Behavioural Brain Research
March 30, 2017
Andrea Gogos, Snezana Kusljic, Shane J Thwaites et al.
Acute amphetamine caused greater distance traveled (locomotor hyperactivity) in female rats than in male rats, while phencyclidine-induced locomotor hyperactivity was similar in both sexes. No sex differences were observed in amphetamine- or phencyclidine-induced disruption of prepulse inhibition. Male rats showed an increased startle response after amphetamine. These findings suggest that sensitivity to amphetamine, but not phencyclidine, differs between male and female rats, and this sex difference is selective to locomotor hyperactivity and startle, not prepulse inhibition.
Behavioural Brain Research
January 1, 2016
Evan J. Kyzar, Adam Michael Stewart, Allan V. Kalueff
The serotonin transporter (SERT) regulates serotonin signaling and is linked to psychiatric disorders like anxiety, autism spectrum disorders (ASD), and obsessive-compulsive disorder (OCD). In mice, removing the Sert gene increases anxiety and grooming behavior. This study examined the effects of the hallucinogen LSD (0.32 mg/kg) on grooming and other behaviors in mice with one copy of the Sert gene (Sert+/-). These mice showed longer self-grooming regardless of LSD treatment. LSD increased serotonin-sensitive behaviors like head twitching and tremors in both normal and Sert+/- mice, with no significant interaction between LSD and Sert gene dosage. The results suggest Sert+/- mice respond to LSD similarly to normal mice.
Behavioural Brain Research
September 15, 2015
Natashia Swalve, Scott T Barrett, Rick A Bevins et al.
Nicotine and phencyclidine (PCP) each separately increased rats' lever-pressing for a brief visual stimulus, indicating a reinforcement-enhancement effect. The effect was dose-dependent for nicotine (0.2 or 0.4 mg/kg) and present with PCP (2.0 mg/kg) across increasing fixed-ratio schedules. Adding PCP to nicotine did not further increase lever-pressing, possibly due to a ceiling effect. PCP's effect appeared driven largely by locomotor stimulation, whereas nicotine's effect was independent of locomotor activity. This dissociation suggests that different pharmacological properties underlie the reinforcement-enhancement effects of these substances.
Behavioural Brain Research
January 15, 2012
Luigi De Gennaro, Cristina Marzano, Carlo Cipolli et al.
Recent findings confirm that the neurophysiological mechanisms for encoding and recalling episodic memories are largely comparable across wakefulness and sleep. Brain lesion and neuroimaging studies indicate that the temporo-parieto-occipital junction and ventromesial prefrontal cortex play a crucial role in dream recall. Morphoanatomical measurements reveal direct relations between volumetric and ultrastructural measures of the hippocampus-amygdala and specific qualitative features of dreaming. Intracranial recordings in epileptic patients support the notion that hippocampal nuclei mediate memory formation during sleep as in wakefulness. Surface EEG studies show that sleep cortical oscillations associated with successful dream recall are the same as those involved in encoding and recall of episodic memories during wakefulness. These converging pieces of evidence strengthen the view that episodic/declarative memory mechanisms may be the same across different states of consciousness.
Behavioural Brain Research
January 20, 2010
Luigi De Gennaro, Cristina Marzano, Fabio Moroni et al.
After 40 hours of prolonged wakefulness, a recovery night of sleep almost completely abolished dream recall, reducing it by about 75% compared to adaptation and baseline nights. The number of dreams recalled by those who did remember dreams did not differ significantly between nights, and gender or sleep stage at awakening did not affect recall. The drastic impairment of dream recall was associated with a larger increase in slow-wave sleep and shorter REM sleep duration. The authors suggest dream recall may be impaired due to fewer spontaneous awakenings, less dreamlike mental experiences during SWS, and poorer consolidation of dream content as episodic memory during recovery sleep.
Behavioural Brain Research
August 22, 2008
Sally Martin, Maarten Van den Buuse
Depleting serotonin in the forebrain of mice, specifically by destroying serotonin neurons projecting from the median raphe nucleus, made the animals hyperactive at baseline and increased their hyperactivity response to phencyclidine, a drug that can induce psychosis-like behaviors. The same lesion did not affect hyperactivity caused by amphetamine or a measure of sensorimotor gating called prepulse inhibition. Serotonin levels dropped by 68% in the hippocampus and 31% in the striatum. These results, consistent with earlier rat studies, suggest that serotonin release in the dorsal hippocampus normally dampens excessive behavioral stimulation. Disruption of this pathway may contribute to psychosis, and enhancing it could be a mechanism for antipsychotic drugs.
Behavioural Brain Research
January 6, 2006
Rainer Wolf, Henrik Dobrowolny, Kay Matzke et al.
Mice with lower NMDA receptor density in the hippocampus (CPB-K strain) show weaker sensorimotor gating—measured by prepulse inhibition (PPI)—compared to mice with higher receptor density (BALB/cJ strain). CPB-K mice also had a significantly higher acoustic startle response. PPI was reliably measured across repeated sessions over 13 weeks. The authors propose that the CPB-K mouse strain may serve as an animal model for schizophrenia, consistent with the hypo-glutamatergic hypothesis of the disorder, but further behavioral experiments are needed to establish this.
Behavioural Brain Research
August 31, 2004
John Mastropaolo, Richard B Rosse, Stephen I Deutsch
A reduced level of the alpha7-nicotinic acetylcholine receptor in certain brain areas may contribute to sensory and movement deficits in schizophrenia and might be a necessary condition for the disorder. This has led to interest in drugs that activate this receptor. In a mouse model, the drug anabasine, a selective alpha7-nicotinic receptor agonist, reduced popping behavior caused by MK-801 (a drug that mimics schizophrenia-like symptoms) at a dose that did not cause seizures. The findings suggest potential therapeutic benefit for schizophrenia, but also highlight the need to consider seizure risk.
Behavioural Brain Research
January 1, 1996
R E Steinpreis
Phencyclidine (PCP) produces a psychotic reaction in humans that closely resembles an acute episode of schizophrenia, making it a valuable model for the disorder. This review examines the behavioral and neurochemical effects of PCP in both humans and animals, comparing them with those of amphetamine where possible. It discusses the roles of dopamine and NMDA/PCP receptors in mediating PCP-induced psychosis and emphasizes the importance of selecting behavioral models that capture the expression of psychosis rather than just the motor effects of psychotomimetic drugs.