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• W2004331010 abstract "In 1979, Joshua Lederburg, recently appointed president of Rockefeller University, was in recruiting mode. Based on his long-term interest in the brain and psychiatry, Josh approached me with an attractive offer for myself and my colleagues Joe Coyle and Mike Kuhar. I visited our Dean, Richard Ross, to say goodbye, as I knew that Hopkins could never provide us Rockefeller-like resources. While Ross couldn't match the Rockefeller offer for a professor, he had an alternative proposal. Years earlier, an advisory committee had recommended that Hopkins establish a Department of Neuroscience. Dr. Ross suggested a mini-department comprised solely of myself, Coyle, and Kuhar, which might integrate Hopkins neuroscience. In contrast to the tens of millions of dollars provided nowadays as dowries for new departmental directors, the Dean offered only a modest annual budget that could be “saved” for the three years till a single floor would become available for our department. Dan Nathans, Director of Microbiology and a valued confidant, advised that a new department must be done “right” so I should ask for triple the offered space. The Dean agreed, and on July 1, 1980, our department commenced operations. Today, Neuroscience is the largest basic science department at Hopkins. Our faculty has done well. Among present and emeritus members, three of our primary faculty have been elected to the National Academy of Sciences, four are fellows of the Academy of Arts and Sciences, two of the American Philosophical Society, two have received the Lasker Award, two the National Medal of Science, and various faculty members have accumulated more than 13 honorary doctorates. Science citation analysis indicates that of the eight most highly cited Johns Hopkins medical scientists, five are appointed in our department. For the decade 1989–1998, four of the world's 16 most highly cited neuroscientists were from Hopkins, with no other institution having more than one. But neuroscience at Hopkins did not begin in 1980. Johns Hopkins has a long tradition of contributions in the field. More than most other institutions, Hopkins’ efforts in the neurosciences encompass clinical as well as basic science. Let me relate some of these in a brief panorama that is not meant to be exhaustive but merely to illustrate a few major themes, especially the breadth of research and the uniquely collegial relationships of Hopkins neuroscientists. The founding fathers of Hopkins were giants in American medicine, with William Welch, the first Dean, orchestrating these talents and himself making major contributions to pathology. William Osler defined the field of internal medicine, and William Halstead inaugurated modern surgery. There was no Neurology Department nor even a neurology division of Medicine. Neurosurgery remained a subdivision of the surgery department for almost 70 years till Donlin Long was appointed the director of a new Neurosurgery Department. In 1906, Harvey Cushing was appointed the first head of neurosurgery at Hopkins (Figure 1). He revolutionized pituitary surgery and, by carefully monitoring symptoms following removal of pituitary tumors, he was able to elucidate the role of excess or deficient secretion of the anterior pituitary and to confirm his clinical observations with studies in animals (Cushing, 1909Cushing H. The hypothesis cerebri: Clinical aspects of hyperpituitarism and of hypopituitarism.JAMA. 1909; 53: 249-255Crossref Scopus (39) Google Scholar). He showed that hormonally active tumors arising in young people lead to gigantism and, in adults, to acromegaly. Walter Dandy succeeded Cushing as head of the neurosurgery division. In 1913, he elucidated the circulation of cerebrospinal fluid (CSF), showing how selective blockade leads to hydrocephalus (Dandy and Blackfan, 1913Dandy W. Blackfan K. An experimental and clinical study of internal hydrocephalus.JAMA. 1913; 61: 2216-2217Crossref Scopus (85) Google Scholar). In dogs, obstructing the Sylvian Aqueduct caused dilation of the third and lateral ventricles, while blocking the Foramen of Monro elicited a similar ballooning of the lateral ventricle. In the same study, he provided the first definitive evidence that the choroid plexus elaborates CSF, as its removal prevented hydrocephalus. He discovered how CSF is absorbed into subarachnoid blood vessels. He extended this basic research into patients, observing that every case of “idiopathic hydrocephalus” was associated with obstruction of the Sylvian Aqueduct or one of the critical foramina. Even more important was Dandy's development in 1918 of pneumoencephalography, conceptualized when he noticed in the chest X-ray of a patient with a perforated intestine, free air outlining the structure of various abdominal viscera. Might injected air outline the cerebral ventricles? In short-order he injected gas into the cerebral ventricles, inaugurating pneumoencephalography, which, until the advent of CAT scans, remained the most powerful means of identifying brain tumors and other abnormalities (Dandy, 1918Dandy W. Ventriculography following the injection of air into the cerebral ventricles.Ann. Surg. 1918; 68: 5-11Crossref PubMed Google Scholar). Systems neuroscience began with operative ablation of various brain regions to mimic abnormalities associated with brain tumors or surgical removal of brain tissue to cope with injuries or epilepsy. Phillip Bard, the fourth Director of Physiology at Hopkins, arrived in Baltimore in 1933 following training at Harvard with Walter Cannon. Work in Cannon's laboratory had revealed that disconnecting the cerebral cortex from the brainstem of cats elicited rage responses. As these responses were not associated with “real” anger and were not directed toward the triggering stimulus, they were designated “sham rage.” At Hopkins, Bard attempted to localize the specific brain regions responsible for sham rage. After decorticating cats to elicit rage, he made various transactions through the brain stem. Successive transactions in a caudal direction failed to alter sham rage until he cut through the posterior hypothalamus. Directed posterior hypothalamic lesions eliminated sham rage, while electrical stimulation in this region caused rage. This work lead to conceptualizations of emotional behavior determined by the limbic system of brain structures. Bard soon realized that behavioral observations were insufficient to clarify brain function and that electrical recordings would be critical. In 1933, Ralph Gerard, working at the University of Chicago, had identified cerebral action potentials, and, with Wade Marshall, he employed this approach to characterize sensory activity in the cerebral cortex. In the late 1930s, Marshall moved to Hopkins, and, with Bard and Clinton Woolsey, he developed technology for measuring evoked cortical potentials and mapped the sites for cutaneous touch sensation on the primate postcentral gyrus (Marshall et al., 1937Marshall W. Woolsey S. Bard P. Cortical representation of tactile sensibility as indicated by cortical potentials.Science. 1937; 85: 388-390Crossref PubMed Scopus (54) Google Scholar). Vernon Mountcastle, Bard's successor in 1964 as Director of Physiology, took up the challenge of mapping the somatic sensory system with greater refinement. In the mid-1950s, utilizing newly developed microelectrodes that permitted single-cell recoding, Mountcastle discovered that submodalities of touch and pressure sensation were localized to vertical columns running from the surface of the brain to underlying white matter. All cells in an individual column responded to selective sites on the skin and to either superficial or deep pressure (Mountcastle, 1957Mountcastle V. Modality and topographic properties of single neurons of cat's somatic sensory cortex.J. Neurophysiol. 1957; 20: 408-434PubMed Google Scholar). This columnar organization is now appreciated as a universal organizing principle of brain function. At about the same time that Mountcastle was doing his pioneering work in the Physiology Department, Stephen Kuffler spent 12 years in a laboratory in the basement of the Ophthalmology Department. In one body of work, he characterized synaptic inhibition in stretch receptor neurons of crustacea, which led to subsequent work of his later colleagues David Potter and Edward Kravitz establishing GABA as the principal inhibitory neurotransmitter. Perhaps Kuffler's most important contribution was his discovery of center-surround interactions in the retina (Kuffler, 1952Kuffler S. Neurons in the retina: Organization, inhibition and excitation problems.Cold Spring Harb. Symp. Quant. Biol. 1952; 17: 281-292Crossref PubMed Scopus (103) Google Scholar). Utilizing a multibeam ophthalmoscope that had been developed in the Ophthalmology Department, he recorded from single retinal ganglion cells and observed diametrically opposite responses depending on whether light impacted the central or peripheral field. In 1959, Kuffler moved to Harvard where in 1966 he established a Department of Neurobiology. Torsten Wiesel and David Hubel joined Kuffler at Hopkins in the mid-1950s, initially working on the retina and then turning their attention to the visual cortex. They discovered center-surround and other organizational principles in the cortex (Hubel and Wiesel, 1959Hubel D. Wiesel T. Receptive fields of single neurones in the cat's striate cortex.J. Physiol. 1959; 148: 574-591PubMed Google Scholar). Most importantly, they detected parallel receptive fields for neighboring cells in the visual cortex, pointing to a universal role for Mountcastle's concept of columnar organization of the cerebral cortex. They moved with Kuffler to Harvard in 1959 where they continued their elegant assessment of how visual information is organized in the cortex, leading to their receipt of the Nobel Prize for Physiology or Medicine in 1981. Psychiatry provides the ultimate systems approach to the brain and behavior. Adolph Meyer was the first Director of Psychiatry at Hopkins. In the Henry Phipps Psychiatric Clinic, which opened in 1913, Meyer inaugurated an unprecedented approach to psychiatry with laboratories of neuroanatomy, neurophysiology, and behavior and a clinical program that emphasized a comprehensive approach to each patient integrating psychological and biological factors, an essentially new discipline that he dubbed “psychobiology” (Meyer, 1915Meyer A. Objective psychology or psychobiology with subordination of the medically useless contrast of mental and physical.JAMA. 1915; 65: 860-863Crossref Scopus (21) Google Scholar). Among the early scientists Meyer recruited was John Watson, the founder of behaviorism. Watson did not remain long at Hopkins, his principal contribution being his graduate student Curt Richter who, when Watson left, took over the laboratory and remained in it for about 70 years. Among his many contributions, Richter developed precise means for monitoring all aspects of a rat's life in a laboratory using a cage containing a running wheel to assess temporal aspects of activity initiation. With this simple but elegantly powerful system, Richter explored the molecular and neuroanatomical regulation of the “biological clock” (Richter, 1960Richter C. Biological clocks in medicine and psychiatry.Proc. Natl. Acad. Sci. USA. 1960; 46: 1506-1530Crossref PubMed Google Scholar). In 1965, when I arrived at Johns Hopkins for psychiatry residency, one of my first visits was to Richter's laboratory. I had worked with Julie Axelrod at the NIH on circadian rhythms in the serotonin content of the pineal gland and sought Richter's advice. He showed me his experiments making discrete brain lesions to localize the clock, which he had narrowed down to a small area in the hypothalamus. Because of his obsessive drive to “be sure” of his results, he did not publish these findings, although his lesions, in the vicinity of the suprachiasmatic nucleus, anticipated the discovery years later by Robert Moore of this nucleus as the locus of the mammalian “clock.” Richter's contributions were remarkably diverse. For instance, he pioneered the notion that rodents will self-select an optimal diet and, in this way, he established the minimal daily requirement for vitamins and minerals (Richter et al., 1938Richter C. Holt L.J. Barelar B.J. Nutritional requirements for normal growth and reproduction in rats studied by the self-selection method.Am. J. Physiol. 1938; 122: 734-744Google Scholar). His work on the galvanic skin response was critical in the evolution of the lie detector test. W. Horsley Gantt, a contemporary of Richter's in the Psychiatry Department, studied with Ivan Pavlov and was a pioneer in introducing Pavlovian psychiatry into the United States. He utilized Pavlov's techniques to develop models of mental illness in dogs. For his contributions, he received a Lasker Award in 1946, the inaugural year of these prizes. Today, most cellular-molecular neuroscience research employs tissue culture as routine methodology. The first successful use of tissue culture employed neurons and was carried out at Johns Hopkins by Ross G. Harrison (Harrison, 1907Harrison R. Observations on the living developing nerve fiber.Proc. Soc. Exp. Biol. Med. 1907; 4: 140-143Crossref Scopus (242) Google Scholar). At the time of this research in 1907, the cellular source of neuronal fibers was not at all clear. Harrison placed small portions of frog embryo spinal cords in lymph on a microscope slide and was able to observe clearcut neuronal sprouting. In 1917, the Nobel Prize Committee voted to award the prize in Physiology or Medicine to Harrison but ultimately did not award a prize that year. Research underlying the Nobel Prize in 1956 for the growth of polio virus in kidney cell cultures did employ Harrison's methodology. Harrison's innovations in tissue culture at Hopkins were continued by George Gey (Gey et al., 1952Gey G. Coffman W. Kubicek M. Tissue culture studies of the proliferative capacity of cervical carcinoma and normal epithelium.Cancer Res. 1952; 12: 264-265Google Scholar). Utilizing a cervical tumor from Henrietta Lacks, Gey created the HeLa cell line, which to this day is the most widely employed tissue culture preparation and was particularly valuable for growing the three types of polio virus. Gey made myriad advances in tissue culture, including the use of collagen as substratum and the roller-tube technique used by John Enders for his Nobel Prize-winning cultivation of the polio virus. The crucial research for growing polio virus in tissue culture took place at Johns Hopkins in the laboratory of David Bodian, who also employed some of Gey's procedures. Bodian was able to differentiate nerve cells that were resistant or sensitive to viral infection, laying the groundwork for much polio vaccine research (Bodian, 1955Bodian D. Emerging concept of poliomyelitis infection.Science. 1955; 122: 105-108Crossref PubMed Scopus (162) Google Scholar). At that time, large numbers of viral strains had been identified, but it wasn't clear which were relevant for vaccine development. Bodian established that there were only three major immunologic forms of the virus, permitting development of a practical vaccine. Besides his work on the polio virus, Bodian, who served as Director of the Anatomy Department, was one of the world's great neuroanatomists. Utilizing his staining technique, the “Bodian Stain,” he identified the existence of neurofilaments. Because of his interest in spinal cord defects in polio, he focused on the ultrastructure of neurons in the spinal cord and was the first to obtain strong evidence that spherical synaptic vesicles were associated with excitation and flat vesicles with synaptic inhibition (Bodian, 1966Bodian D. Electron microscopy: Two major synaptic types on spinal motorneurons.Science. 1966; 151: 1093-1094Crossref PubMed Scopus (141) Google Scholar). John Jacob Abel founded the Department of Pharmacology at Hopkins. Based on his strong background in chemistry, Abel attempted to isolate biologically active substances. One of his first triumphs was the identification of epinephrine as the hormone of the adrenal medulla (Abel and Crawford, 1897Abel J.J. Crawford A. On the blood-pressure raising constituent of the suprarenal capsule.Trans. Assoc. Am. Phys. 1897; 12: 461Google Scholar). Much later in his career, he obtained the first crystals of insulin, establishing its protein nature (Abel, 1926Abel J.J. Crystalline insulin.Proc. Natl. Acad. Sci. USA. 1926; 12: 132-136Crossref PubMed Google Scholar). As with some of the other early departmental directors at Hopkins', Abel set standards for the rest of the country. He regarded pharmacology primarily as a medical discipline and so never trained Ph.D. students, with Hopkins finally establishing a pharmacology graduate program under my initial direction in 1968. Abel's national influence was evident in his founding the Journal of Pharmacology and Experimental Therapeutics and the Journal of Biological Chemistry. Clinical neuropharmacology played an important role at Hopkins. In the late 1940s, Leslie Gay, who directed the allergy clinic, was treating a lady for hives with antihistamines. She mentioned that her severe motion sickness evaporated when she took the new antihistamine. Working through the auspices of Army Chief of Staff General Omar Bradley, Gay directed the most sophisticated clinical drug trial of that era, a randomized study of 1500 soldiers on a north Atlantic trip to Europe. He showed definitively that the antihistamine, Dramamine, both prevented and relieved sea sickness (Gay et al., 1949Gay L. Carliner P. Moore J. The prevention and treatment of motion sickness.Trans. Assoc. Am. Physicians. 1949; 52: 196-203Google Scholar). In 1954, Louis Lasagna, Hopkins' first Head of Clinical Pharmacology, discovered a novel approach to creating less-addicting opiates. He was investigating interactions in humans of opiate agonists and antagonists, specifically morphine and nalorphine. As a control, he administered nalorphine alone and was astounded to detect analgesic efficacy equivalent to that of morphine (Lasagna and Beecher, 1954Lasagna L. Beecher H.K. The analgesic effectiveness of nalorphine and nalorphine-morphine combinations in man.J. Pharmacol. Exp. Ther. 1954; 112: 356-363PubMed Google Scholar). Thus, nalorphine was a mixed agonist-antagonist. Its antagonist properties decreased addictive propensities leading to major efforts in the pharmaceutical industry to develop mixed agonist-antagonist opiates as safer analgesics. Drugs that emerged from this program, such as pentazocine and buprenorphine, remain the least-addictive commercially marketed opiates. I came to Johns Hopkins for psychiatry residency in 1965 and, during the second year of residency, was appointed a full-time Assistant Professor of Pharmacology while still a full-time psychiatry resident. At that time, systems neuroscience was a dominant presence in the Department of Physiology, directed by Vernon Mountcastle. David Bodian, the Director of Anatomy and himself a distinguished neuroanatomist, had recruited numerous neuroanatomists to his department. Neither neurochemistry nor neuropharmacology existed at Hopkins. After I completed psychiatry residency in 1968 and was promoted (Associate Professor, Pharmacology and Psychiatry; 1970 Full Professor), Paul Talalay, Director of Pharmacology, appointed new faculty in a nascent “division” of neuropharmacology. These included Michael Kuhar, my first graduate student, who did postdoctoral training at Yale with George Aghajanian, and Joseph Coyle, my first medical student trainee and subsequently Research Associate with Julie Axelrod. Elliott Richelson, a Hopkins medical student who had worked with me and was subsequently an NIH Research Associate with Marshall Nirenberg, was for a few years a member of our division. Early research in my laboratory with Coyle and Kuhar focused on neurotransmitter uptake. Axelrod had established reuptake by sympathetic nerve endings of norepinephrine as the mode of its synaptic activation in experiments utilizing injections of radiolabeled norepinephrine into rodents. To study transmitter uptake in vitro and examine its kinetic properties, we sought to employ isolated nerve endings, synaptosomes. However, synaptosomes could only be prepared in sucrose solutions, while an ionic environment was required for transmitter uptake. As a medical student, Coyle devised a simple solution to this dilemma, homogenizing the brain first in hypertonic sucrose and then adding ionic buffers with the sucrose protecting the synaptosomes from degradation. This system permitted the evaluation of numerous putative neurotransmitters, especially the demonstration that amino acids that seemed to be good candidates as neurotransmitters, glutamate, aspartate, and glycine (in the spinal cord), possessed high-affinity sodium-requiring uptake systems which were not evident for “ordinary” amino acids (Logan and Snyder, 1971Logan W.J. Snyder S.H. Unique high affinity uptake systems for glycine, glutamic and aspartic acids in central nervous tissue of the rat.Nature. 1971; 234: 297-299Crossref PubMed Scopus (238) Google Scholar). At the Lilly Research Laboratories, David Wong adopted this crude synaptosomal preparation to screen drugs for selective inhibition of serotonin versus norepinephrine uptake, permitting the discovery of fluoxetine (Prozac) (Wong et al., 2005Wong D.T. Perry K.W. Bymaster F.P. Case history: the discovery of fluoxetine hydrochloride (prozac).Nat. Rev. Drug Discov. 2005; 4: 764-774Crossref PubMed Scopus (2) Google Scholar). In 1973, utilizing simple reversible ligand-binding techniques with crude brain membranes, we were able to identify opiate receptors in the nervous system (Pert and Snyder, 1973Pert C.B. Snyder S.H. Opiate receptor: demonstration in nervous tissue.Science. 1973; 179: 1011-1014Crossref PubMed Scopus (1482) Google Scholar). We extended this finding to receptors for numerous neurotransmitters by seeking drugs with high affinity and selectivity for receptors and obtaining from our valued collaborators at the New England Nuclear Corporation (now Perkin-Elmer) tritiated versions of the drugs (Snyder, 2002Snyder S.H. Forty years of neurotransmitters: a personal account.Arch. Gen. Psychiatry. 2002; 59: 983-994Crossref PubMed Scopus (15) Google Scholar). Such studies permitted the demonstration that the relative potencies of neuroleptics in blocking dopamine receptors predicts their antipsychotic actions. Ligand binding permitted clarification of anticholinergic sedative and hypotensive side effects of neuroleptics and antidepressants. In his own laboratory, Kuhar developed ligand-binding techniques for autoradiography, permitting him to localize opiate and other neurotransmitter receptors at a microscopic level and to explain with reasonable precision most of the therapeutic and adverse effects of opiates (Young and Kuhar, 1979Young 3rd, W.S. Kuhar M.J. A new method for receptor autoradiography: [3H]opioid receptors in rat brain.Brain Res. 1979; 179: 255-270Crossref PubMed Scopus (636) Google Scholar). Subsequently, in collaboration with Henry Wagner, Chair of the Division of Nuclear Medicine, he participated in the first imaging of neurotransmitter receptors in human brain by PET scanning, technology subsequently employed with virtually all neurotransmitter receptors (Wagner et al., 1983Wagner Jr., H.N. Burns H.D. Dannals R.F. Wong D.F. Langstrom B. Duelfer T. Frost J.J. Ravert H.T. Links J.M. Rosenbloom S.B. et al.Imaging dopamine receptors in the human brain by positron tomography.Science. 1983; 221: 1264-1266Crossref PubMed Scopus (516) Google Scholar). Coyle and his students employed receptor pharmacology to develop selective brain lesions. Following reports that the rigid glutamate derivative kainate destroys neurons by excitotoxicity, Coyle employed kainate lesions to destroy cell bodies in the caudate/putamen, eliciting a model of Huntington's disease (Coyle and Schwarcz, 1976Coyle J.T. Schwarcz R. Lesion of striatal neurones with kainic acid provides a model for Huntington's chorea.Nature. 1976; 263: 244-246Crossref PubMed Scopus (1009) Google Scholar). He utilized similar kainate lesions in the nucleus basalis of Meynert to establish that these cells are the source of the major cholinergic innervation of the cerebral cortex. In collaboration with Peter Whitehouse, Donald Price, and Mahlon DeLong in Neuropathology and Neurology, he delineated the loss of the cholinergic projection to the brain in Alzheimer's disease (Whitehouse et al., 1982Whitehouse P.J. Price D.L. Struble R.G. Clark A.W. Coyle J.T. Delon M.R. Alzheimer's disease and senile dementia: loss of neurons in the basal forebrain.Science. 1982; 215: 1237-1239Crossref PubMed Scopus (2878) Google Scholar). This work provided part of the background for the subsequent use of cholinesterase inhibitors in treating the memory loss of Alzheimer's disease. Other important work on cholinergic transmission was taking place in the laboratory of Daniel Drachman in the Neurology Department. Drachman had long been interested in the pathophysiology of myasthenia gravis. As cholinesterase inhibitors were therapeutic, it was assumed that something about cholinergic synapses was abnormal. Once it was possible to measure nicotinic cholinergic receptors with radiolabeled α-bungarotoxin, Drachman and Douglas Fambrough in the Biology Department at Hopkins demonstrated a profound depletion of cholinergic receptors in muscle biopsies of patients (Fambrough et al., 1973Fambrough D. Drachman D. Satymurti S. Neuromuscular junction in myasthenia gravis: Deceased acetylcholine receptors.Science. 1973; 182: 293-295Crossref PubMed Scopus (477) Google Scholar). At about the same time, others showed that rodents that were immunized with nicotinic cholinergic receptors develop symptoms resembling myasthenia gravis. Drachman injected serum of myasthenic patients into mice and reproduced symptoms of the disease, establishing myasthenia gravis as an autoimmune disease associated with degradation of cholinergic receptors (Toyka et al., 1977Toyka K.V. Drachman D.B. Griffin D.E. Pestronk A. Winkelstein J.A. Fishbeck K.H. Kao I. Myasthenia gravis. Study of humoral immune mechanisms by passive transfer to mice.N. Engl. J. Med. 1977; 296: 125-131Crossref PubMed Scopus (343) Google Scholar). A major body of work in Neuropathology/Neurology was carried out by Donald Price and Sangram Sisodia, elucidating mechanisms of amyloid β-peptide formation in Alzheimer's disease. They employed elegantly designed transgenic mice to establish how mutations of the amyloid precursor protein and its processing enzymes elicit Alzheimer's pathology (Price et al., 1998Price D.L. Sisodia S.S. Borchelt D.R. Genetic neurodegenerative diseases: the human illness and transgenic models.Science. 1998; 282: 1079-1083Crossref PubMed Scopus (213) Google Scholar). They employed similar strategies to clarify the role of certain types of superoxide dismutase in amyotrophic lateral sclerosis. The Department of Biomedical Engineering has always housed distinguished neurophysiologists with special expertise in auditory and vestibular studies. David Robinson pioneered in elucidating the vestibulo-ocular reflex. The reflex maintains constancy of images on the fovea of the retina as the head rotates. It does this by causing the eyes to rotate at the same speed as the head but in an opposite direction. In one classic study, Robinson showed that this presumably “hard-wired” reflex is modulated by experience, with the cerebellum critical for such modulation (Robinson, 1976Robinson D. Adaptive gain control of vestibulo-ocular reflex by the cerebellum.J. Neurophysiol. 1976; 39: 954-969PubMed Google Scholar). He also showed that the cerebellum detects and repairs dysmetria, a midjudgement of distances in motor movements. Murray Sachs, presently Director of the Department of Biomedical Engineering, and Eric Young pioneered in defining the code for detecting speech sounds, especially vowels. They showed that vowel perception is encoded by increased firing rates but that there is a dynamic range wherein the discharge rate of auditory nerve fibers is capped (Sachs and Young, 1980Sachs M. Young E. Effects of nonlinearities on speech encoding in the auditory nerve.J. Acoust. Soc. Am. 1980; 68: 858-875Crossref PubMed Scopus (128) Google Scholar). Although our department was founded in 1980, we had no independent laboratory space until 1983, when our first recruits, Richard Mains and Elizabeth Eipper, joined Kuhar, Coyle, and myself as full professors (Figure 2). Mains and Eipper had done postdoctoral work with Edward Herbert at the University of Oregon, where they discovered pro-opiomelanocortin, the protein precursor of ACTH and β-endorphin. They then pioneered in the biochemistry of neuropeptide processing (Eipper et al., 1992Eipper B.A. Stoffers D.A. Mains R.E. The biosynthesis of neuropeptides: peptide alpha-amidation.Annu. Rev. Neurosci. 1992; 15: 57-85Crossref PubMed Scopus (540) Google Scholar). I felt it important to begin with senior faculty who could share some of the administrative responsibilities of a new department. Mains and Eipper rose to the challenge, launching our graduate program. Besides developing a curriculum and recruiting students, they set up a departmental seminar series and a substantial number of graduate courses. When Kuhar left Hopkins in 1985, we recruited Jay Baraban, a Yale M.D./Ph.D., who trained with George Aghajanian and, following psychiatry residency at Columbia, did postdoctoral research with me. The next major impetus for departmental expansion came with the launching by the Howard Hughes Medical Institute (HHMI) of a neuroscience initiative. In those days, HHMI operated by setting up “institut" @default.
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• W2004331010 hasConcept C15744967 @default.
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• W2004331010 hasConceptScore W2004331010C15744967 @default.
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