Get access

Lesion of medial prefrontal dopamine terminals abolishes habituation of accumbens shell dopamine responsiveness to taste stimuli

Authors

  • Zisis Bimpisidis,

    1. Department of Biomedical Sciences, University of Cagliari, Cagliari, Italy
    Search for more papers by this author
  • Maria Antonietta De Luca,

    Corresponding author
    1. INN, National Institute of Neuroscience, Italy
    • Department of Biomedical Sciences, University of Cagliari, Cagliari, Italy
    Search for more papers by this author
  • Augusta Pisanu,

    1. National Council of Italy (CNR), Institute of Neuroscience, Cagliari Section, Italy
    Search for more papers by this author
  • Gaetano Di Chiara

    1. Department of Biomedical Sciences, University of Cagliari, Cagliari, Italy
    2. INN, National Institute of Neuroscience, Italy
    3. Centre of Excellence “Neurobiology of Addiction”, Cagliari, Italy
    4. National Council of Italy (CNR), Institute of Neuroscience, Cagliari Section, Italy
    Search for more papers by this author

Correspondence: Dr M. A. De Luca, as above.

E-mail: deluca@unica.it

Abstract

Taste stimuli increase extracellular dopamine (DA) in the nucleus accumbens (NAc) and in the medial prefrontal cortex (mPFC). This effect shows single-trial habituation in NAc shell but not in core or in mPFC. Morphine sensitization abolishes habituation of DA responsiveness in NAc shell but induces it in mPFC. These observations support the hypothesis of an inhibitory influence of mPFC DA on NAc DA. To test this hypothesis, we used in vivo microdialysis to investigate the effect of mPFC 6-hydroxy-dopamine (6-OHDA) lesions on the NAc DA responsiveness to taste stimuli. 6-OHDA was infused bilaterally in the mPFC of rats implanted with guide cannulae. After 1 week, rats were implanted with an intraoral catheter, microdialysis probes were inserted into the guide cannulae, and dialysate DA was monitored in NAc shell/core after intraoral chocolate. 6-OHDA infusion reduced tissue DA in the mPFC by 75%. Tyrosine hydroxylase immunohistochemistry showed that lesions were confined to the mPFC. mPFC 6-OHDA lesion did not affect the NAc shell DA responsiveness to chocolate in naive rats but abolished habituation in rats pre-exposed to the taste. In the NAc core, mPFC lesion potentiated, delayed and prolonged the stimulatory DA response to taste but failed to affect DA in pre-exposed rats. Behavioural taste reactions and motor activity were not affected. The results indicate a top-down control of NAc DA by mPFC and a reciprocal relationship between DA transmission in these two areas. Moreover, habituation of DA responsiveness in the NAc shell is dependent upon an intact DA input to the mPFC.

Ancillary