Topic: hippocampal long-term potentiation

Aim: Acid-sensing ion channels 1a (ASIC1a) are widely distributed in the mammalian nervous system and in particular brain areas including the hippocampus. ASIC1a is highly permeable to Ca2+ and its activation has a crucial importance in numerous physiological and pathological processes, including synaptic plasticity, learning and memory. To further understand the role of ASIC1a channels in the synaptic alterations induced by Aβ, we carried out electrophysiological experiments investigating the effects of a ASIC1a-blocking monoclonal antibody ASC06-IgG on hippocampal long-term potentiation (LTP

The prefrontal cortex is one of the most commonly studied structures in depression. Synaptic loss and prefrontal circuits deficits have been widely described in depression physiopathology, and their restoration by antidepressant drugs is at the center of their therapeutic effect. Aims: This project aims to test the antidepressant potential of a specific manipulation of prefrontal circuits. Methods: Using the Chronic Despair Model (CDM) of depression, and the DREADDs chemogenetic technique, we counteracted the hypofrontality characteristic of a depressive-like state, and assessed the behavioura

Dopamine D3 receptors (D3Rs) regulate several brain functions such as reward and social behavior by modulating neuronal activity in different brain regions. Although mostly expressed in dopaminergic areas, D3Rs are also present in the hippocampus. Previous results obtained in our laboratory suggested that D3 pharmacological blockade or genetic deletion in D3-knock-out (KO) mice enhanced hippocampal long-term potentiation (LTP) and memory. Based on these findings, here, we aimed to explore the molecular bases underlying this pro-cognitive effect.To determine whether D3R blockade acted via pre-

Down syndrome (Trisomy 21, Ts21) is the most common cause of early onset Alzheimer’s disease. We previously reported that secretomes of induced pluripotent stem cell (iPSC)-derived human Ts21 cortical neurons inhibited hippocampal long-term potentiation (LTP) in a tau-dependent manner (Hu et al., Cell Reports, 2018). Here, we employed electrophysiological recording from the CA1 area of the hippocampus of live rats under urethane anaesthesia to assess the ability of anti-tau antibodies to immunodeplete Ts21 iPSC-derived neuron synaptotoxic tau. We found that the mid-region (amino acids 210-241)