Chronic lithium treatment rectifies maladaptive dopamine release in the nucleus accumbens.

Chronic lithium treatment effectively reduces behavioral phenotypes of mania in humans and rodents. The mechanisms by which lithium exerts these actions are poorly understood. Pre-clinical and clinical evidence have implicated increased mesolimbic dopamine (DA) neurotransmission with mania.

Effects of Ketamine and Ketamine Metabolites on Evoked Striatal Dopamine Release, Dopamine Receptors, and Monoamine Transporters.

Following administration at subanesthetic doses, (R,S)-ketamine (ketamine) induces rapid and robust relief from symptoms of depression in treatment-refractory depressed patients. Previous studies suggest that ketamine's antidepressant properties involve enhancement of dopamine (DA) neurotransmission. Ketamine is rapidly metabolized to (2S,6S)- and (2R,6R)-hydroxynorketamine (HNK), which have antidepressant actions independent of N-methyl-d-aspartate glutamate receptor inhibition.

Olanzapine Treatment of Adolescent Rats Alters Adult D2 Modulation of Cortical Inputs to the Ventral Striatum.

Background: The striatal dopamine system undergoes vast ontogenetic changes during adolescence, making the brain vulnerable to drug treatments that target this class of neurotransmitters. Atypical antipsychotic drugs are often prescribed to children and adolescents for off-label treatment of neuropsychiatric disorders, yet the long-term impact this treatment has on brain development remains largely unknown.

Methods: Adolescent male rats were treated with olanzapine or vehicle for 3 weeks (during postnatal day 28-49) using a dosing condition designed to approximate closely D2 receptor occupancies in the human therapeutic range.

Olanzapine antipsychotic treatment of adolescent rats causes long term changes in glutamate and GABA levels in the nucleus accumbens.

Atypical antipsychotic drugs (AAPDs) are widely used in children and adolescents to treat a variety of psychiatric disorders. However, little is known about the long-term effects of AAPD treatment before the brain is fully developed. Indeed, we and others have previously reported that treatment of adolescent rats with olanzapine (OLA; a widely prescribed AAPD) on postnatal days 28-49, under dosing conditions that approximate those employed therapeutically in humans, causes long-term behavioral and neurobiological perturbations.

Olanzapine treatment of adolescent rats causes enduring specific memory impairments and alters cortical development and function.

Antipsychotic drugs are increasingly used in children and adolescents to treat a variety of psychiatric disorders. However, little is known about the long-term effects of early life antipsychotic drug treatment. Most antipsychotic drugs are potent antagonists or partial agonists of dopamine D2 receptors; atypical antipsychotic drugs also antagonize type 2A serotonin receptors.

Olanzapine treatment of adolescent rats alters adult reward behaviour and nucleus accumbens function.

Antipsychotic drugs are increasingly used in children and adolescents to treat a variety of psychiatric disorders. However, little is known about the long-term effects of early life antipsychotic drug (APD) treatment. Most APDs are potent antagonists or partial agonists of dopamine (DA) D₂ receptors; atypical APDs also have multiple serotonergic activities.

Experience and the developing prefrontal cortex.

The prefrontal cortex (PFC) receives input from all other cortical regions and functions to plan and direct motor, cognitive, affective, and social behavior across time. It has a prolonged development, which allows the acquisition of complex cognitive abilities through experience but makes it susceptible to factors that can lead to abnormal functioning, which is often manifested in neuropsychiatric disorders. When the PFC is exposed to different environmental events during development, such as sensory stimuli, stress, drugs, hormones, and social experiences (including both parental and peer interactions), the developing PFC may develop in different ways.

Early exposure to haloperidol or olanzapine induces long-term alterations of dendritic form.

Exposure of the developing brain to a wide variety of drugs of abuse (e.g., stimulants, opioids, ethanol, etc.

Effects of trkB knockout on topography and ocular segregation of uncrossed retinal projections.

TrkB is an important receptor for brain-derived neurotrophic factor and NT4, members of the neurotrophin family. TrkB signaling is crucial in many activity-dependent and activity-independent processes of neural development. Here, we investigate the role of trkB signaling in the development of two distinct, organizational features of retinal projections--the segregation of crossed and uncrossed retinal inputs along the "lines of projection" that represent a single point in the visual field and the "retinotopic" mapping of retinofugal axons within their cerebral targets.

Factors influencing frontal cortex development and recovery from early frontal injury.

Background: Neocortical development represents more than a simple unfolding of a genetic blueprint but rather represents a complex dance of genetic and environmental events that interact to adapt the brain to fit a particular environmental context. Although most cortical regions are sensitive to a wide range of experiential factors during development and later in life, the prefrontal cortex appears to be unusually sensitive to perinatal experiences and relatively immune to many adulthood experiences relative to other neocortical regions.

Methods And Results: One way to examine experience-dependent prefrontal development is to conduct studies in which experiential perturbations are related neuronal morphology.

The fibroblast growth factor system is downregulated following social defeat.

The fibroblast growth factor (FGF) system has previously been found to be altered in post-mortem brains of individuals with major depressive disorder (MDD). The present study tested whether the FGF system is altered following acute social defeat. Rats were exposed to four consecutive days of either a social defeat paradigm or novel cages.

Neuroplasticity and schizophrenia.

This article's title is also the name of a workshop sponsored by the International Congress on Schizophrenia Research that was focused on an appraisal of the potential role of neuroplastic processes in the etiology or course of schizophrenia. The workshop brought together clinical investigators of schizophrenia and basic scientists who study various aspects of neuroplasticity, including central nervous system (CNS) development, learning and memory, and drug action. The goal was to identify special opportunities to advance knowledge and understanding of schizophrenia pathology, treatment, or prevention by applying neuroplasticity concepts as a framework to theories of the illness.

TrkB receptor signaling regulates developmental death dynamics, but not final number, of retinal ganglion cells.

We investigated the effects of endogenous neurotrophin signaling on the death-survival of immature retinal ganglion cells (RGCs) in vivo. Null mutation of brain-derived neurotrophic factor [(BDNF) alone or in combination with neurotrophin 4 (NT4)] increases the peak rate of developmental RGC death as compared with normal. Null mutation of NT4 alone is ineffective.

Complexity in the modulation of neurotrophic factor mRNA expression by early visual experience.

The expression of mRNA for brain-derived neurotrophic factor (BDNF) is regulated by early visual experience. In this study, we sought to determine whether other neurotrophic factor mRNAs are similarly regulated. We reared pigmented rats from birth to postnatal day 21 in a normal light cycle, constant light (LR) or constant darkness (DR).