The 25th annual meeting of the Canadian College of Neuropsychopharmacology. Ottawa, Ontario, Canada, June 9-12, 2002 (original) (raw)
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Journal of Psychiatry …, 2007
The 30th Annual Meeting of the Canadian College of Neuropsychopharmacology (CCNP) was held in Banff, Alberta, June 15 to June 19, 2007. This report summarizes the 3 CCNP award lectures and 10 symposia. CCNP Heinz Lehmann Award lecture Dr. Hymie Anisman (Carleton University, Ottawa) was the recipient of this year's Heinz Lehmann award, and his talk was entitled "Stress, cytokines and depressive illness." As Dr. Anisman noted, in recent years it has become clear that stressors can affect the immune system. This led to the converse question: can the immune system affect psychological states? Investigations of these associations have benefited from distinguishing between different types of stressors: predictable versus unpredictable, chronic versus intermittent, and processive (e.g., cognitive) versus systemic (e.g., disease activated). Depending on these stressor features, along with intensity and duration, the elicited response can facilitate coping, or it can lead to dysfunction and disease. For example, mild, controllable stressors activate monoamine release and lead to increased synthesis plus an enhanced coping response on subsequent re-exposure. In comparison, severe, uncontrollable stressors deplete monoamine stores, and synthesis rates are unable to compensate adequately. Similarly, monoamine sensitization might simultaneously enhance short-term coping but, in the absence of adequate increases in synthesis, increase vulnerability to the effects of prolonged stressors. The latter change might be related to the progressive acceleration of relapse rates in patients with recurrent major depression. Marked individual and rodent strain differences in these responses are also evident. Recent work by Dr. Anisman's group has identified a neurobiological pathway that could mediate many of these effects: stress-induced activation of immune signalling cytokines. Inflammatory cytokines such as interleukin-1 (IL-1) and interferon-γ (IFN-γ) are present in the brain, and their activation can affect cell death, neurogenesis, and cell metabolism. Patients suffering from severe stress and depression exhibit increased cytokine activity, whereas cytokine immunotherapy (e.g., interferon-α, tumour necrosis factor-α [TNF-α]) can induce antidepressant-reversible depressions. In Dr. Anisman's studies, administration of IL-1, like stress, increases norepinephrine (NE) metabolism and serotonin (5-HT) release. The bacterial endotoxin (LPS) increases dopamine (DA) release in the nucleus accumbens (NAc), whereas chronic stressor regimens can decrease responding for electrical brain stimulation (EBS) reward. Following exposure to a cytokine such as TNF-α, there is an increase in sicklike behavioural responses (e.g., ptosis, ruffled fur, altered body posture), corticosterone release and NE metabolism, and this response becomes greater after repeated exposures followed by extended intertest intervals. These associations have recently been followed up in studies
Neuropsychopharmacology advance online publication
2020
Abnormalities in the regulation of neurotransmitter release and/or abnormal levels of extracellular neurotransmitter concentrations have remained core components of hypotheses on the neuronal foundations of behavioral and cognitive disorders and the symptoms of neuropsychiatric and neurodegenerative disorders. Furthermore, therapeutic drugs for the treatment of these disorders have been developed and categorized largely on the basis of their effects on neurotransmitter release and resulting receptor stimulation. This perspective stresses the theoretical and practical implications of hypotheses that address the dynamic nature of neurotransmitter dysregulation, including the multiple feedback mechanisms regulating synaptic processes, phasic and tonic components of neurotransmission, compartmentalized release, differentiation between dysregulation of basal vs activated release, and abnormal release from neuronal systems recruited by behavioral and cognitive activity. Several examples illustrate that the nature of the neurotransmitter dysregulation in animal models, including the direction of drug effects on neurotransmitter release, depends fundamentally on the state of activity of the neurotransmitter system of interest and on the behavioral and cognitive functions recruiting these systems. Evidence from evolving techniques for the measurement of neurotransmitter release at high spatial and temporal resolution is likely to advance hypotheses describing the pivotal role of neurotransmitter dysfunction in the development of essential symptoms of major neuropsychiatric disorders, and also to refine neuropharmacological mechanisms to serve as targets for new treatment approaches. The significance and usefulness of hypotheses concerning the abnormal regulation of the release of extracellular concentrations of primary messengers depend on the effective integration of emerging concepts describing the dynamic, compartmentalized, and activitydependent characteristics of dysregulated neurotransmitter systems.
Encyclopedia of Clinical Neuropsychology
2011
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Downey et al 2016 Eur Neuropsychopharmacology.pdf
Intravenous infusion of lanicemine (formerly AZD6765), a low trapping non-selective N-methyl-D-aspartate (NMDA) receptor antagonist, induces antidepressant effects with a similar time course to ketamine. We investigated whether a single dose lanicemine infusion would reproduce the previously reported decrease in subgenual anterior cingulate cortex (sgACC) activity evoked by ketamine, a potential mechanism of antidepressant efficacy. Sixty unmedicated adults meeting the criteria for major depressive disorder were randomly assigned to receive constant intravenous infusions of ketamine, lanicemine or saline during a 60 min pharmacological magnetic resonance imaging (phMRI) scan. Both ketamine and lanicemine gradually increased the blood oxygen level dependent signal in sgACC and rostral ACC as the primary outcome measure. No decreases in signal were seen in any region. Interviewer-rated psychotic and dissociative symptoms were minimal following administration of lanicemine. There was no significant antidepressant effect of either infusion compared to saline. The previously reported deactivation of sgACC after ketamine probably reflects the rapid and pronounced subjective effects evoked by the bolus-infusion method used in the previous study. Activation of the ACC was observed following two different NMDA compounds in both Manchester and Oxford using different 3 T MRI scanners, and this effect predicted improvement in mood 1 and 7 days post-infusion. These findings suggest that the initial site of antidepressant www.elsevier.com/locate/euroneuro http://dx.161 275 7428. 1 former employee. European Neuropsychopharmacology (2016) 26, 994-1003 action for NMDA antagonists may be the ACC (NCT01046630. A Phase I, Multi-centre, Doubleblind, Placebo-controlled Parallel Group Study to Assess the pharmacoMRI Effects of AZD6765 in Male and Female Subjects Fulfilling the Criteria for Major Depressive Disorder; http:// clinicaltrials.gov/show/NCT01046630).
2012
Charles F. Albright, Randy C. Dockens, Jere E. Meredith Jr., Richard E. Olson, Randy Slemmon, Kimberley A. Lentz, Jun-Sheng Wang, R. Rex Denton, Gary Pilcher, Paul W. Rhyne, Joseph J. Raybon, Donna M. Barten, Catherine Burton, Jeremy H. Toyn, Sethu Sankaranarayanan, Craig Polson, Valerie Guss, Randy White, Frank Simutis, Thomas Sanderson, Kevin W. Gillman, John E. Starrett, Jr., Joanne Bronson, Oleksandr Sverdlov, Shu-Pang Huang, Lorna Castaneda, Howard Feldman, Vlad Coric, Robert Zaczek, John E. Macor, John Houston, Robert M. Berman, and Gary Tong