Golgi cell afterhyperpolarization [13], unless one can assume mechanisms which prolong the effect of each Golgi cell spike. While the synaptic GABAA channels already have relatively slow kinetics, the much slower spillover mechanism seems well suited to having a function in gain control. As a result of spillover, increased Golgi cell activity -- through either direct mossy fiber activation or indirect parallel fiber activation -- will reduce excitability of all granule cells participating in a glomerulus. This would provide for rather a slow gain control mechanism, which may not prevent fast swings in granule cell activity [13]. But how does the stronger tetrodotoxin-resistant tonic inhibition fit into this picture? It could provide a constant baseline, raising the threshold for spike initiation in granule cells. But if this is desired, it seems more straightforward to reduce the intrinsic excitability of granule cells, as observed in transgenic mice that lack the GABAA receptor 6 and subunits and so have no tonic current [18]. A more attractive idea is that tonic inhibition itself is regulated somehow. This could occur at the receptor side, for example by phosphorylation depending on subunit expression [19], or by changing the baseline GABA concentration in the glomerulus. Reduced tonic inhibition may explain the evidence for spike-mediated inhibition in vivo [13, 17], which is difficult to reconcile with the in vitro observation that only 3% of the GABAA current is spike mediated [1]. If tonic inhibition is regulated, it could have additional effects beyond controlling information flow through the cerebellum. Long-term potentiation LTP ; of mossy fiber-to-granule cell synapses can only be reliably evoked in vitro when inhibition is blocked [20]. Any mechanism that reduces tonic inhibition will enhance LTP of this synapse. If it turns out that extrasynaptic inhibition can be regulated separately in each individual glomerulus, there could be very interesting implications for the possible computational functions of the glomerulus and testosterone. Assessing the practical burdens on poor countries of administering patent systems and resolving disputes over rights. National governments need to develop mechanisms to ensure funding for research and development for neglected diseases Innovative approaches to stimulating research in essential medicines need to be devised, including: Increased public and donor funding of health care research. Compulsory research obligations, such as requirements that companies reinvest a percentage of pharmaceutical sales into research and development , either directly or through public or private sector research and development programmes. Development of a "Neglected Disease Act" that could be used to stimulate private investment for communicable disease vaccines and medicines.