It has been shown that the peptide anxiolytic drug Selank recovers learning and memory impaired by damage of the noradrenergic (NA) brain system in Wistar rats after injection of the NA-synthesis inhibitor disulfiram, administration of neurotoxic compound 6-OHDA, or a combined induction of hypoxic hypoxia and hypercapnia. The main component of the Selank action is the stimulation of the search reflex aimed to distinguish an adequate adaptive response in the first trials of the learning session. The enhancement of memory consolidation and retrieval shows evidence for stimulation of the brain motivation mechanisms impaired by the NA system damage.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Therapeutic Efficacy of Hemodynamic Management Using Norepinephrine on Cardiorespiratory Function Following Cervical Spinal Cord Contusion in Rats.
J Neurotrauma
December 2024
Department of Biological Sciences, College of Science, National Sun Yat-sen University, Kaohsiung, Taiwan.
Cervical spinal cord injury usually leads to cardiorespiratory dysfunction due to interruptions of the supraspinal pathways innervating the phrenic motoneurons and thoracic sympathetic preganglionic neurons. Although clinical guidelines recommend maintaining the mean arterial pressure within 85-90 mmHg during the first week of injury, there is no pre-clinical evidence from animal models to prove the therapeutic efficacy of hemodynamic management. Accordingly, the present study was designed to investigate the therapeutic efficacy of hemodynamic management in rats with cervical spinal cord contusion.
View Article and Find Full Text PDFPrevention and management of hypertensive crises in children with pheochromocytoma and paraganglioma.
Front Endocrinol (Lausanne)
September 2024
Endocrinology, Diabetes and Metabolism; Department of Medical Sciences; University of Turin, Turin, Italy.
Article Synopsis
- - Hypertensive crises in children are rare and often occur without a prior hypertension diagnosis, potentially linked to underlying issues like pheochromocytoma/paraganglioma (PPGL) that cause catecholamine excess.
- - The type of catecholamine excess varies by tumor type: noradrenergic tumors typically lead to sustained hypertension, while adrenergic tumors may cause paroxysmal hypertension due to a mix of adrenergic receptor stimulation.
- - Treatment for these hypertensive crises mainly involves alpha-blockers, and sometimes beta-blockers for tachyarrhythmias, with the administration route depending on whether it's a hypertensive emergency or urgency.
The Projection-Specific Noradrenergic Modulation of Perseverative Spatial Behavior in Adult Male Rats.
eNeuro
August 2024
Department of Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, 72076 Tübingen, Germany
Adaptive behavior relies on efficient cognitive control. The anterior cingulate cortex (ACC) is a key node within the executive prefrontal network. The reciprocal connectivity between the locus ceruleus (LC) and ACC is thought to support behavioral reorganization triggered by the detection of an unexpected change.
View Article and Find Full Text PDFAn Expanded Narrative Review of Neurotransmitters on Alzheimer's Disease: The Role of Therapeutic Interventions on Neurotransmission.
Mol Neurobiol
February 2025
Neuropharmacology Research Laboratory, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, 47500, Bandar Sunway, Selangor, Malaysia.
Alzheimer's disease (AD) is a progressive neurodegenerative disease. The accumulation of amyloid-β (Aβ) plaques and tau neurofibrillary tangles are the key players responsible for the pathogenesis of the disease. The accumulation of Aβ plaques and tau affect the balance in chemical neurotransmitters in the brain.
View Article and Find Full Text PDFComparison of Protective Effects of Antidepressants Mediated by Serotonin Receptor in Aβ-Oligomer-Induced Neurotoxicity.
Biomedicines
May 2024
Department of Pharmacology, Showa University Graduate School of Medicine, Tokyo 142-8555, Japan.
Amyloid β-peptide (Aβ) synthesis and deposition are the primary factors underlying the pathophysiology of Alzheimer's disease (AD). Aβ oligomer (Aβo) exerts its neurotoxic effects by inducing oxidative stress and lesions by adhering to cellular membranes. Though several antidepressants have been investigated as neuroprotective agents in AD, a detailed comparison of their neuroprotection against Aβo-induced neurotoxicity is lacking.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!