Lab mission statement
Welcome to the Vargas-Caballero Lab!
We are a research group at School of Biological Sciences, University of Southampton. Dr. Vargas-Caballero brings 25 years of experience in analysing neuronal excitability in health and disease, with a focus on studying synaptic mechanisms involved in cognition.
Our mission is to cultivate an environment of collaborative research that contributes new knowledge to the scientific community, while also fostering the professional growth of every lab member.
Our team is driven by values that we actively put into practice. In a recent poll of lab members, the following core values emerged as central to our research endeavours:
Research overview
The brain enables everything from perception and memory to decision-making and action. It’s composed of billions of neurons that communicate with one another through specialised contact points known as synapses.
Synapses are dynamic structures whose ability to strengthen or weaken in response to activity, known as synaptic plasticity, is fundamental to how we learn and form memories. This process depends on the coordinated function of hundreds of proteins, including those that control electrical signalling.
A key focus of the Vargas-Caballero Laboratory is to understand the properties of neurons that drive activity and synaptic transmission, and how synapses support plasticity. Our research pays special attention to the role of ion channels, proteins that regulate the flow of ions across neuronal membranes and underpin excitability. Ion channels are crucial for generating and modifying synaptic responses, and their dysfunction has been implicated in neurodevelopmental disorders, memory loss and neurodegeneration.
Research Interests
Ion channels and neuronal excitability
Ion channels are essential for the proper functioning of neurons, as they control the flow of ions that generate electrical signals and regulate neuronal communication. Our lab focuses on how ion channel activity influences neuronal excitability and synaptic function in both health and disease. Dysregulation of ion channels can alter the balance of excitation and inhibition in the brain, contributing to neuropsychiatric and neurodegenerative disorders.
We assess ion channel function and excitability in cell lines transfected with specific ion channels, neuronal cultures, and brain slices. We combine electrophysiological, molecular, and imaging approaches to investigate how changes in ion channel function impact neuronal networks and behaviour. Our goal is to uncover mechanisms that underpin excitability and synaptic function and to identify potential therapeutic targets for early intervention when these processes are disrupted.
See this publication for our contribution to understanding of the effects of haemoglobin on neural function, such as after subarachnoid haemorrhage.
Schizophrenia and Synaptic Dysfunction
We are researching how disruptions at the synaptic level contribute to the development of schizophrenia. This complex psychiatric disorder is associated with impairments in cognition, perception, and behaviour, and growing evidence points to alterations in synaptic plasticity and ion channel function as key underlying mechanisms.
We investigate how neurotransmitter-activated ion channels in the prefrontal cortex and hippocampus shape the way neurons respond to synaptic inputs. We are currently focusing on analysing NMDA receptor function. These channels play a critical role in regulating neuronal excitability and plasticity, both of which are disrupted in schizophrenia. By examining the molecular and electrophysiological changes in experimental models, we aim to reveal how early synaptic alterations may drive circuit-level dysfunctions that underlie the cognitive symptoms of the disorder.
Alzheimer’s Disease
In parallel, we investigate how synaptic and ion channel dysfunction contributes to memory loss in Mild Cognitive Impairment, the earliest clinical phase of Alzheimer’s disease. Our work explores how early synaptic dysfunction and impaired plasticity may lead to cognitive decline in Alzheimer’s and understanding the key mechanisms that could be targeted. See this post for more discussion on that topic.