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. Author manuscript; available in PMC: 2017 May 3.
Published in final edited form as: Neuroscience. 2015 Aug 24;321:163–188. doi: 10.1016/j.neuroscience.2015.08.041

Table 2.

Pharmacological and environmental mouse models of bipolar mania

Validity
Manipulation Face Predictive Construct
Amphetamine-induced hyperactivity Hyperactivity, cognitive deficits with chronic treatment Activity reversed by acute lithium and haloperidol Hyperdopaminergia
Amphetamine + CDP Hyperactivity Activity reversed with acute lithium Hyperdopaminergia, anxiolytic effects of CDP
Ouabain Hyperactivity, spatial learning deficits Activity reversed by haloperidol, lithium and valproate. Some neurodegenerative markers were reversed by lithium and valproate Increased levels of oxidative stress, changes in BDNF levels
D2 receptor stimulation Hyperactivity Activity reversed by valproate and carbamazepine Increased dopaminergic signaling
Sleep deprivation Hyperactivity, insomnia, aggressive behavior, hypersexuality, increased stereotypy, cognitive deficits, circadian rhythm disruption Sleep latency and hyperactivity reversed by lithium and haloperidol. PKC changes reversed by lithium Acute circadian rhythm and sleep changes can precipitate mania in humans. PKC signaling is altered.
Resident-intruder paradigm Increased aggression Aggression reduced by lithium and valproate Stress is associated with changes in mood state