Erich Hirschberg
University of Wisconsin-Madison
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Science | 1971
Erich Hirschberg; I. Bernard Weinstein
cuneate cells (1, 4), while the P wave has been postulated to be due to prolonged depolarization of the presynaptic terminals of cuneate tract fibers (4, 5, 7). Brief flashes or clicks generated similar N and P waves on the surface of the cuneate nucleus (Fig. 1). In response to photic and acoustic stimuli, however, the N wave (10 msec latency) was more prolonged and the P wave reached its peak at 55 msec and lasted about 80 msec. When a P wave was evoked in the cuneate nucleus in response to conditioning photic or acoustic stimuli, it depressed the test P wave evoked by an ipsilateral cutaneous volley. This P wave depression reached its maximum at conditioning-testing interval of about 50 msec and lasted over 200 msec (Fig. 1). This was similar to the effects on the P wave by conditioning stimulation of the adjacent forelimb nerves (7), the contralateral sensorimotor cortex (7), or remote skin areas in the other limb (11). Another evidence for a visual and auditory influence on the cuneate nucleus was observed by the method of excitability testing (5, 12). Microelectrode stimulation within the cuneate nucleus evoked an antidromic response in the superficial radial nerve consisting of an initial spike complex conducted antidromically over the faster cutaneous nerves and a second spike complex that is analogous to the dorsal root reflex (5). Conditioning photic or acoustic stimuli caused an increase in the initial spike complex and a depression in the secondary spike complex (Fig. 2), with a similar time course for both effects. This time course was also similar to that observed during the P wave interaction just described. These changes and their time courses are suggestive of presynaptic inhibition (5, 11). A third line of evidence was observed from the effects of photic and
Archive | 1971
I. Bernard Weinstein; Erich Hirschberg
Paul Ehrlich, the father of “Molecular Pharmacology”, formulated a strategy of chemotherapy based on designing toxic agents containing binding sites that specifically complex with receptor sites present in the parasite or cell type which is to be attacked (Ehrlich, 1890). Only within the past few years, however, has it become apparent that for certain drugs, including agents closely related structurally to some of the dyestuffs tested by Ehrlich, the cellular receptor site is DNA. One of these compounds is the subject of this report.
Cancer Research | 1952
Erich Hirschberg; Jacob Kream; Alfred Gellhorn
Cancer Research | 1968
Erich Hirschberg; I. Bernard Weinstein; Naola Gersten; Emily Marner; Theodore Finkelstein; Richard A. Carchman
The Journal of General Physiology | 1954
Stanley L. Einhorn; Erich Hirschberg; Alfred Gellhorn
Cancer Research | 1958
Erich Hirschberg
Cancer Research | 1953
Erich Hirschberg; Margaret R. Murray; Edith R. Peterson; Jacob Kream; Raoul Schafranek; J. Lawrence Pool
Cancer Research | 1953
John E. Ultmann; Erich Hirschberg; Alfred Gellhorn
Cancer Research | 1957
Erich Hirschberg; Alfred Gellhorn; William S. Gump
Archive | 1962
Alfred Gellhorn; Erich Hirschberg; C. B. Anfinsen