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Does learned helplessness induction by haloperidol involve serotonin mediation?

F Petty1, G Kramer, M Moeller

  • 1Veterans Affairs Medical Center, Dallas 75216.

Pharmacology, Biochemistry, and Behavior
|July 1, 1994
PubMed
Summary
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Learned helplessness (LH) is a behavioral depression linked to inescapable stress. Dopamine D2 receptor blockade with haloperidol in rats increased serotonin release in the medial prefrontal cortex, contributing to LH.

Area of Science:

  • Neuroscience
  • Behavioral Science
  • Psychopharmacology

Background:

  • Learned helplessness (LH) is a behavioral state of depression following inescapable stress.
  • The neurochemical underpinnings of LH, particularly the roles of dopamine and serotonin, are not fully elucidated.

Purpose of the Study:

  • To investigate the role of dopamine (DA) and serotonin (5-HT) in the medial prefrontal cortex (MPC) in the development of learned helplessness.
  • To determine if haloperidol-induced LH in rats is associated with altered neurotransmitter release in the MPC.

Main Methods:

  • Learned helplessness was induced in rats using the dopamine D2 receptor antagonist haloperidol (HDL).
  • In vivo microdialysis was employed to measure neurotransmitter release (dopamine and serotonin) in the medial prefrontal cortex (MPC).

Related Experiment Videos

  • The effects of direct HDL perfusion and dopamine/apomorphine perfusion in the MPC on 5-HT release were assessed.

    • Main Results:

    • Haloperidol administration induced helpless behavior in a dose-dependent manner.
    • Haloperidol increased serotonin (5-HT) release in the medial prefrontal cortex (MPC).
    • Direct perfusion of haloperidol, dopamine, or apomorphine into the MPC increased cortical 5-HT release, suggesting a role for dopamine in modulating serotonin.

    Conclusions:

    • Increased dopamine (DA) release in the MPC, observed with both inescapable stress and haloperidol, is a necessary but not sufficient factor in learned helplessness development.
    • Elevated DA activity in the MPC appears to drive increased 5-HT release, leading to behavioral depression characteristic of learned helplessness.