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The Max Planck Institute (MPI) for Biophysical Chemistry (Karl-Friedrich Bonhoeffer Institute) was founded in 1971 in Göttingen. Two of the 11 departments at the institute had a neuroscientific focus. Otto D. Creutzfeldt (1927–1992) and Victor P. Whittaker (1919–2016) were directors of the Neurobiological and Neurochemical Departments, respectively. Creutzfeldt's department researched the structure and function of the cerebral cortex, and Whittaker's department concentrated on the biochemical analysis of synapses and synaptic vesicles. Creutzfeldt and Whittaker were already internationally respected scientists when they were appointed to Göttingen. The next generation of departmental directors, Erwin Neher and Bert Sakmann, were "home-grown" researchers from the institute and, during their time as junior group leaders, they developed the so-called patch clamp technique, with which they were able to measure single ion channels in nerve cells. This technique revolutionized neurophysiology, and Neher and Sakmann were awarded the 1991 Nobel Prize in Physiology or Medicine for their work in this area. Neher was appointed director of the Membrane Biophysics Department in 1983 and, since then, his department has mainly examined the role of Ca2+ in the release of neurotransmitters at synapses and in the secretion of catecholamines from chromaffin cells. From 1985, Sakmann was director of the Cell Physiology Department, and his laboratory concentrated on the molecular and physiological characterization of transmitter receptors in postsynaptic membranes. In 1989, he was appointed to the MPI for Medical Research in Heidelberg. Reinhard Jahn became director of the Neurobiology Department in 1997, researching the molecular mechanisms of the release of neurotransmitters from the presynaptic terminals, and he discovered several proteins associated with the synaptic vesicles. With their work, Neher, Sakmann, and Jahn have made the MPI for Biophysical Chemistry one of the world's leading research centers for the transmission of signals at synapses. [ABSTRACT FROM AUTHOR]

Diets high in sucrose and fat are becoming more prevalent the world over, accompanied by a raised prevalence of cardiovascular diseases, cancers, diabetes, obesity, and metabolic syndrome. Clinical studies link unhealthy diets with the development of mental health disorders, particularly depression. Here, we investigate the effects of 12 days of sucrose consumption administered as 2 L of 25% sucrose solution daily for 12 days in Göttingen minipigs on the function of brain receptors involved in reward and motivation, regulating feeding, and pre- and post-synaptic mechanisms. Through quantitative autoradiography of cryostat sections containing limbic brain regions, we investigated the effects of sucrose restricted to a 1-h period each morning, on the specific binding of [3H]raclopride on dopamine D2/3 receptors, [3H]UCB-J at synaptic vesicle glycoprotein 2A (SV2A), [3H]MPEPγ at metabotropic glutamate receptor subtype 5 (mGluR5) and [3H]SR141716A at the cannabinoid receptor 1 (CB1). Compared to control diet animals, the sucrose group showed significantly lower [3H]UCB-J and [3H]MPEPγ binding in the prefrontal cortex. The sucrose-consuming minipigs showed higher hippocampal CB1 binding, but unaltered dopamine D2/3 binding compared to the control group. We found that the sucrose diet reduced the synaptic density marker while increasing CB1 binding in limbic brain structures, which may subserve maladaptive changes in appetite regulation and feeding. Further studies of the effects of diets and lifestyle habits on brain neuroreceptor and synaptic density markers are warranted. • We investigated 12 days of excessive sucrose consumption in Göttingen minipigs. • Sucrose reduced synaptic vesicle glycoprotein 2A binding, marking presynaptic density. • Sucrose reduced prefrontal metabotropic glutamate receptor 5 binding. • Sucrose increased hippocampal cannabinoid receptor 1 binding. • Sucrose ingestion can alter brain systems involved in appetite regulation and feeding. [ABSTRACT FROM AUTHOR]

Purpose: Loss of neuronal synapse function is associated with a number of brain disorders. The [11C]UCB-J positron emission tomography (PET) tracer allows for in vivo examination of synaptic density, as it binds to synaptic vesicle glycoprotein 2A (SV2A) expressed in presynaptic terminals. Here, we characterise [11C]UCB-J imaging in Göttingen minipigs.Procedures: Using PET imaging, we examined tracer specificity and compared kinetic models. We explored the use of a standard blood curve and centrum semiovale white matter as a reference region. We compared in vivo [11C]UCB-J PET imaging to in vitro autoradiography, Western blotting and real-time quantitative polymerase chain reaction.Results: The uptake kinetics of [11C]UCB-J could be described using a 1-tissue compartment model and blocking of SV2A availability with levetiracetam showed dose-dependent specific binding. Population-based blood curves resulted in reliable [11C]UCB-J binding estimates, while it was not possible to use centrum semiovale white matter as a non-specific reference region. Brain [11C]UCB-J PET signals correlated well with [3H]UCB-J autoradiography and SV2A protein levels.Conclusions: [11C]UCB-J PET is a valid in vivo marker of synaptic density in the minipig brain, with binding values close to those reported for humans. Minipig models of disease could be valuable for investigating the efficacy of putative neuroprotective agents for preserving synaptic function in future non-invasive, longitudinal studies. [ABSTRACT FROM AUTHOR]