The cerebellar interneuron network
Interneurons (stellate and basket cells) of the molecular layer are interconnected by gabaergic synapses. This network is functionnally isolated in slice preparations because excitatory inputs are inactive. We are studying this network in detail, focussing on the excitability of interneurons, on synaptic interactions (Chavas and Marty, 2003), on the characterisation of parameters governing release at these synapses (Auger and Marty, 1997; Kondo and Marty, 1998a; Auger and Marty, 2000) and on modulations through neuroamines (Kondo and Marty, 1997; 1998b).

Retrograde signalling at interneuron-> Purkinje synapses
We have found that, following a calcium elevation in Purkinje cells, the strength of incoming GABAergic synapses is sequentially inhibited and excited (Llano, Leresche and Marty, 1991; Vincent, Armstong and Marty, 1992). The initial effect has been called Depolarization-induced Suppression of Inhibition (DSI).It is due to the emission of a retrograde messenger which has recently been identified as an endogenous cannabinoid (Diana and al., 2002). The second effect, rebound potentiation, is due to an augmentation of the sensitivity of the Purkinje cell to GABA. We are currently investigating the cellular mechanisms underlying DSI (Diana and Marty, 2003; Galante and Diana, 2004).

Presynaptic calcium stores
Work from the laboratory has shown that MLI terminals contain ryanodine-sensitive calcium stores, and that these stores give rise to spontaneous calcium transients (that we called ScaTs). SCaTs are in turn responsible for large amplitude, multivesicular miniature currents (´maximinis´: Llano et al., 2000). We showed that presynaptic calcium stores regulate evoked synaptic transmission by examining the effects of drugs which interfere with calcium stores on the efficiency of interneurone-Purkinje cell synapses (Galante and Marty, 2003).

Autoreceptors and presynaptic receptors
We have recently shown that, following the release of GABA from interneuron terminals, GABA binds to axonal receptors located on the releasing cell and elicits GABAA (bicuculline-sensitive) currents (Pouzat and Marty, 1999). We are presently studying the functional role of these autoreceptor currents (Mejia-Gervacio and Marty, 2006).

Osmotic GABA response
Following sustained (>1 s) activation of ionotropic GABA receptors, MLIs display a calcium response. Contrary to current theories in other systems, we found that this calcium rise is not mediated by voltage dependent calcium channels (Chavas et al., 2004). Since it is associated with an expansion of the size of dendrites, we propose that it arises from osmotic unbalance following accumulation of Cl- ions, and is part of the regulatory volume decrease reaction of the cell. For this reason we call it the osmotic GABA response. This response may reveal a completely novel facet of neuronal signalling, and is presently under intensive study in the group.

Stell BM, Rostaing P, Triller A, Marty A (2007):Activation of presynaptic GABAA receptors induces glutamate release from parallel fiber synapses..J. Neurosc. 27:9022-9031.

Mejia-Gervacio S, Collin T, Pouzat C, Tan YP, Llano I and Marty A (2007):Axonal speeding: Shaping synaptic potentials in small neurons by the axonal membrane compartment..Neuron. 53:843-855.

Mejia-Gervacio S, Marty A (2006):Autoregulation of neuronal activity by presynaptic GABAARs..Physiology News 64:19-20.

Mejia-Gervacio S, Marty A (2006):Control of interneuron firing pattern by axonal autoreceptors in the juvenile rat cerebellum..J. Physiol. 571:43-55.

Collin T, Marty A , Llano I (2005):Presynaptic calcium stores and synaptic transmission..Curr. Opin. Neurobiol. 15:275-281.