Dysbindin-1 Mutation Alters Prefrontal Cortex Extracellular Glutamate and Dopamine In Vivo.

Elevated risk for schizophrenia is associated with a variation in the gene encoding dysbindin-1, which may underpin cognitive impairments in this prevalent neuropsychiatric disorder. The cognitive symptoms of schizophrenia involve anomalies in glutamate and dopamine signaling, particularly within the prefrontal cortex (PFC). Indeed, mice with mutations exhibit spatial and working memory deficits that are associated with deficits in glutamate release and NMDA receptor function as determined by slice electrophysiology.

Investigation into the biomolecular bases of blunted cocaine-induced glutamate release within the nucleus accumbens elicited by adolescent exposure to phenylpropanolamine.

Globally, phenylpropanolamine (PPA) is a prevalent primary active ingredient in over-the-counter cough and cold, as well as weight-loss medications. Previously, we showed that a sensitization of cocaine-induced glutamate release within the nucleus accumbens (NAC) and the expression of cocaine-conditioned reward is not apparent in adult mice with a prior history of repeated PPA exposure during adolescence. As NAC glutamate is a purported driver of cocaine reward and reinforcement, the present study employed in vivo microdialysis and immunoblotting approaches to inform as to the receptor and transporter anomalies that might underpin the disrupted glutamate response to cocaine in adolescent PPA-exposed mice.

Enduring dysregulation of nucleus accumbens catecholamine and glutamate transmission by developmental exposure to phenylpropanolamine.

For over 50 years, the sympathomimetic phenylpropanolamine (PPA; ±-norephedrine) was a primary active ingredient in over-the-counter nasal decongestants for both children and adults and continues to be prevalent in the vast majority of countries today. Previously, we reported that juvenile PPA exposure alters the developmental trajectory of catecholamine and amino acid neurotransmitter systems in the nucleus accumbens (NAC), impacting the motivational valence of cocaine in later life. The present study employed a combination of in vivo microdialysis and immunoblotting approaches to better understand how juvenile PPA exposure impacts catecholamine and glutamate function within the NAC.

Behavioral and Neurochemical Phenotyping of Mice Incapable of Homer1a Induction.

Immediate early and constitutively expressed products of the gene regulate the functional assembly of post-synaptic density proteins at glutamatergic synapses to influence excitatory neurotransmission and synaptic plasticity. Earlier studies of gene knock-out (KO) mice indicated active, but distinct, roles for IEG and constitutively expressed gene products in regulating cognitive, emotional, motivational and sensorimotor processing, as well as behavioral and neurochemical sensitivity to cocaine. More recent characterization of transgenic mice engineered to prevent generation of the IEG form (a.

Methamphetamine Addiction Vulnerability: The Glutamate, the Bad, and the Ugly.

Background: The high prevalence and severity of methamphetamine (MA) abuse demands greater neurobiological understanding of its etiology.

Methods: We conducted immunoblotting and in vivo microdialysis procedures in MA high/low drinking mice, as well as in isogenic C57BL/6J mice that varied in their MA preference/taking, to examine the glutamate underpinnings of MA abuse vulnerability. Neuropharmacological and Homer2 knockdown approaches were also used in C57BL/6J mice to confirm the role for nucleus accumbens (NAC) glutamate/Homer2 expression in MA preference/aversion.