Roles of micro-opioid receptors in GABAergic synaptic transmission in the striosome and matrix compartments of the striatum

Mol Neurobiol. Apr-Jun 2008;37(2-3):104-15. doi: 10.1007/s12035-008-8023-2. Epub 2008 May 13.


The striatum is divided into two compartments, the striosomes and extrastriosomal matrix, which differ in several cytochemical markers, input-output connections, and time of neurogenesis. Since it is thought that limbic, reward-related information and executive aspects of behavioral information may be differentially processed in the striosomes and matrix, respectively, intercompartmental communication should be of critical importance to proper functioning of the basal ganglia-thalamocortical circuits. Cholinergic interneurons are in a suitable position for this communication since they are preferentially located in the striosome-matrix boundaries and are known to elicit a conditioned pause response during sensorimotor learning. Recently, micro-opioid receptor (MOR) activation was found to presynaptically suppress the amplitude of GABAergic inhibitory postsynaptic currents in striosomal cells but not in matrix cells. Disinhibition of cells in the striosomes is further enhanced by inactivation of the protein kinase C cascade. We discuss in this review the possibility that MOR activation in the striosomes affects the activity of cholinergic interneurons and thus leads to changes in synaptic efficacy in the striatum.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Corpus Striatum* / anatomy & histology
  • Corpus Striatum* / metabolism
  • Cyclic AMP-Dependent Protein Kinases / metabolism
  • Dopamine / metabolism
  • Excitatory Postsynaptic Potentials / physiology
  • Humans
  • Mental Disorders / metabolism
  • Mental Disorders / pathology
  • Nervous System Diseases / metabolism
  • Nervous System Diseases / pathology
  • Neurons / cytology
  • Neurons / metabolism
  • Presynaptic Terminals / metabolism
  • Protein Kinase C / metabolism
  • Receptors, Opioid, mu / metabolism*
  • Synaptic Transmission / physiology*
  • gamma-Aminobutyric Acid / metabolism*


  • Receptors, Opioid, mu
  • gamma-Aminobutyric Acid
  • Cyclic AMP-Dependent Protein Kinases
  • Protein Kinase C
  • Dopamine