title: Basolateral amygdala modulates terminal dopamine release in the nucleus accumbens and conditioned responding.
abstract: BACKGROUND
  Dopamine signaling in the nucleus accumbens (NAc) is essential for goal-directed behaviors and primarily arises from burst firing of ventral tegmental area neurons. However, the role of associative neural substrates such as the basolateral amygdala (BLA) in regulating phasic dopamine release in the NAc, particularly during reward seeking, remains unknown.
  
  
  METHODS
  Male Sprague-Dawley rats learned to discriminate two cues: a discriminative stimulus (DS) that predicted sucrose reinforcement contingent upon a lever press and a nonassociated stimulus (NS) that predicted a second lever never reinforced with sucrose. Following training, a test session was completed in which NAc dopamine was measured using fast-scan cyclic voltammetry in conjunction with inactivation of the ipsilateral BLA (gamma-aminobutyric acid agonists; baclofen/muscimol) to determine the contribution of BLA activity to dopamine release in the NAc core during the task.
  
  
  RESULTS
  Under vehicle conditions, DS and NS presentation elicited dopamine release within the NAc core. The DS evoked significantly more dopamine than the NS. Inactivation of the BLA selectively attenuated the magnitude of DS-evoked dopamine release, concurrent with an attenuation of DS-evoked conditioned approaches. Other behavioral responses (e.g., lever pressing) and dopamine release concomitant with those events were unaltered by BLA inactivation. Furthermore, neither ventral tegmental area electrically stimulated dopamine release nor the probability of high concentration dopamine release events was altered following BLA inactivation.
  
  
  CONCLUSIONS
  These results demonstrate that the BLA terminally modulates dopamine signals within the NAc core under specific, behaviorally relevant conditions, illustrating a functional mechanism by which the BLA selectively facilitates responding to motivationally salient environmental stimuli.
authors.affiliation: Department of Psychology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA.
authors.forename: Joshua L
authors.initials: JL
authors.lastname: Jones
authors.forename: Jeremy J
authors.initials: JJ
authors.lastname: Day
authors.forename: Brandon J
authors.initials: BJ
authors.lastname: Aragona
authors.forename: Robert A
authors.initials: RA
authors.lastname: Wheeler
authors.forename: R Mark
authors.initials: RM
authors.lastname: Wightman
authors.forename: Regina M
authors.initials: RM
authors.lastname: Carelli
mesh_terms: D000679:Amygdala / Q000502:physiology*; D000818:Animals; D001418:Baclofen / Q000494:pharmacology; D003216:Conditioning, Operant / Q000502:physiology*; D003627:Data Interpretation, Statistical; D004298:Dopamine / Q000378:metabolism* / Q000502:physiology; D004563:Electrochemistry; D018755:GABA Agonists / Q000494:pharmacology; D008297:Male; D008845:Microinjections; D009118:Muscimol / Q000494:pharmacology; D009714:Nucleus Accumbens / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects; D017557:Ventral Tegmental Area / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
chemical_list: D018755:GABA Agonists; D009118:Muscimol; D005680:gamma-Aminobutyric Acid; D001418:Baclofen; D004298:Dopamine