Does gene deletion of AMPA GluA1 phenocopy features of schizoaffective disorder?

Glutamatergic dysfunction is strongly implicated in schizophrenia and mood disorders. GluA1 knockout (KO) mice display schizophrenia- and depression-related abnormalities. Here, we asked whether GluA1 KO show mania-related abnormalities.

Evidence that altered amygdala activity in schizophrenia is related to clinical state and not genetic risk.

Objective: Although amygdala dysfunction is reported in schizophrenia, it is unknown whether this deficit represents a heritable phenotype that is related to risk for schizophrenia or whether it is related to disease state. The purpose of the present study was to examine amygdala response to threatening faces among healthy siblings of schizophrenia patients in whom a subtler heritable deficit might be observed.

Method: Participants were 34 schizophrenia patients, 29 unaffected siblings, and 20 healthy comparison subjects.

A validated network of effective amygdala connectivity.

Regulatory interactions with the amygdala are thought to be critical for emotional processing in the extended limbic system. Structural equation modeling (path analysis) is a widely used method to quantify interactions among brain regions based on connectivity models, but is often limited by lack of precise anatomical and functional constraints. To address this issue, we developed an automated elaborative path analysis procedure guided by known anatomical connectivity in the macaque.

Environmental and immune stressors enhance alcohol-induced motor ataxia in rat.

Infection is now accepted as a stressor, consequently we sought to compare the short- and longer-term consequences of several environmental stressors versus an endotoxin challenge on alcohol-induced motor ataxia. The present set of studies examined the impact of intermittent electric shock (SHOCK), intermittent cold water swim (ICWS), or lipopolysaccharide (LPS) administration on the motor ataxic effects of an intraperitoneal (i.p.

Effects of mild early life stress on abnormal emotion-related behaviors in 5-HTT knockout mice.

A low-expressing polymorphic variant of the serotonin transporter (5-HTT) gene has been associated with emotional disorders in humans and non-human primates following exposure to early life trauma. 5-HTT gene knockout (KO) mice exhibit increased anxiety- and depression-related behaviors, and provide a model to study interactions between 5-HTT gene variation and early life stress. The present study assessed the effects of postnatal footshock stress on the development of emotion-related behaviors in 5-HTT KO mice.

Ethanol-related behaviors in serotonin transporter knockout mice.

Background: Increasing evidence supports a role for 5-hydroxytryptamine (5-HT) and the 5-HT transporter (5-HTT) in modulating the neural and behavioral actions of ethanol (EtOH) and other drugs of abuse.

Methods: We used a 5-HTT knockout (KO) mouse model to further study this relationship. 5-Hydroxytryptamine transporter KO mice were tested for the sedative/hypnotic, hypothermia-inducing, motor-incoordinating (via accelerating rotarod), and depression-related (via tail suspension test) effects of acute EtOH administration.

The acute intoxicating effects of ethanol are not dependent on the vasopressin 1a or 1b receptors.

Studies of the role of vasopressin (Avp) in mediating the effects of ethanol have focused on Avp's role in altering kidney function via its action through the vasopressin 2 receptor. However, alcohol consumption also has central effects that are poorly understood. There is evidence that Avp may mediate ethanol consumption as well as some of ethanol's behavioral effects.

Ethanol inhibits clearance of brain serotonin by a serotonin transporter-independent mechanism.

Brain serotonin (5-HT) modulates the neural and behavioral effects of ethanol in a manner that remains poorly understood. Here we show that treatment with physiologically relevant (i.e.