from amygdala, affecting structures critically involved in depersonalization. I speculate that, in depersonalization disorder, the increased... (More)
Low-dose ketamine administration mimics, both clinically and on gross neuroimaging, depersonalization disorder. The perceptual effects of ketamine may be due to secondary stimulation of glutamate release and lamotrigine, possibly by inhibited glutamate release, may reduce some of ketamine's so-called dissociative effects. However, lamotrigine does not seem to be useful in the treatment of depersonalization disorder. Glutamate release in prefrontal cortex is increased by subanaesthetic doses of ketamine, resulting in increased inhibition, possibly via intercalated GABAerg cells, of projections from amygdala, affecting structures critically involved in depersonalization. I speculate that, in depersonalization disorder, the increased glutamate activity in prefrontal cortex is due to intrinsic imbalance, resulting in long-term potentiation, at the postsynaptic glutamate receptors on the GABAerg interneurons while the same receptor abnormality at the synapses on the intercalated GABAerg cells of the amygdala result in long-term depression in the case of either normal or high glutamate release. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Medical Hypotheses
volume
77
pages
593 - 594
publisher
Churchill Livingstone
external identifiers
  • wos:000295440300027
  • pmid:21742442
  • scopus:80052626088
ISSN
1532-2777
DOI
10.1016/j.mehy.2011.06.041
language
English
LU publication?
yes
id
d8116bd2-d14a-4248-a55e-5d1cbcae71e4 (old id 2058778)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/21742442?dopt=Abstract
date added to LUP
2011-08-01 19:33:52
date last changed
2017-01-01 07:54:05
@article{d8116bd2-d14a-4248-a55e-5d1cbcae71e4,
  abstract     = {Low-dose ketamine administration mimics, both clinically and on gross neuroimaging, depersonalization disorder. The perceptual effects of ketamine may be due to secondary stimulation of glutamate release and lamotrigine, possibly by inhibited glutamate release, may reduce some of ketamine's so-called dissociative effects. However, lamotrigine does not seem to be useful in the treatment of depersonalization disorder. Glutamate release in prefrontal cortex is increased by subanaesthetic doses of ketamine, resulting in increased inhibition, possibly via intercalated GABAerg cells, of projections from amygdala, affecting structures critically involved in depersonalization. I speculate that, in depersonalization disorder, the increased glutamate activity in prefrontal cortex is due to intrinsic imbalance, resulting in long-term potentiation, at the postsynaptic glutamate receptors on the GABAerg interneurons while the same receptor abnormality at the synapses on the intercalated GABAerg cells of the amygdala result in long-term depression in the case of either normal or high glutamate release.},
  author       = {Pikwer, Andreas},
  issn         = {1532-2777},
  language     = {eng},
  pages        = {593--594},
  publisher    = {Churchill Livingstone},
  series       = {Medical Hypotheses},
  title        = {Depersonalization disorder may be related to glutamate receptor activation imbalance.},
  url          = {http://dx.doi.org/10.1016/j.mehy.2011.06.041},
  volume       = {77},
  year         = {2011},
}