The use of dendrograms to describe the electrical activity of motoneurons underlying behaviors in leeches.

The present manuscript aims at identifying patterns of electrical activity recorded from neurons of the leech nervous system, characterizing specific behaviors. When leeches are at rest, the electrical activity of neurons and motoneurons is poorly correlated. When leeches move their head and/or tail, in contrast, action potential (AP) firing becomes highly correlated.

The dynamics of group formation among leeches.

Leeches exploring a new environment continuously meet each other and merge in temporary groups. After 2-3 h, leeches become attracted to each other eventually forming a large and stable group. When their number is reduced, leeches remain solitary, behaving independently.

The elementary events underlying force generation in neuronal lamellipodia.

We have used optical tweezers to identify the elementary events underlying force generation in neuronal lamellipodia. When an optically trapped bead seals on the lamellipodium membrane, Brownian fluctuations decrease revealing the underlying elementary events. The distribution of bead velocities has long tails with frequent large positive and negative values associated to forward and backward jumps occurring in 0.

Statistical characterization of social interactions and collective behavior in medicinal leeches.

In the present study we analyzed the behavior and interactions among leeches in the same observation tank. Colored beads were glued onto their skin so that their behavior could be followed and quantified. When two or three leeches were present in the observation tank, they searched around for a maximum of 2 h and their motion and behavior were independent from those of their conspecifics.

Force generation in lamellipodia is a probabilistic process with fast growth and retraction events.

Polymerization of actin filaments is the primary source of motility in lamellipodia and it is controlled by a variety of regulatory proteins. The underlying molecular mechanisms are only partially understood and a precise determination of dynamical properties of force generation is necessary. Using optical tweezers, we have measured with millisecond (ms) temporal resolution and picoNewton (pN) sensitivity the force-velocity (Fv) relationship and the power dissipated by lamellipodia of dorsal root ganglia neurons.

Control of GABA Release at Mossy Fiber-CA3 Connections in the Developing Hippocampus.

In this review some of the recent work carried out in our laboratory concerning the functional role of GABAergic signalling at immature mossy fibres (MF)-CA3 principal cell synapses has been highlighted. While in adulthood MF, the axons of dentate gyrus granule cells release onto CA3 principal cells and interneurons glutamate, early in postnatal life they release GABA, which exerts into targeted cells a depolarizing and excitatory action. We found that GABA(A)-mediated postsynaptic currents (MF-GPSCs) exhibited a very low probability of release, were sensitive to L-AP4, a group III metabotropic glutamate receptor agonist, and revealed short-term frequency-dependent facilitation.

Sequential steps underlying neuronal plasticity induced by a transient exposure to gabazine.

Periods of intense electrical activity can initiate neuronal plasticity leading to long lasting changes of network properties. By combining multielectrode extracellular recordings with DNA microarrays, we have investigated in rat hippocampal cultures the temporal sequence of events of neuronal plasticity triggered by a transient exposure to the GABA(A) receptor antagonist gabazine (GabT). GabT induced a synchronous bursting pattern of activity.

Increased spontaneous activity of a network of hippocampal neurons in culture caused by suppression of inhibitory potentials mediated by anti-gad antibodies.

Introduction: Anti-glutamic acid decarboxylase autoantibodies (GAD-Ab) are commonly considered the marker of autoimmune diabetes; they were first described in patients affected by stiff-person syndrome and recently, in ataxic or epileptic patients. The pathogenetic role of GAD-Ab remains unclear but inhibition of GABA synthesis or interference with GABA exocytosis are hypothesized. The aim of the study was to assess whether GAD-Ab interfere with neuronal transmission.