Digital rat brain: a computerized atlas.

Digital brain mapping provides the techniques required for 3 dimensional (3D) reconstruction and display. This paper describes work which extends the data published in the Paxinos and Watson (1982) atlas of the rat brain to a computerized form. The product of these experiments is a 3D digital neuroanatomic atlas. The data were transformed from 2D outlines to 3D volumes each associated with a specific neuroanatomic structure. The system which manages this transformation also provides tools to manipulate the composition, orientation and appearance of the displays interactively.

Regional distribution of flunitrazepam binding constants: visualizing Kd and Bmax by digital image analysis.

We demonstrate direct visualization of benzodiazepine binding parameters collected in a 3H-flunitrazepam saturation study. In this way the relationship between anatomy and specific binding, Kd and Bmax, can be appreciated. These experiments have resulted in image representations of specific flunitrazepam binding, Kd and Bmax. The images retain the anatomic localization inherent in the original autoradiogram and hence make these parameters amenable to visual survey. Binding constants were consistent with data presented elsewhere in the literature. The image of Bmax showed regional heterogeneity. Kd, on the other hand, was relatively homogeneous. These results demonstrate a means by which autoradiographic binding experiments can be extended to saturation studies without significant loss of data.

Physiology of excitatory synaptic transmission in cultures of dissociated rat hippocampus.

Cultures of dissociated rat hippocampal neurons were used to study the physiology and pharmacology of excitatory synaptic transmission. Rat hippocampal neurons depolarized when they were exposed to the excitatory transmitter candidates, glutamate (Glu) and aspartate (Asp), as well as to the pure excitatory amino acid agonists, N-methyl-D-aspartate (NMDA) and kainate (KA). Quisqualate (QUIS) produced responses in about two-thirds of these cells. Glu responses were much more effectively blocked by the excitatory amino acid antagonists cis-2,3-piperidine dicarboxylic acid (PDA) and gamma-D-glutamylglycine (DGG) than by D-2-amino-5-phosphonovaleric acid (APV) or D-alpha-aminoadipic acid (DAA). Asp depolarizations were depressed by all four antagonists. Monosynaptic excitatory postsynaptic potentials (EPSPs) were only decreased by PDA and DGG. Postsynaptic responses to both Glu and Asp were very voltage dependent, decreasing as the membrane potential was hyperpolarized up to 70 mV below resting levels. The EPSP, however, increased linearly in the hyperpolarized range. NMDA responses were also voltage dependent, while KA and QUIS responses behaved like EPSPs. DGG very effectively blocked KA, but not QUIS, depolarizations. APV, which only partially depressed Glu responses, markedly diminished their voltage sensitivity. These results all suggest that EPSPs in this preparation are produced by Glu acting at KA-type synaptic receptors. Exogenous Glu probably acts at both synaptic KA receptors and extrasynaptic NMDA receptors, which explains why it produces a voltage-dependent response different from the EPSP.