This project investigated how dopamine affects the metabolic function of astrocytes, using primary astrocyte cultures derived from the rat brain. The work focused on three main areas: establishing the presence of dopamine receptors in astrocytes, measuring how dopamine regulates intracellular signalling and metabolism, and exploring how these responses are altered when key receptor-related genes are suppressed. First, we confirmed that astrocytes in our cultures expressed the dopamine D1 receptor, although another receptor type, the β-adrenoreceptor, was present at much higher levels. This suggested that dopamine might act through multiple pathways in these cells. Next, we used live-cell fluorescence imaging to track how astrocytes respond to dopamine. Dopamine increased levels of intracellular messengers such as cAMP and calcium, and also stimulated the production of L-lactate, a molecule that helps support neurons. Through pharmacological testing, we found that this lactate increase was mainly mediated by beta-adrenoreceptors, rather than D1 receptors. To better understand the role of these receptors, we reduced the expression of β1-adrenoreceptors using gene-silencing techniques. When these receptors were knocked down, dopamine-induced L-lactate production was significantly reduced. These results confirmed that β1-adrenoreceptors are involved in the metabolic response of astrocytes to dopamine. Together, these experiments provide new insight into how dopamine shapes astrocyte metabolism under laboratory conditions. The findings highlight receptor-specific pathways that may be important for future research on brain energy regulation and its potential relevance to mental health. The results were also presented at several scientific conferences and seminars, helping to communicate the results to the wider research community. Moreover, a manuscript is being prepared to be submitted to a peer-reviewed journal.
