Showing papers in "Neuropharmacology in 2012"

TL;DR: A paradigm shift from a monoamine hypothesis of depression to a neuroplasticity hypothesis focused on glutamate may represent a substantial advancement in the working hypothesis that drives research for new drugs and therapies.

TL;DR: Results from prospective longitudinal and retrospective cross-sectional studies investigating executive function associated with PTSD are summarized and a model is presented concerning how such impairments may contribute to the clinical profile of PTSD and lead to the use of alternative coping styles such as avoidance.

TL;DR: This article shall review cellular and molecular mechanisms, as well as recent work on individual differences in anxiety-like behavior and also developmental influences that bias how the brain responds to stressors.

TL;DR: Together these studies indicate that ketamine rapidly reverses the atrophy of spines in the PFC and thereby causes a functional reconnection of neurons that underlies the rapid behavioral responses.

TL;DR: Initial clinical evidence comes from the significantly enhanced antidepressant therapeutic response when eszopicole, an anxiolytic/hypnotic acting preferentially on α(2)/α(3) and α(1) GABA(A) receptors, was coadministered with an antidepressant.

TL;DR: It is suggested that in schizophrenia the specific ability of fast-spiking interneurons to control and synchronize disparate cortical circuits is disrupted and that this disruption may underlie many of the schizophrenia symptoms.

TL;DR: Overall, PTSD subjects demonstrate a lack of safety signal learning and an inability to modulate the fear responses with safety cues, according to a conditional discrimination paradigm used in combat and civilian PTSD populations.

TL;DR: This work evaluates established and novel approaches to uncover the molecular substrates, genetic pathways and neural circuits of anxiety using adult zebrafish, and provides a conceptual framework for the wider application of zebra fish and other aquatic models in anxiety research.

TL;DR: The traditional as well as endocrine roles of adipose tissue in controlling energy metabolism and their dysregulation in obesity that leads to development of cardiometabolic disorders, with a focus on the resident macrophage-derived adipokines.

TL;DR: It is proposed that analogous signal-to-noise deficits in the flow of cortical information in preclinical models are useful targets for the development of new drugs that target the treatment-resistant symptoms of schizophrenia.

TL;DR: A touchscreen method that satisfies a proposed 'wish-list' of desirables for a cognitive testing method for assessing rodent models of schizophrenia and is capable of detecting not just impairments in function, but enhancements as well, which is essential for testing putative cognitive therapies.

TL;DR: The current evidence in the literature is examined which offers insight into the premise that both central and systemic inflammation may contribute to neurodegeneration in PD, and the emerging possibility of the use of diagnostic tools such as imaging technologies for PD patients is discussed.

TL;DR: Results indicate that TNF-α produces a depressive-like state in mice, reinforcing the notion that an inflammatory component may play an important role in the pathophysiology of depression and suggesting that the central administration of T NF-α may be a novel approach to study the inflammatory component of depressive disorder.

TL;DR: Improvements in transgenic mouse technology, rodent behavioral analyses, and the understanding of the neurogenesis process will allow us to refine the authors' conclusions and perform ever more specific experiments, and highlight work showing that adult-generated neurons are functionally important for the behavioral response to social stress.

TL;DR: This review discusses the neuropeptides that regulate feeding behaviour and how their function can be altered through cross-talk with hormones and neuropePTides that also regulate the hypothalamo-pituitary-adrenal axis.

TL;DR: Results demonstrate that the nausea response accompanying peripheral exendin-4 occurs via a vagal-independent pathway involving GLP-1R activation in the brain as the exend in-4-induced pica response is attenuated with CNS co-administration of the GLP -1R antagonist ex endin-(9-39), but not by vagotomy.

TL;DR: The poly(I:C) model seems highly suitable for the exploration of novel pharmacological and neuro-immunomodulatory strategies for both symptomatic and preventive treatments against psychotic disease, as well as for the identification of neurobiological mechanisms underlying gene-environment and environment-environment interactions presumably involved in the etiology of schizophrenia and related disorders.

TL;DR: The mechanisms of action of hypothalamic neuropeptides with established roles in feeding, including melanin-concentrating hormone (MCH), the orexins, α-melanocyte stimulating hormone (α-MSH), agouti-gene related protein (AgRP), neuropeptic Y, and oxytocin are reviewed, with emphasis laid on both their effects on appetite regulating centres throughout the brain, and on examining the evidence for their physiological roles.

TL;DR: Neurochemical evidence of reward-related brain dysfunctions obtained through animal models of binge eating, bulimia nervosa, or anorexia nervosa suggest alterations in dopamine, acetylcholine, and opioid systems in reward- related brain areas occur in response to binge eating of palatable foods.

TL;DR: Therapeutic approaches that focus on normalizing hippocampal function may prove to be more effective treatment avenues for the schizophrenia patient.

TL;DR: 6-Shogaol showed significant neuroprotective effects in vivo in transient global ischemia via the inhibition of microglia, suggesting that 6-shogaol is an effective therapeutic agent for treating neurodegenerative diseases.

TL;DR: A picture begins to emerge of DISC1 as a key hub for multiple critical developmental pathways within the brain, disruption of which can lead to a variety of psychiatric illness phenotypes.

TL;DR: Results suggest an enhanced negative glucocorticoid feedback within the HPA axis of 51KO mice, possibly modulated by an increased sensitivity of the GR.

TL;DR: It is suggested that the selective partial agonist EVP-6124 improves memory performance by potentiating the acetylcholine response of α7 nAChRs and support new therapeutic strategies for the treatment of cognitive impairment.

TL;DR: A combined analysis of environmental, genetic, endophenotype and epigenetic data will be necessary to better understand pathomechanisms in PTSD.

TL;DR: Key strengths and weaknesses of each of the NMDAR hypofunction hypothesis approaches are described with regard to their ability to recapitulate the deficits seen in patients, and it is surprisingly difficult to identify any single aspect of cognitive function that possesses complete translational integrity.

TL;DR: Knowledge of the genetic underpinnings and neuronal pathways involved in the etiology and maintenance of PTSD will allow for improved targeting of primary prevention amongst vulnerable individuals or populations, as well as timely, targeted treatment interventions.

TL;DR: This review will discuss established pharmacological interventions for PTSD as well as highlight novel therapeutic strategies undergoing extensive pre-clinical and ongoing clinical research, including modulation of stress effects on memory consolidation after trauma.

TL;DR: It is proposed that ECM abnormalities may contribute to several aspects of the pathophysiology of this disease, including disrupted connectivity and neuronal migration, synaptic anomalies and altered GABAergic, glutamatergic and dopaminergic neurotransmission.

TL;DR: Clinical and preclinical literature is examined to support a theory of hippocampal dysfunction as a primary contributory factor to the etiology of PTSD, and future research required to test these hypotheses are discussed.