Building a virtual archive using brain architecture and Web 3D to deliver neuropsychopharmacology content over the Internet.

The vast amount of heterogeneous data generated in various fields of neurosciences such as neuropsychopharmacology can hardly be classified using traditional databases. We present here the concept of a virtual archive, spatially referenced over a simplified 3D brain map and accessible over the Internet. A simple prototype (available at http://aquatics.crs4.it/neuropsydat3d) has been realized using current Web-based virtual reality standards and technologies. It illustrates how primary literature or summary information can easily be retrieved through hyperlinks mapped onto a 3D schema while navigating through neuroanatomy. Furthermore, 3D navigation and visualization techniques are used to enhance the representation of brain's neurotransmitters, pathways and the involvement of specific brain areas in any particular physiological or behavioral functions. The system proposed shows how the use of a schematic spatial organization of data, widely exploited in other fields (e.g. Geographical Information Systems) can be extremely useful to develop efficient tools for research and teaching in neurosciences.

Gamma-hydroxybutyric acid (GHB) and the mesoaccumbens reward circuit: evidence for GABA(B) receptor-mediated effects.

Gamma-hydroxybutyric acid (GHB) is a short-chain fatty acid naturally occurring in the mammalian brain, which recently emerged as a major recreational drug of abuse. GHB has multiple neuronal mechanisms including activation of both the GABA(B) receptor, and a distinct GHB-specific receptor. This complex GHB-GABA(B) receptor interaction is probably responsible for the multifaceted pharmacological, behavioral and toxicological profile of GHB. Drugs of abuse exert remarkably similar effects upon reward-related circuits, in particular the mesolimbic dopaminergic system and the nucleus accumbens (NAc). We used single unit recordings in vivo from urethane-anesthetized rats to characterize the effects of GHB on evoked firing in NAc "shell" neurons and on spontaneous activity of antidromically identified dopamine (DA) cells located in the ventral tegmental area. GHB was studied in comparison with the GABA(B) receptor agonist baclofen and antagonist (2S)(+)-5,5-dimethyl-2-morpholineacetic acid (SCH50911). Additionally, we utilized a GHB analog, gamma-(p-methoxybenzil)-gamma-hydroxybutyric acid (NCS-435), devoid of GABA(B) binding properties, but with high affinity for specific GHB binding sites. In common with other drugs of abuse, GHB depressed firing in NAc neurons evoked by the stimulation of the basolateral amygdala. On DA neurons, GHB exerted heterogeneous effects, which were correlated to the baseline firing rate of the cells but led to a moderate stimulation of the DA system. All GHB actions were mediated by GABA(B) receptors, since they were blocked by SCH50911 and were not mimicked by NCS-435. Our study indicates that the electrophysiological profile of GHB is close to typical drugs of abuse: both inhibition of NAc neurons and moderate to strong stimulation of DA transmission are distinctive features of diverse classes of abused drugs. Moreover, it is concluded that addictive and rewarding properties of GHB do not necessarily involve a putative high affinity GHB receptor.