E-neuroforum 

Abstract: Neural stem cells in various regions of the vertebrate brain continuously generate neurons throughout life1,2,3,4. In the mammalian hippocampus, a region important for spatial and episodic memory5,6, thousands of new granule cells are produced per day7, with the exact number depending on environmental conditions and physical exercise1,8. The survival of these neurons is improved by learning and conversely learning may be promoted by neurogenesis8,9,10. Although it has been suggested that newly generated neurons may have specific properties to facilitate learning2,10,11, the cellular and synaptic mechanisms of plasticity in these neurons are largely unknown. Here we show that young granule cells in the adult hippocampus differ substantially from mature granule cells in both active and passive membrane properties. In young neurons, T-type Ca2+ channels can generate isolated Ca2+ spikes and boost fast Na+ action potentials, contributing to the induction of synaptic plasticity. Associative long-term potentiation can be induced more easily in young neurons than in mature neurons under identical conditions. Thus, newly generated neurons express unique mechanisms to facilitate synaptic plasticity, which may be important for the formation of new memories.

Abstract: Understanding how neural activity in sensory cortices relates to perception is a central theme of neuroscience. Action potentials of sensory cortical neurons can be strongly correlated to properties of sensory stimuli and reflect the subjective judgements of an individual about stimuli. Microstimulation experiments have established a direct link from sensory activity to behaviour, suggesting that small neuronal populations can influence sensory decisions. However, microstimulation does not allow identification and quantification of the stimulated cellular elements. The sensory impact of individual cortical neurons therefore remains unknown. Here we show that stimulation of single neurons in somatosensory cortex affects behavioural responses in a detection task. We trained rats to respond to microstimulation of barrel cortex at low current intensities. We then initiated short trains of action potentials in single neurons by juxtacellular stimulation. Animals responded significantly more often in single-cell stimulation trials than in catch trials without stimulation. Stimulation effects varied greatly between cells, and on average in 5% of trials a response was induced. Whereas stimulation of putative excitatory neurons led to weak biases towards responding, stimulation of putative inhibitory neurons led to more variable and stronger sensory effects. Reaction times for single-cell stimulation were long and variable. Our results demonstrate that single neuron activity can cause a change in the animal's detection behaviour, suggesting a much sparser cortical code for sensations than previously anticipated.

Abstract: Desert ants, Cataglyphis, navigate in their vast desert habitat by path integration. They continuously integrate directions steered (as determined by their celestial compass) and distances traveled, gauged by as-yet-unknown mechanisms. Here we test the hypothesis that navigating ants measure distances traveled by using some kind of step integrator, or "step counter." We manipulated the lengths of the legs and, hence, the stride lengths, in freely walking ants. Animals with elongated ("stilts") or shortened legs ("stumps") take larger or shorter strides, respectively, and concomitantly misgauge travel distance. Travel distance is overestimated by experimental animals walking on stilts and underestimated by animals walking on stumps.

Abstract: Neurotrophine sind Proteine, die, ähnlich wie Nervenwachstumsfaktoren, die Entwicklung, das Überleben und Funktionieren von Neuronen gewährleisten bzw. fördern (Barde 1989). Dafür binden die Neurotrophine an Rezeptoren in der neuronalen Membran, die zu der Familie der Tyrosin-Rezeptor-Kinasen (Trk) gehören. Christine Rose und weitere Mitglieder der Arbeitsgruppe von Arthur Konnerth vom Physiologischen Institut der LM Universität München haben in ihrem Artikel jetzt eine neue Rolle dieser Proteine beschrieben, und zwar bei dem Dialog wenig von dem vollständigen TrkB-Rezeptor exprimieren, dafür aber um so mehr von dem verkürzten Rezeptor TrkB-T1. BDNF löst in Gliazellen über diesen verkürzten Rezeptor eine Signalkaskade aus, die nicht eine Tyrosinkinase aktiviert (die fehlt ja eben bei diesen Rezeptoren), sondern, wie viele Liganden metabotroper Rezeptoren, an ein G-Protein gekoppelt ist. So konnte erstmals gezeigt werden, dass auch die unvollständigen TrkB-T1-Rezeptoren funktionelle Rezeptoren darstellen, die, zumindest in Gliazellen, eine Signalkaskade in Gang setzen.