Disorders Of Action Control And Learning-related Plasticity In The Basal Ganglia
Funder
National Health and Medical Research Council
Funding Amount
$434,874.00
Summary
Disorders of the basal ganglia have long been known to produce severe cognitive symptoms including a deficit in the control of voluntary action. This project will assess the learning processes through which humans and other animals acquire such actions. We will systematically investigate changes in cellular plasticity associated with the acquisition of new actions to establish the role that it plays in action control under normal and pathological conditions.
Pathologies Of Action Control: Amygdala-striatal Interactions And The Development Of Habits.
Funder
National Health and Medical Research Council
Funding Amount
$431,867.00
Summary
Changes in basal ganglia function, whether produced by neurodegenerative disorders, stroke, injury or disease, can produce pathological changes in action control. This proposal will assess the role of amygdala afferents on basal ganglia structures, most notably the dorsal striatum, in this process. Using an animal model we will compare the role of central and basolateral amygdala inputs to striatum in decision-making, choice and the transition of actions to reflexive, habitual responses.
Dysfunctions In Decision-making And The Cognitive Control Of Action
Funder
National Health and Medical Research Council
Funding Amount
$647,341.00
Summary
The aim of this research project is to establish the neural bases of dysfunctions in decision-making associated with deficits in the cognitive control of action. Decision-making is a complex capacity dependent on the interaction between neural systems that mediate cognition and the selection of specific actions. To this end we will examine the intracellular, cellular and circuit level processes controlling the influence of predictive information on choice between goal-directed actions.
The aim of this research project is to provide critical new information on the functional changes in brain circuits mediating cognitive-emotional integration during decision-making. This project will use a powerful and unique combination of behavioural, circuit-level, cellular, genetic and imagining tools to assess decision processes in healthy rodent and human subjects, and in animal models of, and humans suffering from, specific psychiatric disorders.
High-resolution Brain Imaging Of Basal Ganglia Function
Funder
National Health and Medical Research Council
Funding Amount
$589,083.00
Summary
This project will develop new methods for high resolution MRI imaging of the human brain. We will assess functions of deep brain areas known as the basal ganglia that play a critical role in movement planning and co-ordination. Dysfunction within the basal ganglia is responsible for the motor impairments seen in people with Parkinson’s disease. In this project, we will examine changes in basal ganglia function and structure that lead to individual differences in movement control and learning.
Determining Neuronal Connections Involved In Parkinson's Disease And Cocaine Addiction
Funder
National Health and Medical Research Council
Funding Amount
$343,300.00
Summary
Addictive behaviours in response to cocaine use and fine motor coordination that is affected in Parkinson's disease are both controlled by the same type of cells/neurons, i.e., dopamine neurons. However, the circuitry of these neurons varies from where they originate and the type of connections they make. By understanding the neuronal circuitry of these two circuitries in concert we will be able to gain important insight into their roles in adaptive and pathological brain function.
Hypothalamic Orexin Neurons And The Medullary Sympathoadrenal Centre: A Key Role In Glucose Homeostasis
Funder
National Health and Medical Research Council
Funding Amount
$577,957.00
Summary
Hypoglycaemia or low blood sugar is a major side-effect of the treatment of diabetes. Exposure to hypoglycaemia results in changes in the brain (neuroplasticity) that reduce the awareness of hypoglycaemia, often with serious consequences. Hypoglycaemia triggers the production of several hormones including adrenaline which restore normal blood glucose. This process is incompletely understood. This research project will identify key components of the neurocircuitry that controls blood sugar.
The brain regulates body temperature by a series of mechanisms, including the control of how much blood flows to the skin to lose or retain heat. The project aims to locate the brain temperature receptors and brain pathways that do this, using an animal model, the rat. At present they are not known.
Which Neurons Maintain Sympathetic Vasomotor Tone?
Funder
National Health and Medical Research Council
Funding Amount
$567,918.00
Summary
High blood pressure is a major risk factor for cardiovascular disease, a major burden of disease worldwide. High levels of nerve activity that cause the blood vessels to constrict elevating blood pressure are characteristic of hypertension. We do not know which brain cells set and maintain this nerve activity. We will identify these cells, determine how they function and what regulates them. Ultimately we could control these cells treating the cause of hypertension or when clinical need arises.
Brain Pathways For Neurally-mediated Fever: From Vagal Afferent To Sympathetic Output To Brown Adipose Tissue Via Brain
Funder
National Health and Medical Research Council
Funding Amount
$405,223.00
Summary
Fever is one of the immune defence reactions to the invasion of microorganisms such as bacteria and viruses. Fever reflects increased heat production and decreased heat loss. Systems regulating heat production and heat loss are under brain control. To trigger fever, the immune system must alert the brain to the presence of infection. The general view of how the alerting system triggers fever is that it develops in sequential steps. Macrophages ingest microorganisms, and then regulatory proteins ....Fever is one of the immune defence reactions to the invasion of microorganisms such as bacteria and viruses. Fever reflects increased heat production and decreased heat loss. Systems regulating heat production and heat loss are under brain control. To trigger fever, the immune system must alert the brain to the presence of infection. The general view of how the alerting system triggers fever is that it develops in sequential steps. Macrophages ingest microorganisms, and then regulatory proteins (cytokines) are released. The cytokines enter the blood stream and are transported to the brain. Recently, the existence of another signalling pathway has been demonstrated. The pathway is via a special peripheral sensory nerve, the abdominal vagal sensory nerve. However, special neural pathways in the brain have not yet been clarified, even though several neural relay stations have been proposed. To elucidate neural pathways transmitting information of infection to the brain, both input and output of the pathway need to be specified. Specific outputs other than body temperature have not been determined, so far. I have recently developed a new reflex model, in which I focus on sympathetic nerves supplying the specialised fat tissue as an output as well as the vagus sensory nerve as an input. The fat tissue, brown adipose tissue (BAT), generates heat. When the vagus sensory nerve is stimulated electrically, BAT sympathetic nerve is activated. We were very exited when we discovered the potency of the combination in our rat model. We are now ready to elucidate brain pathways for neurally-mediated fever, using our new reflex model. Signalling to the brain via the nervous system is faster than via the blood stream, and thus must be very important for the earliest phase of fever. Understanding the neural pathways by which the brain perceives peripheral infection and triggers fever may promote beneficial aspects of the acute-phase immune reaction.Read moreRead less