Dopaminergic mechanisms underlying catalepsy, fear and anxiety: Do they interact?

• Published in: Behavioural brain research 2013-11, Vol.257, p.201-207
• Main Authors: Colombo, Ana Caroline, de Oliveira, Amanda Ribeiro, Reimer, Adriano Edgar, Brandão, Marcus Lira
• Format: Article
• Language: English
• Subjects: Analysis of Variance; Animals; Anxiety - etiology; Anxiety - physiopathology; Biological and medical sciences; Catalepsy; Catalepsy - chemically induced; Catalepsy - metabolism; Conditioned fear; Conditioning, Classical - drug effects; Dopamine - metabolism; Dopamine Antagonists - toxicity; Dose-Response Relationship, Drug; Ear and associated structures. Auditory pathways and centers. Hearing. Vocal organ. Phonation. Sound production. Echolocation; Exploratory Behavior - drug effects; Exploratory Behavior - physiology; Fear - drug effects; Fear - psychology; Fundamental and applied biological sciences. Psychology; Haloperidol; Haloperidol - toxicity; Male; Medical sciences; Neuropharmacology; Open-field; Pharmacology. Drug treatments; Psycholeptics: tranquillizer, neuroleptic; Psychology. Psychoanalysis. Psychiatry; Psychopharmacology; Rats; Rats, Wistar; Receptors, Dopamine D2 - metabolism; Time Factors; Ultrasound vocalization; Vertebrates: nervous system and sense organs; Vocalization, Animal - drug effects; Vocalization, Animal - physiology
• ISSN: 0166-4328; 1872-7549
• DOI: 10.1016/j.bbr.2013.10.002

•Haloperidol did not cause 22kHz USVs during catalepsy or open-field test.•Pre-training haloperidol did not change USVs or conditioned freezing response.•Pre-testing haloperidol decreased USVs.•D2 receptors seem to be important for the expression of conditioned fear.•Dopamine mechanisms in catalepsy seem to be dissociated from those related to fear. Haloperidol is a dopamine D2 receptor antagonist that induces catalepsy when systemically administered to rodents. The haloperidol-induced catalepsy is a state of akinesia and rigidity very similar to that seen in Parkinson's disease. There exists great interest in knowing whether or not some degree of emotionality underlies catalepsy. If so, what kind of emotional distress would permeate such motor disturbance? This study is an attempt to shed some light on this issue through an analysis of ultrasound vocalizations (USVs) of 22kHz, open-field test, and contextual conditioned fear in rats with some degree of catalepsy induced by haloperidol. Systemic administration of haloperidol caused catalepsy and decreased exploratory activity in the open-field. There was no difference in the emission of USVs between groups during the catalepsy or the exploratory behavior in the open-field test. In the contextual conditioned fear, when administered before training session, haloperidol did not change the emission of USVs or the freezing response. When administered before testing session, haloperidol enhanced the freezing response and decreased the emission of USVs on the test day. These findings suggest that the involvement of dopaminergic mechanisms in threatening situations depends on the nature of the aversive stimulus. Activation of D2 receptors occurs in the setting up of adaptive responses to conditioned fear stimuli so that these mechanisms seem to be important for the emission of 22kHz USVs during the testing phase of the contextual conditioned fear, but not during the training session or the open-field test (unconditioned fear stimuli). Catalepsy, on the other hand, is the result of the blockage of D2 receptors in neural circuits associated to motor behavior that appears to be dissociated from those directly linked to dopamine-mediated neural mechanisms associated to fear.