1,721,057 research outputs found
A human translational model based on neuroplasticity for pharmacological agents potentially effective in Treatment-Resistant Depression: Focus on dopaminergic system
Major Depressive Disorder (MDD) is a common psychiatric condition characterised by two core symptoms, low mood and anhedonia (or lack of pleasure). About 15-30% of people suffering from MDD do not respond to standard-of-care antidepressants, e.g., the serotonin re-uptake inhibitors (SSRI), and are considered affected by Treatment Resistant Depression (TRD). The neurobiology of this condition is presently unknown. Recent attempts of developing novel treatments for TRD have been driven by four major breakthroughs: (1) Increasing dopaminergic neurotransmission improves TRD symptoms; (2) Anhedonia occurs when central dopaminergic neurotransmission is low; (3) Enhanced neuroplasticity is critical for the action of antidepressants; (4) Ketamine shows antidepressant properties in TRD patients and triggers neuroplasticity in preclinical animal models. These breakthroughs are at the basis of a putative human translational cellular model for antidepressant agents that we are proposing in this article. The rationale is briefly described here
Neural substrate of nicotine addiction as defined by functional brain maps of gene expression.
Stress-like effects of intermittent exposures to a strong magnetic field in weanling mice
NMDA-mediated modulation of dopamine release is modified in rat prefrontal cortex and nucleus accumbens after chronic nicotine treatment
Pressor responses to hyperventilation in elderly subjects differentiate essential from secondary hypertension
Chronic uridine treatment reduces the level of [3H]spiperone-labelled dopamine receptors and enhances their turnover rate in striatum of young rats: relationship to dopamine-dependent behaviours.
Corrigendum: Negative Symptoms of Schizophrenia and Dopaminergic Transmission: Translational Models and Perspectives Opened by iPSC Techniques (Front. Neurosci., (2020), 14, (632), 10.3389/fnins.2020.00632)
In the original article, we neglected to include an Acknowledgments section. The added Acknowledgements section is below: We would like to thank the “VAnviteLli pEr la RicErca: VALERE” program of the University of Campania Luigi Vanvitelli that assigns contributions for the diffusion of open access research products. The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated
Characterization of a 7% carbon dioxide (C02) inhalation paradigm to evoke anxiety symptoms in healthy subjects
The present study is aimed at characterizing the carbon dioxide (CO2) procedure in healthy subjects to achieve reliable provocation of anxiety symptoms. Thirty healthy subjects inhaled in single-blind both compressed air and 7% CO2 mixture. Panic Symptom List (PSLIII-R), Visual Analogue Scale-Anxiety (VAS-A), State Anxiety Inventory (STAI-Y/1), respiratory parameters and skin conductance were measured. 'Responders' were classified depending on PSLIII-R scores after CO2. Twelve out of the 21 'responders' performed a second test to assess test-retest repeatability. In 21 subjects Delta%VAS-A (45.4 +/- 32.1) and PSLIII-R (pre-test 2.3 +/-2.1, post-test 17.5 +/- 8.2) but not STAI-Y/1, significantly increased during CO2 inhalation. Respiratory Rate, Minute Volume, end-Tidal CO2 and skin conductance rose in 'responders'. Repeatability was studied with Bland-Altman plots, revealing mean difference between tests close to 0 for both Delta%VAS-A and PSLIII-R. Among physiologic parameters, end-Tidal CO2 and Respiratory Rate showed good repeatability, with a within-subject CV of 9.2% and 6%, respectively. The challenge produced measurable response in healthy subjects. Good test-retest repeatability was observed in 'responders'. These data indicate that the test can be suitable for testing putative anti-panic or anxiolytic drugs in clinical studies using a within subject, crossover design
Neurohistochemical studies on striatal lesions induced by transient forebrain ischemia. Evidence for protective effects of the ganglioside analogue AGF2
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