Why Us? >>

  • - Open Access
  • - Peer-reviewed
  • - Rapid publication
  • - Lifetime hosting
  • - Free indexing service
  • - Free promotion service
  • - More citations
  • - Search engine friendly

Free SCIRP Newsletters>>

Add your e-mail address to receive free newsletters from SCIRP.

 

Contact Us >>

WhatsApp  +86 18163351462(WhatsApp)
   
Paper Publishing WeChat
Book Publishing WeChat
(or Email:book@scirp.org)

Article citations

More>>

Marquette, P., Vendier, D., Kodala, A., et al. (2015) An Astrocyte-Dependent Mechanism of Neuronal Rhythmogenesis. Nature Neuroscience, 18, 844-854.
https://doi.org/10.1038/nn.4013

has been cited by the following article:

  • TITLE: Psychobiological Model of Bipolar Disorder: Based on Imbalances of Glial-Neuronal Information Processing

    AUTHORS: Bernhard J. Mitterauer

    KEYWORDS: Bipolar Disorder, Glial-Neuronal Interactions, Synaptic Imbalances, Hyperintentionality

    JOURNAL NAME: Open Journal of Medical Psychology, Vol.7 No.4, September 29, 2018

    ABSTRACT: A psychobiological model of the etiopathology of bipolar disorder is proposed. Based on genetic-epigenetic and chronobiological factors a hyperintentional personality structure, if faced with non-feasible intentional programs in the environment, suffers from inner and outer stress. This stress situation leads to imbalances in information processing in glial-neuronal synaptic units, called tripartite synapses. In depression the overexpression of astrocytic receptors and of gap junctions in the astroglial network causes a prolonged information processing which affects the behavior generating systems in the brainstem reticular formation. Because the activation of the behavior generating systems is protracted, they are unable to select an appropriate mode of behavior (e.g. communicating, eating, working, sleeping, etc.) from sensory information in real time. Inversely, in mania astrocytic receptors and gap junctions are underexpressed causing a shortened synaptic information processing with rapid changes in behavior. Switching may represent a coping-attempt with depression by mania and vice versa. Towards a comprehensive model of the pathophysiology of bipolar disorder the role of microglia and their devastating effects on glial-neuronal interactions are outlined. Finally, the testing of the model is discussed.