1. Multiple-barreled microelectrodes were used to record from neurons in the area postrema of anesthetized dogs and to test the responses of the neurons to a variety of substances in this structure, which is known to function as the chemoceptive trigger zone for emesis. 2. The neurons in area postrema were silent at rest but could be "found" by virtue of their response to ionophoretic glutamate. The glutamic response was brief and of short latency with high frequency of discharge. 3. Dog area postrema neurons were also excited by over 20 other substances, including acetylcholine, the biogenic amines, several peptides, and at least two hormones. Not all agents were excitatory, however. 4. The responses to all excitatory agents except glutamate were similar and unusual. All responses showed a relatively long latency (3-20 s), a long duration of excitation (30 s to many minutes), and a low discharge frequency (1-3 Hz). 5. There was a good correlation between substances that were excitatory on area postrema neurons and substances known to cause emesis. Because emesis due to intravenous application of these substances is known to be abolished in animals with ablation of the area postrema, it is very likely that recordings were from the neurons which trigger the response. 6. Because so many substances elicit the same type of response there is a possibility that all utilize a common second messenger. Neurons were not excited by ionophoresis of guanosine 3',5'-cyclic monophosphate (cGMP) but were excited by 8-bromo-adenosine 3',5'-cyclic monophosphate (cAMP) and by forskolin, an activator of adenylate cyclase. 7. Behavioral studies were performed looking for emetic responses in awake dogs following intravenous injection of apomorphine, insulin, angiotensin II, and leucine enkephalin. For each a threshold concentration could be determined, which would consistently evoke emesis. 8. Dogs pretreated with phosphodiesterase inhibitors (theophylline, 3-isobutyl-1-methylxanthine, or RO 1724) showed a shift in the threshold concentration of the above substances that triggered emesis, such that emesis was evoked by lower concentrations than in the control. 9. These results suggest that neurons of the dog area postrema trigger the emetic reflex in response to specific receptors for a great variety of transmitters, peptides, and hormones, and that these receptors act through a common second messenger, cAMP.

Brains fixed in paraformaldehyde or in Clarke's solution were blocked coronaily. Blocks from brains fixed in paraformaldehyde were either frozen in liquid nitrogen or embedded in paraffin. Tissue fixed in Clarke's solution was embedded in paraffin. Sections from each block were stained by the peroxidase-antiperoxidase method for adenosine deaminase or complexing protein using affinity-purified goat antibodies. Adenosine deaminase and complexing protein did not co-localize. Adenosine deaminase was detected in oligodendroglia and in endotheial cells lining blood vessels, whereas complexing protein was concentrated in neurons. The subcellular location and appearance of the peroxidase reaction product associated with individual cells was also quite distinctive. The cell bodies ofadenosine deaminase-positive oligodendroglia were filled with intense deposits ofperoxidase reaction product. In contrast to oligodendroglia, the reaction product as-If the regulatory actions of adenosine depend on binding to cell surface receptors, it seems reasonable that the concentration ofextracellular adenosine should also be subject to regulation. Wu and Phillis (1984) have suggested that uptake and metabolism of

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A study was made to determine the efferent projections of the subthalamic nucleus in the monkey. Because of the impossibility of producing lesions in this nucleus, not involving adjacent structures, lesions were produced by different stereotaxic approaches. Comparisons were made with degeneration resulting from localized lesions in substantia nigra and globus pallidus. Degeneration resulting from these lesions was studied in transverse and sagittal sections stained by the NautaGygax method.Efferent fibers from the subthalamic nucleus pass through the internal capsule into the medial pallidal segment; a few fibers are distributed to the lateral pallidum. Some subthalamic efferent fibers pass to the contralateral globus pallidus via the dorsal supraoptic decussation, but none projection to the thalamus.Nigral efferent fibers project to parts of the ventral anterior (VAmc) and ventral lateral (VLm) thalamic nuclei. The medial pallidal segment gives fibers to: (1) ventral anterior (VA), ventral lateral (VLo) and centromedian (CM) thalamic nuclei, and (2) the pedunculopontine nucleus. The lateral pallidal segment projects exclusively to the subthalamic nucleus. Thalamic projections of the substania nigra and globus pallidus are distinctive. Subthalarnic projections to the globus pallidus are more profuse than those of the substantia nigra.Subthalamic dyskinesia, due to lesions in the subthalamic nucleus, is a consequence of removal of inhibitory influences acting upon the medial segment of the globus pallidus.The following hypothesis is presented:Clinicopathological reports (Martin, '27; Whittier, '47; Juba, '65) and experimental studies (Whittier and Mettler, '49b; Carpenter, Whittier and Mettler, '50; Carpenter, '61) indicate that discrete lesions in the subthalamic nucleus, which fulfill certain criteria, almost invariably results in severe dyskinesia in the contralateral extremities. This dyskinesia, the most forceful and violent variety known, has been referred to as hemiballism or hemichorea. Experimental studies in the monkey (Carpenter, Whittier and Mettler, '50; Carpenter, '61) suggest that this dyskinesia is the physiological expression of removal of inhibitory influences that normally act upon the neurons of the globus pallidus. This thesis is supported by the fact that lesions in the medial segment of the globus pallidus abolish or ameliorate the dyskinesia. Lesions in the ventral lateral nucleus of the thalamus also can reduce or abolish this form AM. J. ANAT., 121: 41-72.of dyskinesia (Martin and McCaul, '59; Andy and Brown, '60) presumably by interruption of pallidothalamic fiber systems and thalamocortical projections.Although a number of studies (Carpenter and Brittin, '58; Carpenter, Correll and Hinman, '60; Strominger and Carpenter, '65; Carpenter, Strominger and Weiss, '65; Stein and Carpenter, '65) have been done to establish structures involved in the neural mechanism of this dyskinesia in the monkey, many questions remain unanswered. A full understanding of the basic neural me...