Publications by authors named "Jana Kroll"

Synaptic vesicles (SVs) store and transport neurotransmitters to the presynaptic active zone for release by exocytosis. After release, SV proteins and excess membrane are recycled via endocytosis, and new SVs can be formed in a clathrin-dependent manner. This process maintains complex molecular composition of SVs through multiple recycling rounds.

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Article Synopsis
  • The release of neurotransmitters at synapses relies on a series of protein interactions, particularly involving complexins, which play a role in regulating synaptic transmission.
  • Research on the N-terminus of complexin II, focusing on its hydrophobic amino acids, shows that preserving this property supports its stimulatory function, while changes disrupt neurotransmitter release.
  • Specific mutations in the N-terminus, particularly residue changes, can enhance spontaneous release but negatively affect evoked release, highlighting the importance of precise amino acid composition in managing synaptic neurotransmitter dynamics.
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Article Synopsis
  • - The study investigates the role of complexin II (Cpx) in regulating neurotransmitter release at central synapses, focusing specifically on its N-terminal region (amino acids 1-27) which plays a critical role in both stimulating and inhibiting synaptic transmission.
  • - Through experiments such as mutagenesis and membrane fusion assays, the research reveals that the hydrophobic characteristics of the N-terminus are important for enhancing spontaneous neurotransmitter release, while alterations in specific amino acids can impair evoked release and affect the release pool size.
  • - The findings highlight the nuanced functions of Cpx in synaptic activity, emphasizing its effect on the balance between spontaneous and evoked neurotransmitter release in mouse hippocampal neurons.
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Cholesterol is crucial for neuronal synaptic transmission, assisting in the molecular and structural organization of lipid rafts, ion channels, and exocytic proteins. Although cholesterol absence was shown to result in impaired neurotransmission, how cholesterol locally traffics and its route of action are still under debate. Here, we characterized the lipid transfer protein ORP2 in murine hippocampal neurons.

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Inner hair cells (IHCs) are the primary receptors for hearing. They are housed in the cochlea and convey sound information to the brain via synapses with the auditory nerve. IHCs have been thought to be electrically and metabolically independent from each other.

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Endophilins-A are conserved endocytic adaptors with membrane curvature-sensing and -inducing properties. We show here that, independently of their role in endocytosis, endophilin-A1 and endophilin-A2 regulate exocytosis of neurosecretory vesicles. The number and distribution of neurosecretory vesicles were not changed in chromaffin cells lacking endophilin-A, yet fast capacitance and amperometry measurements revealed reduced exocytosis, smaller vesicle pools and altered fusion kinetics.

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High-throughput neurotransmission at ribbon synapses of cochlear inner hair cells (IHCs) requires tight coupling of neurotransmitter release and balanced recycling of synaptic vesicles (SVs) as well as rapid restoration of release sites. Here, we examined the role of the adaptor protein AP180 (also known as SNAP91) for IHC synaptic transmission by comparing AP180-knockout (KO) and wild-type mice using high-pressure freezing and electron tomography, confocal microscopy, patch-clamp membrane capacitance measurements and systems physiology. AP180 was found predominantly at the synaptic pole of IHCs.

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Ribbon synapses of cochlear inner hair cells (IHCs) operate with high rates of neurotransmission; yet, the molecular regulation of synaptic vesicle (SV) recycling at these synapses remains poorly understood. Here, we studied the role of endophilins-A1-3, endocytic adaptors with curvature-sensing and curvature-generating properties, in mouse IHCs. Single-cell RT-PCR indicated the expression of endophilins-A1-3 in IHCs, and immunoblotting confirmed the presence of endophilin-A1 and endophilin-A2 in the cochlea.

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Toxoplasma gondii infects virtually any nucleated cell type of warm-blooded animals and humans including skeletal muscle cells (SkMCs). Infection of SkMCs by T. gondii, differentiation from the highly replicative tachyzoites to dormant bradyzoites and tissue cyst formation are crucial for parasite persistence in muscle tissue.

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