Rat cerebral cortex showing autoradiographically labeled nerve fibers that appear as whitish bands by dark-field illumination through the microscope. The radiolabeled amino acid marker was injected into the thalamic laterodorsal nucleus, a member of the so-called nonspecific thalamic nuclei that send axons to superficial and deep layers of widespread areas of cortex, providing the anatomical basis for integration of cortical responsiveness. The cortical areas shown are the primary visual cortex (area 17, with axonal termination in layers I and V) surrounded by secondary visual cortex (area 18, with axonal termination in layers I and IV).

The distribution of opiate receptors, labeled with tritiated naloxone, in the striatum (caudate-putamen and accumbens) of the rat brain. The image was produced on tritium-sensitive film and captured by a computer that generated colors in accordance with receptor density. The study showed the registration of opiate receptor-dense patches, acetylcholinesterase-poor "striosomes," and axonal projections from the thalamus.

Opiate receptors marked by tritiated naloxone in rhesus monkey cortex showing laminar patterns of receptor distribution in visual cortex (area 17) and surrounding area 18. The layering of receptor densities changed abruptly at the border of the two cortical areas.

A paradigm for showing delayed effects of therapeutic antidepressant drug treatment at the molecular level is demonstrated. Animals given daily therapeutic doses of imipramine showed changes in gene expression for key neurotransmitters and enzymes in key anatomically defined areas that are thought to be important in responding to stressful stimuli. The changes were seen only after long-term (8 weeks) administration. The delay in change in levels of gene expression is significant because clinically effective antidepressant treatments are associated with similar delays in onset of efficacy. The picture shows glucocorticoid receptor mRNA expression in the hippocampus, a site implicated in negative feedback control of the stress axis.

Horizontal section of rat brain showing the distribution of cannabinoid receptors labeled by a tritiated synthetic cannabinoid drug. This study was the first complete description of the pattern of distribution of the receptors for marijuana and other cannabinoid drugs in the rat brain. High levels of receptors were seen in the basal ganglia, hippocampus, and cerebellum. These areas are known to be involved in movement control and memory formation.

Article called "Smoking out the marijuana receptor" summarized the recent avalanche of scientific findings about the nature of the cannabinoid receptor. The picture showed cannabinoid receptors in the hippocampus. The film image was color-coded by the computer.

Article in Science News summarizing recent studies of the characterization, localization, and cloning of the cannabinoid receptor. The hippocampal image was color coded sing a different color scale.

Expression of CRH mRNA in the hypothalamic paraventricular nucleus (PVN) is decreased in aged rats. The technique of in situ hybridization histochemistry was used to show that neurons in the PVN express lower levels of the mRNA for the important neurotransmitter in old rats. CRH regulates levels of cortisol in the blood.

Article about the mRNA expression of the fragile X gene in the hippocampus following several experimental manipulations that alter levels of neural activity. The picture shows Golgi-stained neurons of the dentate gyrus. These are called granule cells, and they show plastic changes associated with learning and memory.

Localization of cannabinoid receptors in the spinal cord. The paper was part of a series of studies localizing cannabinoid receptors to key sensory way-stations that process nociception that we perceive as pain.

Article about the localization of cannabinoid receptor mRNA (CB1) bearing neurons colocalized with enkephalin and dynorphin mRNA-positive projection neurons in the rat caudate-putamen. The potential role of cannabinoids in movement control was the underlying basis for the study.

In this study, the herbal product St. John's wort was shown to have many effects on neuronal gene transcription in brain stress circuits that are the same as the changes caused by the prototypic antidepressant drug imipramine when administered to rats in a therapeutic regimen of daily administration for 8 weeks. The illustration shows corticotropin releasing hormone (CRH) mRNA expression in the hypothalamic paraventricular nucleus (PVN) of the rat.

An anti-neuronal autoimmune reaction was achieved by immunizing Lewis rats with peptides from the brain-type cannabinoid receptor. The image shows an immune reaction in the cerebellum where dense cannabinoid receptors reside. This is the first demonstration of a cell-mediated autoimmune attack against neuronal elements and is therefore a model of suspected anti-neuronal autoimmune diseases such as Tourette's syndrome, Sydenham's chorea, and Rasmussen's encephalitis.