Thomas A. Ban
Neuropsychopharmacology in Historical Perspective
Education in the Field in the Post-Neuropsychopharmacology Era

Background to An Oral History of the First Fifty Years
Neuropsychopharmacology (Volume Five): 3. Psychopharmacology of Schizophrenia; Psychopharmacology of Depression; Endocrine Measures
(Bulletin 50)



Neuropsychopharmacology of Schizophrenia


            Based on findings which indicated that nicotinic acid, the precursor of nicotinamide adenine dinucleotide (NAD), was effective in the treatment of schizophrenia it was hypothesized that schizophrenia is a NAD deficiency disease, a form of “cerebral pellagra” (Pauling 1968). Yet, Hoffer and Osmond’s dramatic results with NAD treatment could not be replicated and there was no NAD deficiency in schizophrenic blood (Gallant, Bishop and Steele 1966; Hoffer and Osmond 1966; Kline, Barclay,Cole et al. 1967; Meltzer, Greenspoon and Shader 1959).

            Based on pharmacological findings in the mid-1950s which indicated a linear relationship between the sedative and anti-5HT effect of chlorpromazine and its congeners and the demonstrated psychotomimetic effect of dimethyltryptamine (DMT), it was hypothesized that an excess of 5HT and/or DMT formation might be involved in the pathophysiology of schizophrenia (Gyermek, Lazar and Csák 1957).  Yet, Bertlet and his associates found that a diet in which tryptophan, the precursor of 5HT, and methionine (the methyl donor for DMT formation) was reduced, had no effect on schizophrenia (Bertlet, Bull, Himwich et al. 1966).

            Based on the findings of Carlsson and Lindqvist, in 1963 that chlorpromazine and haloperidol increased 3-methoxytyramine and normetanephrine levels in the mouse brainit was assumed that the therapeutic effect of these drugs in schizophrenia was the result of catecholamine receptor blockade andhypothesized that catecholamines were involved in the pathophysiology of schizophrenia (Carlsson and Lindqvist 1963). They were Carlsson and Lindqvist findings which opened the path for the formulation of the dopamine hypothesis of schizophrenia (Van Rossum 1966). Supportive of the dopamine hypothesis were Heath and his associates findings that disulfiram, a dopamine-β-hydroxylase inhibitor, which decreased the breakdown of dopamine (DA), aggravated schizophrenia and, indirectly, Gershon and his associates’ findings that α-methyl-para-tyrosine (AMT), a substance that blocked the formation of NE, had no effect on schizophrenia (Gershon, Hekimian, Floyd and Hollister 1967; Heath, Nesselhof, Bishop and Byers 1965; Seeman 2006).

            There was an inverse relationship between the potency of neuroleptics to produce extrapyramidal signs (EPS), an indicator of DA antagonism, and neuroleptic dose requirements. Yet, the difference was restricted to dose; there was no difference in therapeutic efficacy between drugs like thioproperazine,a potent DA antagonist which produced marked EPS and drugs like methotrimeprazine that produced only mild EPS (Ayd 1961; Ban, Papathomopoulos and Schwarz 1962; Ban and Schwarz 1963; Brook 1956; Flűgel 1953).

            In the mid-1950s Hans Joachim Haase suggested that there is a neuroleptic thres hold dose, at which neuroleptics become effective without further increase in effectiveness at higher dosages. He also developed a test for the detection of this dose from the changes in the size of letters in hand-writing (Haase 1965; Haase and Janssen 1965).


Neuropsychopharmacology of Depression


            Developments in the neuropsychopharmacology of depression began with the assumption of a relationship between monoamine oxidase (MAO) inhibition and iproniazid’s antidepressant effect. It was a tenuous relationship because isoniazid, the parent substance of iproniazid, a substance with virtually no MAO inhibiting property, was also reported to have antidepressant effects (Burger 1977; Delay, Laine and Buisson 1952, 1953; Fox and Gibbas 1953; Salter and Lurie 1953, 1955; Zeller, Barsky, Fouts et al. 1952). The clinical effects of iproniazid were confounded by findings which indicated that iproniazid was more of an energizer than an antidepressant possibly with some anxiolytic properties (Ban 1974, 1981a; Crane 1957; Loomers, Saunders and Kline 1957; Rees 1960;Sargant 1961; Sargant and Sally 192; West and Dally 1954, 1962).

            Developments in the neuropsychopharmacology of depression continued with imipramineone of 42 substances selected in the mid-1950s from the chemical library of Geigy in the search for a promethazine-like antihistaminic or chlorpromazine-like tranquilizing drug (Ban 1981b; Kuhn 1957). It took about eight years from the time its effectiveness in some depressed patients was discovered by Kuhn (1957) that Klerman and Cole succeeded in demonstrating its statistically significant superior (65% improvement) efficacy to an inactive placebo (65% vs. 31% improvement rate) in patients with depression (Klerman and Cole 1965; Kuhn1957).

            Pharmacological studies in the late 1950s indicated that imipramine has antihistaminic, anticholinergic, noradrenergic and serotonergic properties without offering any clues which of these actions might be related to its antidepressant effect (Domenjoz and Theobald 1959).  The finding that imipramine antagonized and reversed reserpine- induced sedation, hypothermia, ptosis and diarrhoea did not advance this issue, because reserpine, in addition to depleting NE and 5HT from brain storage sites, also has cholinomimetic effects (Costa, Garattini and Valzelli 1960). Furthermore, far from being clearly a mood depressant, reserpine was classified by the World Health Organization as a neurolepticand was even reported to be effective in the treatment of anxious and depressed patients (Davies and Shepherd 1955; Mueller, Pryor, Gibbons and Orgain 1955; World Health Organization 1967).

            Imipramine blocks muscarinic acetylcholine receptors and has central and peripheral anticholinergic effects (Sulser and Watts 1960).

            In 1961 Helmut Selbach attributed the antidepressant effect of imipramine to its action on autonomic regulation, producing an imbalance in which the parasympathetic-trophotropic, acetylcholine system is more strongly inhibited than the sympathetic-ergotropic, adrenaline-epinephrine system (Selbach 1962; Sigg 1959). He also described three successive stages in the course of treatment, the first characterized by “trophotropic actions,” such as feelings of tiredness and decrease of blood pressure; the second by “lability,” manifest in tremor and fluctuation of blood pressure;and the third by “ergotropic actions” displayed in elation and increased interest (Selbach 1962). 

            The noradrenergic properties of imipramine were further elaborated in the late 1950s by Ernest Sigg, who demonstrated that imipramine enhanced and prolonged physiological responses to exogenous NE and to endogenous NE released by pre-or postganglionic sympathetic nerve stimulation (Sigg 1959). The only findings which indicated that the noradrenergic properties of the substance might translate into an effect on behaviour and psychopathology were from Elmadjian and  his associates who reported a correlation between urinary excretion of NE and aggression, and Ström-Olsen and Weil-Malherbe, who reported  higher urinary excretion of epinephrine and NE in the manic compared to the depressive phase of manic-depressive psychosis (Elmadjian, Hope and Lawson 1957; Ström-Olsen and Weil-Malherbe 1958).                

            In 1961, Axelrod and his associates discovered that imipramine and amitriptyline blocked neuronal reuptake of NE and in 1964 Sulser and his associates demonstrated that imipramine’s reserpine reversal was blocked after depletion of NE in the brain (Hertting, Axelrod and Whitby 1961; Sulser, Bickel and Brodie 1964). These preclinical findings were instrumental in the formulation of a catecholamine hypothesis of depression. However, in clinical studies the therapeutic efficacy of desipramine, the demethylated metabolite of imipramine, a selective NE reuptake inhibitor,was not found to be superior to the parent substance in the treatment of depression (Ban and Lehmann 1962; Brodie, Dick, Kielholz, Poldinger and Theobold 1961; Kline, Simpson and Brodie 1962; Mann 1962; Oltman and Freedman 1962).    

            The serotonergic properties of imipramine were first elaborated in 1960 by Gyermek and Posemanto who demonstrated that the pharmacological effects of 5HT were enhanced by administration of the drug (Gyermek and Posemanto 1960).  There were some indications that imipramine’s serotonergic action was related to its antidepressant effect. In 1959 Pare and Sandler reported decreased urinary excretion of 5-hydroxyindoleacetic acid (5HIAA), the urinary end product of 5HT,in depressed patients and in 1960 Aschcroft and Sharma found lower concentrations of 5-hydroxyindoles in the cerebrospinal fluid of depressed patients than in normal subjects (Aschcroft and Sharma 1960; Pare and Sandler 1959). Furthermore, in 1963 Coppen, Shaw and Farell had shown that the antidepressant effect of monoamine oxidase inhibitors (MAOIs) was potentiated by tryptophan (Coppen, Shaw and Farrell 1963). Their findings were further substantiated by Pare in the same year (Pare 1963). Yet, the first selective serotonin re-uptake inhibitor, zimelidine, was introduced only almost 20 years later in the early 1980s (Hope and Attley 1982).

            Trimipramine, a structurally similar substance to imipramine which neither blocks NE reuptake nor potentiates the pharmacological effects of tryptophan, was introduced in the treatment of depression in the early 1960s (Ban 1964; Lambert and Guyotat 1961). It is a dopamine-D2 and serotonin-5HT2 antagonist (Baghai, Guze and Sartorius 2007). 


Endocrine Measures


            After some isolated reports in the 1940s, developments in endocrine psychiatry began in 1951 with a Ciba-Foundation Symposium on The Influence of Steroid Hormones on Behavioural and Psychological Reactions (Hemphill 1940). It was followed in 1954 by the controversial publication of Manfred Bleuler’s Endokrinologische Psychiatrie (Endocrine Psychiatry) and in 1958 by Max Reiss’ “Psychoendocrinology” (Bleuler 1954; Reiss 1955). By the end of the 1950s it was shown that increased adrenocortical activity was not restricted to depression but was present in anxiety states, schizophrenia and in both the manic and depressive phases of manic-depressive illness (Bryson and Martin 1954; Lingjaerde 1964; Reiss 1958; Schwartz, Mandell, Green and Ferman 1966). Another early finding was that increased adrenocortical activity correlated with emotional turmoil and stress (Bliss, Migren, Branch and Samuels 1956; Persky 1957; Price, Thaler and Mason 1957; Weil-Malherbe and Szara 1971).

            An elevation of plasma cortisol level in depressive illness was first reported by Gibbons and McHugh in 1962 (Gibbons and McHugh 1962). They also showed that in depression cortisol’s diurnal rhythm was abolished.

            In the mid-1960s it was demonstrated that morning cortisol levels in depressed patients are significantly higher than in normal subjects (Bridges and Jones 1966; Doig, Mummery, Wills and Elkes 1966). It was also in the mid-1960s that Krieger and Krieger discovered that the circadian rise of 17-hydroxycorticosteroids was blocked in a dose dependent manner by atropine and other anticholinergic drugs (Krieger and Krieger 1967).

            Introduction of neuroendocrine tests in neuropsychopharmacological research began in the late 1960s with the first reports indicating that in severely depressed patients dexamethasone might not suppress the morning rise of cortisol and that the resistance to dexamethasone suppression correlated with the severity of depression (Butler and Besser 1968; Matussek 2006).In the 1970s research interest in endocrine psychiatry was extended to growth hormone (GH) and thyroid stimulating hormone (TSH) with reports of a blunted GH response in endogenous depression to insulin in 1971,to L-5-hydroxytryptophan in 1973,to the thyrotropin releasing hormone (TRH) in 1975,to amphetamine in 1976and to clonidine in 1978 (Langer, Heinze, Reim and Matussek 1976; Maeda, Kato, Ohgo et al. 1975; Matussek,  Ackenheil, Hippius et al. 1980; Sachar, Finkelstein and Hellman 1971; Takahashi, Kondo, Yoshimura et al. 1973).   

            The first report on a decreased thyroid stimulating hormone (TSH) response to TRH was published in the late 1970s (Kirkegaard, Bjorum, Cohn and Lauridson 1978).




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December 27, 2018