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CNS stimulants, such as cocaine, amphetamines, and cannabinoids, have varying structures and mechanisms of action that lead to different therapeutic effects and side effects. Cocaine, with its molecular formula C17H21NO4, is a tropane alkaloid and a tertiary amino compound. It has two chemical forms: the hydrochloride salt and the "freebase." The former is in powder form, while the latter involves removing the hydrochloride salt to create a form that can be smoked. Cocaine exerts its...
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Updated: Dec 12, 2025

Assessment of Cocaine-induced Behavioral Sensitization and Conditioned Place Preference in Mice
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Orbitofrontal-striatal potentiation underlies cocaine-induced hyperactivity.

Sebastiano Bariselli1,2, Nanami L Miyazaki1, Meaghan C Creed3,4

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Cocaine boosts activity in both direct and indirect striatal pathways, contrary to prior models. This hyperactivity stems from strengthened orbitofrontal cortex inputs to the dorsomedial striatum, directly impacting locomotion.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Behavioral Science

Background:

  • Psychomotor stimulants like cocaine elevate dopamine levels, influencing locomotion.
  • The precise in vivo effects of stimulants on striatal pathway function remain incompletely understood.
  • Existing models propose differential pathway activation/inhibition, but lack direct in vivo electrophysiological validation.

Purpose of the Study:

  • To investigate the in vivo effects of psychomotor stimulants on direct and indirect striatal pathways.
  • To test the hypothesis that stimulant-induced hyperactivity is mediated by specific striatal pathway modulation.
  • To elucidate the role of orbitofrontal cortex (OFC) inputs in stimulant-induced behavioral changes.

Main Methods:

  • In vivo electrophysiological recordings in awake mice.
  • Administration of cocaine to assess effects on striatal neuron activity.
  • Optogenetic or chemogenetic manipulation of neural pathways (implied by background).
  • High-frequency stimulation protocols to modulate pathway activity.

Main Results:

  • Cocaine increased the activity of both direct and indirect striatal pathways in awake mice.
  • These effects were linked to dopamine-dependent potentiation of OFC-DMS inputs.
  • Inhibition of the OFC-DMS pathway attenuated cocaine-induced locomotor sensitization.

Conclusions:

  • The study challenges existing models by demonstrating cocaine activates both striatal pathways.
  • Strengthened OFC-DMS connectivity is a key mechanism underlying stimulant-induced hyperactivity.
  • Modulating OFC-DMS pathway function offers a potential target for understanding and treating stimulant-induced behaviors.