Welcome to SWEBAGS
The Swedish Basal Ganglia Society, SWEBAGS, is an non-profit scientific organization providing a platform for discussions and education opportunities in the area of basal ganglia research.
We aim to increase the visibility of mainly basic and pre-clinical research, and foster multidisciplinary collaborations across biological scales and methodological approaches. All professionals, students and organisations interested in basal ganglia research are welcome to become members.
– Jeanette Hellgren Kotaleski, Professor, KTH Royal Institute of technology, Chair SWEBAGS
– Angela Cenci Nilsson, Professor, Lund University, Vice Chair SWEBAGS
- Postdoctoral position i neurobiology
A position as post-doctoral researcher (post-doc) is available in professor Åsa Mackenzie´s laboratory where we work with neurocircuitry analysis of the basal ganglia and associated structures. We use viral-genetic, histological and molecular biological methods (including transcriptomics) in rodents to analyze the neuronal building blocks of the basal ganglia with great precision. We also use transgenics and optogenetics methodology to stimulate and inhibit distinct nerve cells and assess activity, both on the neuronal and whole organism level (including behavior analysis). Our goal is to increase current understanding of the basal ganglia in motor and non-motor functions (including aversive and depressive states) in normal conditions and in Parkinson´s disease.
We are now recruiting a well-motivated, knowledgeable postdoc who is eager to perform advanced laboratory analyses and to actively participate in our group´s work towards increased knowledge of the brain´s complex neuronal circuits.
Deadline: May 25, 2022 OBS updated!
- New publication:
Improving well-being and survival in the 6-OHDA lesion model of Parkinson´s disease in mice: Literature review and step-by-step protocol
Adriane Guillaumin, Bianca Vicek & Åsa Wallén-Mackenzie
Parkinson’s disease (PD) is the most common neurodegenerative motor disorder and primarily affects movement control but also a range of non-motor functions. With unknown etiology and lack of cure, much research is dedicated to unravel pathological mechanisms and improve clinical prospects for symptom alleviation, prevention and treatment. To achieve these goals, animal models intended to represent symptoms similar to those observed in the complex clinical display of PD play a key role. It is important to bear in mind that, in any studies with laboratory animals, it is crucial to take the 3Rs principle (Refine, Reduce, Replace) into account. The main pathology of PD includes degeneration of dopamine neurons in the substantia nigra pars compacta (SNc). The 6-hydroxydopamine (6-OHDA) lesion model, in which dopaminergic neurons are chemically destroyed, is often favored as a laboratory model of PD in both rodents and primates. However, while reproducing several features of clinical PD, mice exposed to 6-OHDA frequently experience systemic dysfunction causing premature death. To avoid suffering and unnecessary deaths of laboratory mice, there is a need for improved experimental protocols in accordance with the 3Rs principle. Based on current literature and our own previous experiments, we decided to test the effect of three parameters: 1) reduced dose of the 6-OHDA toxin; 2) daily post-operative care to avoid hypothermia and energy loss; 3) shortened interval from surgical injection of toxin to time of sacrifice.
By implementing a 6-OHDA lesion protocol using a lower dose of toxin than commonly seen in the literature alongside careful post-operative care and decreased time post-injection, a fully recovered weight post-surgery and high survival rate was obtained. This was achieved despite full expression of the 6-OHDA-induced locomotor phenotype. A step-by-step protocol was formulated. Validation using histological analysis confirmed toxin-induced degeneration of midbrain dopamine neurons with concomitant loss of dopaminergic projections in the lesioned hemisphere. Notably, while SNc dopamine neurons were drastically reduced, those located in the ventral tegmental area (VTA) were less affected in a medialhigh survival to laterallow survival manner.
The Refine and Reduce parameters of the 3Rs principle in experimental animal welfare were specifically addressed which allowed us to improve well-being and survival of mice while maintaining characteristic parkinsonian features in the 6-OHDA lesion model. A table summarizing current literature on the 6-OHDA model in rodents as well as our validated step-by-step experimental protocol is provided.