Targeting reconsolidation with propranolol, a blocker of β-adrenergic receptors (β-ARs), emerged as a potential treatment for maladaptive memories such as those involved in posttraumatic stress disorder (PTSD). Reconsolidation targeting treatments for PTSD are becoming a common practice in the clinic and it is important to unveil any side effects upon 'non-targeted' memories. While previous studies have focused on propranolol's effects on the reconsolidation of emotional/distressful memories, the present study asked whether propranolol is involved in the reconsolidation of recognition memories - by assessing its effects on distinct memory components and the role of the dorsal hippocampus. Rats performed an object recognition (OR) task where they were exposed to different objects: A and B presented during the sample phase; A and C presented during the reactivation phase; and D in combination of either A, B, or C during a final test. Intra-hippocampal injections of propranolol (5 µg or 10 µg) were conducted immediately after the reactivation session. Propranolol infusions consistently impaired the addition of novel information to the previously consolidated memory trace regardless of dose, and the retention of familiar objects was not affected. Higher doses of propranolol also hindered memory of a familiar object that was not presented during the reactivation session, but was previously placed at the same location where novel information was presented during reactivation. The present results shed light on the role of β-ARs on the reconsolidation of different memory components and argue for the need for further studies examining possible recognition memory deficits following propranolol treatment.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.neuroscience.2023.02.018 | DOI Listing |
Cureus
December 2024
Infectious Disease, Staten Island University Hospital, Staten Island, USA.
Shingles, also known as herpes zoster, is a reactivation of the chickenpox virus that causes a painful, blistering rash. After a chickenpox infection, the virus lies dormant in nerve cells. When reactivated, usually in older adults or those with weakened immune systems, it travels along nerves, typically affecting a single strip of skin called a dermatome.
View Article and Find Full Text PDFCancer Treat Rev
January 2025
Medical Oncology, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy; Department of Medical and Surgical Sciences (DIMEC), University of Bologna, Bologna, Italy. Electronic address:
Immune-based combinations are the cornerstone of the first-line treatment of metastatic renal cell carcinoma patients, leading to outstanding outcomes. Nevertheless, primary resistance and disease progression is a critical clinical challenge. To properly address this issue, it is pivotal to understand the mechanisms of resistance to immunotherapy and tyrosine kinase inhibitors, that tumor eventually develop under treatment.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Department of Pharmaceutics, School of Pharmacy, Ningxia Medical University, Yinchuan, Ningxia, China. Electronic address:
Herpes zoster is an acute infectious skin disease caused by the reactivation of latent varicella-zoster virus, vaccination, such as subunit vaccine with good safety, can effectively prevent shingles through increasing immunity of the body. However, protein antigens are prone to degradation and inactivation, which alone is generally not sufficient to induce potent immune effect. In this study, the liposomal vaccine platform modified with mPLA (TLR4 agonist) was developed to improve the immunogenicity of glycoprotein E (VZV-gE) derived from herpes zoster virus.
View Article and Find Full Text PDFAm J Clin Dermatol
January 2025
Dr. Phillip Frost Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL, 33136, USA.
Pityriasis rosea (PR) is a prevalent dermatological condition characterized by a distinctive herald patch, followed by secondary eruptions, often forming a "Christmas tree" pattern on the trunk. Despite its recognizable clinical presentation, the etiology of PR remains uncertain, with hypotheses pointing to both infectious and noninfectious origins. Human herpesviruses (HHV) 6 and 7 have been implicated, with evidence suggesting viral reactivation as a potential trigger.
View Article and Find Full Text PDFDiagnostics (Basel)
December 2024
Department of Dermatology, Tokyo Metropolitan Police Hospital, Tokyo 164-8541, Japan.
Fixed drug eruption (FDE) is a type of drug-induced skin inflammation characterized by the recurrence of lesions in the same region following repeated exposure to the causative drug. FDE typically presents as localized spots or plaques without systemic symptoms; however, it can manifest in other forms, such as blisters and papules. In FDE, effector memory CD8-positive T cells that remain dormant in the basal layer after a previous inflammation are reactivated upon re-exposure to the causative drug, leading to the development of erythema at the same sites.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!