Referenzen: [1] American Journal of Psychiatry Narcoanalysis and Criminal Law; John Mcdonald et al. 1954; Band 111; S.283-288 [2] American Journal of Psychiatry Narcoanalysis and Allied Procedures; Harry L. Mackinnon 1948; Band 105; S.224-225 [3] American Journal of Psychiatry Psychic Driving; Donald Ewen Cameron Januar 1956; S.502-509 [4] Bidermann & Zimmer: "Manipulation of Human Behavior" (61) John Wiley & Sons, Inc., New York; London [9] Fraser, F.M., Isbell, H. Eisenmann, A.J., et. al. Chronic Barbiturate Intoxication. Further Studies [10] Donald Ewen Cameron Psychoterapy in Action (1968) [11] Proceedings of the Royal Society of Medicine Vol. XLII p.491, 1949 Professor Jean Delay, M.D. Pharmakological Explorations of the Personality Narco-Analysis and Methedrine Shock [12] The Journal of Sozial Issues Vol. XIII, 1957, 13 (3) Bauer, R.A.: Brainwashing Psychology or Demology, p. 41-47 Miller, J.G.: Brainwashing Present and Future, p. 48-55 [15] Coercive Persuasion; Edgar H. Schein 1961 [19] PZ #3 138.Jahrgang 21.01.1993 p.40 (204) [20] TOXIC PSYCHIATRY Drugs and Eletroconvulsive Therapy Peter Breggin 1993 [21] Strategie und Technik der geheimen Kriegsfuehrung; Paul Chartes 1985 [22] Irrsinn Ost- Irrsinn West; Psychiatrie in Deutschland; Peter Klee [24] ACID DREAMS; Martin A. Lee & Bruce Shlain; 1985 [27] Journey into Madness; Thomas Gordon; 1989 [28] Bericht aus U.S. NEWS & WORLD REPORT; Jan 24.01.94 [29] Artikel aus dem THE ECONOMIST 08.01.1994 [30] Medline Referenzen zur exogenen Induktion einer Modelpsychose siehe naechste Seite [31] Deidenbach, Hans: Zur Psychologie der Bergpredigt Medline- Referencen zur Modelpsychose: TI: [Changes of the dopamine uptake sites in the rat striatum induced by repeated methamphetamine administration: a neurochemical approach to a mechanism of relapse in amphetamine psychosis] AU: Nakayama-M AD: Department of Psychiatry and Neurology, Hokkaido University School of Medicine, Sapporo, Japan. SO: Hokkaido-Igaku-Zasshi. 1993 Jul; 68(4): 507-19 TI: Psychosis following readministration of diethyl proprion: a possible role for kindling? AU: Little-JD; Romans-SE AD: Department of Psychological Medicine, Dunedin Hospital, New Zealand. SO: Int-Clin-Psychopharmacol. 1993 Spring; 8(1): 67-70 TI: Event-related potentials in methamphetamine psychosis during an auditory discrimination task. A preliminary report. AU: Iwanami-A; Suga-I; Kato-N; Nakatani-Y; Kaneko-T AD: Department of Psychiatry, Tokyo Metropolitan Matsuzawa Hospital, Japan. SO: Eur-Arch-Psychiatry-Clin-Neurosci. 1993; 242(4): 203-8 TI: Dopaminergic gene expression during amphetamine withdrawal. AU: Persico-AM; Schindler-CW; Brannock-MT; Gonzalez-AM; Surratt- -CK; Uhl-GR AD: Addiction Research Center, NIDA, Baltimore, MD 21224. SO: Neuroreport. 1993 Jan; 4(1): 41-4 TI: From an animal model of an attentional deficit towards new insights into the pathophysiology of schizophrenia. AU: Feldon- J; Weiner-I AD: Department of Psychology, Tel-Aviv University, Ramat-Aviv, Israel. SO: J-Psychiatr-Res. 1992 Oct; 26(4): 345-66 AB: The paper presents an animal model of schizophrenic-like attentional deficit, consisting of an inability to ignore irrelevant stimuli. It is based on the paradigm of latent inhibition (LI), in which animals learn to ignore repeatedly presented stimuli> not followed by meaningful consequences. In a series of experiments it was demonstrated that the capacity to ignore irrelevant stimuli is lost in rats treated with systemic or intra-accumbens injections of amphetamine, in normal volunteers given amphetamine, in high "psychosis-prone" persons, in acute schizophrenic patients and in untreated male adult rats that were raised until weaning under conditions of extremely restricted stimulation. In addition, LI is lost following the disruption of the hippocampal input to the nucleus accumbens. In all of the above conditions tested for antagonism by anti- psychotic drugs a loss of LI is reversed. On the basis of these results we propose an animal model which accommodates a neurodevelopmental dysfunction, hippocampal pathology, mesolimbic DA overactivity, vulnerability to stress, and gender differences, all of which have been postulated as factors in the pathophysiology of schizophrenia. TI: Repeated methamphetamine-treatment alters brain sigma receptors. AU: Itzhak-Y AD: Department of Biochemistry and Molecular Biology, University of Miami School of Medicine, FL 33101. SO: Eur-J-Pharmacol. 1993 Jan 12; 230(2): 243-4 AB: The present study was undertaken to examine whether repeated exposure of rats to the psychostimulant drug, methamphetamine, induces changes in sigma receptor binding. A significant up-regulation (130-145% of control Bmax) of sigma receptors, labeled w> ith [3H](+)pentazocine, was observed in the substantia nigra, frontal cortex and cerebellum of rats treated with methamphetamine (4.0 mg/kg per day; 10 days). These findings suggest that methamphetamine-induced psychosis may be associated with the up- regulation of sigma receptors in critical brain regions. TI: Mesolimbic deficits exacerbate amphetamine treatment. Clinical implications for drug abusers. AU: Wray-SR; Young-LE; Murthy-NV AD: Programme for Neuroscience, Adolescent Development and Drug Research, U.W.I., Jamaica. SO: West-Indian-Med-J. 1992 Sep; 41(3): 111-5 AB: Amphetamine, a common drug used by abusers, is able to produce a schizophreniform psychosis in man. [...] TI: PET dopamine D2 receptors and susceptibility to methamphetamine psychosis. AU: Iyo-M AD: Division of Drug Dependence and Psychotropic Clinical Research, National Center of Neurology and Psychiatry, Chiba, Japan. SO: Clin-Neuropharmacol. 1992; 15 Suppl 1 Pt A: 652A-653A TI: A lasting vulnerability to psychosis in patients with previous methamphetamine psychosis. AU: Sato-M AD: Department of Psychiatry, Tohoku University School of Medicine, Sendai Miyagi, Japan. SO: Ann-N-Y-Acad-Sci. 1992 Jun 28; 654: 160-70 AB: Chronic MAP abuse may produce a lasting vulnerability of the brain which leads to a paranoid delusional psychosis with hallucinations similar to schizophrenia. [...] TI: Relapse of paranoid psychotic state in methamphetamine model of schizophrenia. AU: Sato-M; Numachi-Y; Hamamura-T AD: Dept. of Psychiatry, Tohoku University School of Medicine, Miyagi, Japan. SO: Schizophr-Bull. 1992; 18(1): 115-22 AB: The study of the clinical course of methamphetamine (MAP) psychosis yields insights into the biological aspect of the relapse of the paranoid psychotic state with hallucination in schizophrenia. A series of MAP psychosis studies in Japan conducted ove> r a period of more than four decades revealed three types of clinical courses of MAP psychosis after discontinuation of MAP: transient type, prolonged type, and persistent type. Identification of the latter two indicates a lasting change in the brain that> produces and maintains a schizophrenia-like paranoid psychotic state without MAP. The characteristic course seen in the transient type is acute recurrence of the psychotic state after a long remission period, almost identical to the initial episode, due to reuse of MAP or to psychological stressors. Such lasting vulnerability of the brain to schizophrenia-like psychotic symptoms may be caused by a lasting sensitization of the brain to the psychotogenic action of MAP resulting from its chronic abuse. Experimental studies using animals sensitized to MAP- induced stereotypy suggest that lasting enhancement of MAP- induced dopamine release in the striatum and nucleus accumbens is related to the development and expression of brain vulnerability to schizophrenic sy> mptoms. TI: Recent advances in the phencyclidine model of schizophrenia [see comments] CM: Comment in: Am J Psychiatry 1992 Jun;149(6):848-9 AU: Javitt-DC; Zukin-SR AD: Department of Psychiatry, Albert Einstein College of Medicine, Montefiore Medical Center, Bronx, N.Y. SO: Am-J-Psychiatry. 1991 Oct; 148(10): 1301-8 AB: OBJECTIVE: Phencyclidine (PCP, "angel dust") induces a psychotomimetic state that closely resembles schizophrenia. As opposed to amphetamine-induced psychosis, PCP- induced psychosis incorporates both positive (e.g., hallucinations, paranoia) and negative (e.g., emotional withdrawal, motor retardation) schizophrenic symptoms. PCP- induced psychosis also uniquely incorporates the formal thought disorder and neuropsychological deficits associated with schizophrenia.[..] CONCLUSIONS: These findings suggest that endogenous dysfunction of NMDA receptor-mediated neurotransmission might contribute to the pathogenesis of schizophrenia. The relative implications of the PCP and amphetamine models of schizophrenia are discussed in relationship to the diagnosis and etiology of schizophrenia. TI: 'Ecstasy' psychosis and flashbacks [see comments] CM: Comment in: Br J Psychiatry 1992 Feb;160:276 AU: Creighton-FJ; Black-DL; Hyde-CE AD: Manchester Royal Infirmary. SO: Br-J-Psychiatry. 1991 Nov; 159: 713-5 TI: Animal models of amphetamine psychosis: neurotransmitter release from rat brain slices. AU: Lillrank-SM; Oja-SS; Saransaari-P; Seppala-T AD: Tampere Brain Research Center, Department of Biomedical Sciences, University of Tampere, Finland. SO: Int-J-Neurosci. 1991 Sep; 60(1-2): 1-15 TI: Chronic atypical psychosis associated with MDMA ("ecstasy") abuse [letter] [see comments] CM: Comment in: Lancet 1991 Dec 14;338(8781):1520. Comment in: Lancet 1992 Mar 14;339(8794):677-8 AU: Schifano-F SO: Lancet. 1991 Nov 23; 338(8778): 1335 TI: Chronic paranoid psychosis after misuse of MDMA [letter; comment] CM: Comment on: BMJ 1991 Mar 23;302(6778):697 AU: Winstock-AR SO: BMJ. 1991 May 11; 302(6785): 1150-1 TI: Chronic paranoid psychosis after misuse of MDMA ("ecstasy") [see comments] CM: Comment in: BMJ 1991 May 11;302(6785):1150-1 AU: McGuire-P; Fahy-T AD: Maudsley Hospital, London. SO: BMJ. 1991 Mar 23; 302(6778): 697 TI: Drug-induced psychoses. AU: Hurlbut-KM AD: Poison Centre, University of Arizona, Tucson 85724. SO: Emerg-Med-Clin-North-Am. 1991 Feb; 9(1): 31-52 AB: Major causes of drug-induced psychoses include cocaine, amphetamines, phencyclidine, cannabinoids, LSD, mescaline, the so-called designer drugs, anticholinergic compounds, and steroids. Most drug-induced psychoses are managed with general supportive measures, reassurance, minimizing patient stimulation, and benzodiazepines as needed; however, specific antidotes such as physostigmine for anticholinergic poisoning or urinary acidification to enhance excretion of amphetamines or phencyclidine may be indicated in some patients. Any patient with a drug-induced psychosis must be evaluated carefully for evidence of other toxic effects of the drug in question. TI: Amphetamine and cocaine induce drug-specific activation of the c-fos gene in striosome-matrix compartments and limbic subdivisions of the striatum. AU: Graybiel-AM; Moratalla-R; Robertson-HA AD: Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge 02139. SO: Proc- Natl-Acad-Sci-U-S-A. 1990 Sep; 87(17): 6912-6 AB: Amphetamine and cocaine are stimulant drugs that act on central monoaminergic neurons to produce both acute psychomotor activation and long- lasting behavioral effects including addiction and psychosis. [.. .] We propose that differential activation of immediate-early genes by psychostimulants may be an early step in drug-specific molecular cascades contributing to acute and long-lasting psychostimulant-induced changes in behavior. TI: Amphetamine psychosis [letter; comment] CM: Comment on: Br J Addict 1990 Jan;85(1):13-23 AU: Caplehorn-JR SO: Br-J-Addict. 1990 Nov; 85(11): 1505-6 TI: Chronic schizophrenia-like states in methamphetamine psychosis. AU: Tomiyama-G AD: Department of Neuropsychiatry, Teikyo University School of Medicine, Ichihara Hospital, Japan. SO: Jpn-J-Psychiatry-Neurol. 1990 Sep; 44(3): 531-9 TI: [Modification of the behavioral effects of drugs after repeated administration--special reference to the reverse tolerance of amphetamines] AU: Tadokoro-S; Kuribara-H AD: Division for Behavior Analysis, Gunma University School of Medicine, Maebashi, Japan. SO: Nippon-Yakurigaku-Zasshi. 1990 May; 95(5): 229-38 AB: It has been well-known that a chronic abuse of amphetamines induces schizophrenia-like psychotic symptoms, namely amphetamine psychosis.[...] The characteristics of reverse tolerance to methamphetamine in animals might be closely correlated to the amphetamine psychosis in humans. [...] TI: Methamphetamine psychosis in Japan: a survey [letter] AU: Nakatani-Y; Yoshizawa-F; Yamada-H; Iwanami-A; Sakaguchi-M; Katoh- N SO: Br-J-Addict. 1989 Dec; 84(12): 1548-9 TI: [The clinical course of chronic methamphetamine psychoses] TO: Ein Beitrag zur Kenntnis klinischer Verlaufe von chronischen Methamphetaminpsychosen. AU: Fujimori-H; Nakatani-Y; Sakaguchi-M AD: Tokyo, Metropolitan Bokuto Hospital, Japan. SO: Fortschr- -Neurol-Psychiatr. 1989 Sep; 57(9): 383-94 TI: Amphetamine psychosis: clinical presentations and differential diagnosis. AU: Hall-RC; Popkin-MK; Beresford-TP; Hall-AK AD: University of Florida, Gainesville. SO: Psychiatr- Med. 1988; 6(1): 73-9 TI: Negative schizophrenic symptomatology and the PCP (phencyclidine) model of schizophrenia. AU: Javitt-DC AD: Albert Einstein College of Medicine/Montefiore Medical Center, Bronx, NY. SO: Hillside-J-Clin-Psychiatry. 1987; 9(1): 12-35 AB: Amphetamine induced psychosis has for the past 30 years provided a useful model for the study of schizophrenia. [...] TI: Paranoid psychoses after abuse of proprietary cold remedies. AU: Lambert-MT AD: Northwick Park Hospital, London. SO: Br-J- Psychiatry. 1987 Oct; 151: 548-50 AB: It is well established that psychosis may arise in the context of the abuse of certain prescribed or illicit drugs. Two cases of paranoid psychosis are described in which proprietary preparations containing amphetamine-like drugs were abused. [...] TI: Enduring changes in brain and behavior produced by chronic amphetamine administration: a review and evaluation of animal models of amphetamine psychosis. AU: Robinson-TE; Becker-JB SO: Brain-Res. 1986 Jun; 396(2): 157-98 AB: Some people who repeatedly use stimulant drugs, such as amphetamine (AMPH), develop an AMPH-induced psychosis that is similar to paranoid schizophrenia. There has been, therefore, considerable interest in characterizing the effects of chronic stimulant drug treatment on brain and behavior in non-human animals, and in developing an animal model of AMPH psychosis. A review of this literature shows that in non-human animals chronic AMPH treatment can produce at least two different syndromes, ...[...] TI: Reverse tolerance to the ambulation-increasing effect of methamphetamine in mice as an animal model of amphetamine- psychosis. AU: Tadokoro-S; Kuribara-H SO: Psychopharmacol-Bull. 1986; 22(3): 757-62 TI: Acute exacerbation of methamphetamine psychosis and lasting dopaminergic supersensitivity--a clinical survey. AU: Sato-M SO: Psychopharmacol-Bull. 1986; 22(3): 751-6 TI: Effect of amphetamine on brain catecholamines, brain beta-endorphin, serum prolactin, catechol-O-methyltransferase and monoamine oxidase of various organs in the rat. AU: Agarwal-DP; Hoo-JJ; Tjaden-A; Nishigaki-I; Beckermann-WJ; Pahnke-V; Goedde-HW SO: Arzneimittelforschung. 1985; 35(11): 1639-42 AB: Rats were treated with amphetamine to induce an amphetamine psychosis which resembles paranoid schizophrenia. TI: [Induced insanity occurring in hospitalized patients of chronic methamphetamine psychosis] AU: Tohhara-S; Miyamoto-Y; Nakajima-T SO: Arukoru-Kenkyuto-Yakubutsu-Ison. 1985 Dec; 20(4): 350-8 TI: Enduring enhancement in frontal cortex dopamine utilization in an animal model of amphetamine psychosis. AU: Robinson-TE; Becker-JB; Moore-CJ; Castaneda-E; Mittleman-G SO: Brain-Res. 1985 Sep 23; 343(2): 374-7 AB: [...] This change in mesocortical dopamine activity may be involved in the behavioral sensitization produced by psychomotor stimulant drugs, and some of the cognitive abnormalities (e.g. amphetamine psychosis) associated with stimulant drug abuse in humans. TI: Hypersensitivity to d-amphetamine several years after early social deprivation in rhesus monkeys. AU: Kraemer-GW; Ebert-MH; Lake-CR; McKinney-WT SO: Psychopharmacology-Berl. 1984; 82(3): 266-71 AB: Social deprivation of rhesus monkeys in infancy results in increased sensitivity to psychotic-like behavioral effects of low doses of d-amphetamine given 2-3 years later. These behavioral effects are associated with increased levels of CSF norepinephrine. These data suggest that social developmental factors could be partially responsible for variation in neurochemical responses and long-lasting differential sensitivity of primates to the psychosis-inducing effects of d-amphetamine. TI: Amphetamine psychosis due to khat leaves [letter] AU: Kalix-P SO: Lancet. 1984 Jan 7; 1(8367): 46 TI: [A case of acute recurrent methamphetamine psychosis characterized by fancy delusions of grandeur] AU: Takezaki-H; Inotani-T; Ikeda-T; Yasuoka-T SO: Seishin-Shinkeigaku-Zasshi. 1984; 86(8): 621-30 TI: CNS stimulants and the look-alike drugs. AU: Lake-CR; Quirk- RS SO: Psychiatr-Clin-North-Am. 1984 Dec; 7(4): 689-701 AB: Abuse of amphetamine and especially the stimulant look-alikes represent a serious problem in the United States. The danger of amphetamine lies in its ability to produce tolerance, psychological addiction, psychosis, hypertensive crisis, and major depression following withdrawal after long-term use. The danger of the look- alikes is of a psychosocial nature and has less to do with the physical properties of the drugs. [...] TI: Amphetamine psychosis in Tokyo--its clinical features and social problems. AU: Yukitake-A SO: Folia-Psychiatr-Neurol-Jpn. 1983; 37(2): 115-20 AB: Japan is presently experiencing a second epidemic of amphetamine abuse, with methamphetamine abusers committing an increasing number of murders and injuries to ordinary citizens. As a result of the author's study of some 60 cases of amphetamine psychosis, the basic symptomatology of the disease was determined to be a paranoid hallucinatory state. Moreover, according to the contents of the paranoid hallucinatory state and the courses of the disease, amphetamine psychotics were divided into two types--the acute and the chronic. Though the former delusions were vivid, realistic and concrete, the latter were generalized, systematized and grandiose. Regarding the course of the disease, the former were episodic and the latter required longer treatments. Thus as the outline of the social background of these addicts had been made clear, it has been emphasized that the authorities must decide to solve this as a social problem. TI: Continuous amphetamine intoxication: an animal model of the acute psychotic episode. AU: Ellison-GD; Eison-MS SO: Psychol- Med. 1983 Nov; 13(4): 751-61 AB: When amphetamines are administered to humans every few hours for several days, either during the 'speed runs' of addicts or in controlled laboratory settings, the psychosis which reliably results is similar to paranoid schizophrenia in a number of important aspects. [...] TI: Apparent hallucinations in monkeys during around-the-clock amphetamine for seven to fourteen days. Possible relevance to amphetamine psychosis. AU: Nielsen-EB; Lyon-M; Ellison-G SO: J- Nerv-Ment-Dis. 1983 Apr; 171(4): 222-33 AB: Schizophrenia-like symptoms have been experimentally produced in humans by a single, large dose of amphetamine or by relatively low level, but continuous administration of the drug. [...] TI: Confusional paranoid psychosis after withdrawal from sympathomimetic amines: two case reports. AU: Deveaugh-Geiss-J; Pandurangi-A SO: Am-J-Psychiatry. 1982 Sep; 139(9): 1190-1 AB: Paranoid psychosis may result from intoxication with, or withdrawal from amphetamines. TI: Effect of chronic amphetamine administration on central dopaminergic mechanisms in the vervet. AU: Owen-F; Baker-HF; Ridley-RM; Cross-AJ; Crow-TJ SO: Psychopharmacology-Berl. 1981; 74(3): 213-6 AB: [...] The results are discussed in relation to the amphetamine psychosis in humans. TI: Amphetamine psychosis and schizophrenia: a dual model. AU: Kokkinidis-L; Anisman-H SO: Neurosci-Biobehav-Rev. 1981 Winter; 5(4): 449-61 TI: Autonomic effects of dextroamphetamine in normal men: implications for hyperactivity and schizophrenia. AU: Zahn-TP; Rapoport-JL; Thompson-CL SO: Psychiatry-Res. 1981 Feb; 4(1): 39- 47 AB: [...] The pattern of ANS effects closely resembles findings on drug-free schizophrenics, suggesting that it may be a matter for biologic changes occurring in amphetamine psychosis and spontaneous psychotic episodes. TI: Dopamine autoreceptor subsensitivity: a mechanism common to the treatment of depression and the induction of amphetamine psychosis. AU: Antelman-SM; Chiodo-LA SO: Biol-Psychiatry. 1981 Aug; 16(8): 717-27 TI: Amphetamine behavioral toxicity: rotational behavior after chronic intrastriatal infusion. AU: Dougherty-GG Jr; Ellinwood-EH Jr SO: Biol-Psychiatry. 1981 May; 16(5): 479-88 AB: The behavioral "reverse tolerance" to d-amphetamine in rats has not been clearly established for the high-dose, sustained d- amphetamine exposure relevant to human behavioral toxicity, especially the amphetamine psychosis. [...] TI: Effects of chronic amphetamine treatment on the glutamate concentration in cerebrospinal fluid and brain: implications for a theory of schizophrenia. AU: Kim-JS; Kornhuber-HH; Brand-U; Menge-HG SO: Neurosci-Lett. 1981 Jun 12; 24(1): 93-6 TI: The regional distribution of d-amphetamine and local glucose utilization in rat brain during continuous amphetamine administration. AU: Eison-MS; Eison-AS; Ellison-G SO: Exp-Brain- -Res. 1981; 43(3-4): 281-8 AB:[...] Animals continuously administered drug were sacrificed in behaviorally distinct stages of the continuous amphetamine syndrome, a potential animal model of amphetamine psychosis.[...] TI: Animal model of psychosis: hallucinatory behaviors in monkeys during the late stage of continuous amphetamine intoxication. AU: Ellison-G; Nielsen-EB; Lyon-M SO: J-Psychiatr-Res. 1981; 16(1): 13-22 TI: Psychopathology induced by "speed drugs". AU: Schiorring-E SO: Pharmacol-Biochem-Behav. 1981; 14 Suppl 1: 109-22 AB: The CNS stimulants produce profound psychopathological conditions in animals and man. The mental and motoric changes in humans make it relevant to retain the amphetamine and cocaine psychoses as possible models for endogenous psychoses, such as certain forms of the schizophrenias and manic-depressive disorders. The following behavioral aberrations in humans were found: (1) motor stereotypies with bizarre movements; repetitive, aimless activities; ("pottering"= "knick-knacking"= "punding") with various> objects, including own body; repetition of single words, phrases or musical expressions; stereotyped drawing and writing (phenomena which are examples of mental stereotypy); (2) social stereotypies: prolonged sexual intercourse without ejaculation; collective monologues; (3) social withdrawal: "autism", social isolation with no or inappropriate responses to social stimuli; (4) paranoia; (5) hallucinations and illusions: auditory, visual, tactile (microhallucinations. Parallels to the overt behaviors have consistently been found in lower and higher animal species. Comparative data from experiments with rats and monkeys are presented. The findings have some important implications: drug addiction, basic understanding of social behavior and mental functions, screening and use of neuroleptic drugs, and side effects on social contact and behavior by the therapeutic use of CNS stimulants. TI: Amphetamine-produced attenuation of latent inhibition is modulated by stimulus preexposure duration: implications for schizophrenia. AU: De-la-Casa-LG; Ruiz-G; Lubow-RE AD: University of Seville, Spain. SO: Biol-Psychiatry. 1993 May 15; 33(10): 707- 11 AB: The relationship between amphetamine-produced dopamine overreactivity and attention to irrelevant stimuli is reflected in an attenuated latent inhibition (LI) effect. This occurs in both animal and human subjects. The present study examines the manner> in which this effect in rats is modulated by the duration of stimulus preexposure. A factorial design was used with three levels of stimulus preexposure duration and either amphetamine or saline administration. In addition, there were corresponding group> s that did not receive stimulus preexposure. It was found that although amphetamine did indeed abolish LI at short exposure intervals (30 sec), the LI effect was normal for long stimulus preexposure durations (150 sec). The data were discussed in terms of the affects of amphetamine on the processing of irrelevant stimuli and the relationship of such a dysfunctional attentional process to schizophrenia. TI: [Effects of antagonists of NMDA receptor on methamphetamine- induced decrease in the dopamine uptake sites in the rat striatum and on the behavioral sensitization] AU: Muraki-A AD: Department of Psychiatry and Neurology, Hokkaido University School of Medicine, Sapporo, Japan. SO: Hokkaido-Igaku-Zasshi. 1993 May; 68(3): 407-18 AB: In humans, repeated use of methamphetamine produces hypersensitivity to the psychotogenic effects of methamphetamine that persists for months to years after the discontinuation of methamphetamine administration. Methamphetamine-induced psychosis has been thought to be a useful experimental model for schizophrenia. [...] TI: 5,7-Dihydroxytryptamine lesions in the fornix-fimbria attenuate latent inhibition. AU: Cassaday-HJ; Mitchell-SN; Williams-JH; Gray-JA AD: Department of Psychology, Institute of Psychiatry, London, England. SO: Behav-Neural-Biol. 1993 May; 59(3): 194-207 AB: When animals are preexposed to a stimulus without consequence they are subsequently slower to associate this stimulus with an important event, such as footshock. This retarding effect of stimulus preexposure is called latent inhibition and can be demonstrated in a variety of classical and instrumental paradigms and in a wide range of species, including man. Latent inhibition is disrupted in acute schizophrenics and by amphetamine treatment in both rat and man.[...] TI: Dopaminergic and noradrenergic modulation of amphetamine- induced changes in auditory gating. AU: Stevens-KE; Fuller-LL; Rose-GM AD: Department of Pharmacology, University of Colorado Health Sciences Center, Denver, CO. SO: Brain-Res. 1991 Jul 26; 555(1): 91-8 AB: Dopaminergic and noradrenergic mediation of central sensory gating were assessed in Sprague-Dawley rats using a condition-test paradigm in which auditory evoked potentials were recorded. In this paradigm, unmedicated rats 'gate', i.e. suppress the re> sponse to the second of a pair of clicks delivered at a 0.5 s interval. Amphetamine-treated rats fail to gate; in this respect, they resemble schizophrenic humans. Previous studies had indicated noradrenergic involvement in the mediation of auditory gating in rats. [...] TI: Cocaine-induced psychosis. AU: Brady-KT; Lydiard-RB; Malcolm- R; Ballenger-JC AD: Department of Psychiatry, Medical University of South Carolina, Charleston 29425. SO: J-Clin-Psychiatry. 1991 Dec; 52(12): 509-12 AB: BACKGROUND: Chronic stimulant use can produce a paranoid psychosis that is similar to acute paranoid schizophrenia. While this phenomenon has been systematically explored in amphetamine abusers, it has been relatively unexplored in a systematic fashion in cocaine abusers. METHOD: [. ..] CONCLUSION: Cocaine-induced paranoia is a common experience among chronic users. Amount and duration of use are related to its development. Implications for a kindling model of cocaine- induced psychosis will be discussed. TI: Chronic schizophrenia-like states in methamphetamine psychosis. AU: Tomiyama-G AD: Department of Neuropsychiatry, Teikyo University School of Medicine, Ichihara Hospital, Japan. SO: Jpn-J-Psychiatry-Neurol. 1990 Sep; 44(3): 531-9 AB: In order to clarify the characteristic psychopathology of chronic methamphetamine (MAP) psychosis, the clinical symptoms of 11 chronic MAP psychotics were compared with those of the same number of chronic schizophrenics matched for sex and age. The positive symptoms were almost similar in both groups. However, the negative symptoms evaluated by the Scale for the Assessment of Negative Symptoms (SANS) differed considerably. According to the SANS, the scores of avolition-apathy, anhedonia-asociality and attentional impairment were moderately high in both groups. The scores of affective flattening or blunting and alogia were lower in the MAP group than those in the schizophrenia group. The SANS scores of negative symptoms increased in accordance with the age of onset in the MAP group, while such a correlation was not observed in the schizophrenia group. Furthermore, detailed clinical observations of the patients revealed the following differences between the two groups: 1) spontaneous affective expression during the interviews was more vivid in the MAP group compared to the schizophrenia group, and 2) affective expressions or interpersonal behaviors changed immediately depending on the situation in the MAP group. From the viewpoint of clinical psychopathology, a group of MAP psychotics whose hallucinatory- delusional state persisted for a long period of one month or more after cessation of MAP use seemed to differ from either chronic schizophrenics or patients with acute MAP psychosis. The author proposed that this group of patients should be a clinical entity and be called as "residual methamphetamine psychosis." TI: Auditory sensory gating in hippocampal neurons: a model system in the rat. AU: Bickford-Wimer-PC; Nagamoto-H; Johnson-R; Adler-LE; Egan-M; Rose-GM; Freedman-R AD: Denver Veterans Administration Hospital, CO 80220. SO: Biol-Psychiatry. 1990 Jan 15; 27(2): 183-92 AB: Diminished evoked response to repeated auditory stimuli, an example of sensory gating normally present in human subjects, is often absent in schizophrenics. To examine the mechanism of the normal response and to delineate possible sites of its abnormality in psychosis, it would be desirable to reproduce the phenomenon in laboratory animals.[...] Amphetamine, which diminished sensory gating in both animals and humans, diminished the gating of the evoked potential recorded in the hippocampus.[...] TI: [Exogenous factors and schizophrenia] TO: Exogene factoren en schizofrenie. AU: de-Groot-L; Stolk-PJ SO: Ned-Tijdschr-Geneeskd. 1989 Aug 26; 133(34): 1673-5 TI: Dopaminergic stimulation disrupts sensorimotor gating in the rat. AU: Mansbach-RS; Geyer-MA; Braff-DL AD: Department of Psychiatry, University of California, San Diego, La Jolla, CA 92093. SO: Psychopharmacology-Berl. 1988; 94(4): 507-14 AB: Prepulse inhibition is a cross-species phenomenon in which reflex responses to discrete sensory events are modified by weak prestimulation. In experiments designed to investigate the neuropharmacological mechanism of this form of information processing, and its relevance to schizophrenic psychopathology, apomorphine (0.125-4.0 mg/kg) and d-amphetamine (0.5-4.0 mg/kg) were administered to rats in an attempt to modify prepulse inhibition of the acoustic startle response. Rats were presented with 40 ms, 118 dB[A] acoustic pulses which were intermittently preceded by a weak 80 dB[A] acoustic prepulse. Both apomorphine and d-amphetamine induced a significant loss of prepulse inhibition, as reflected by increased pulse-preceded-by-prepulse versus pulse-alone startle magnitudes. Haloperidol (0.1 mg/kg), a specific D2 dopamine receptor antagonist, prevented the effects of 2.0 mg/kg apomorphine on prepulse inhibition, while having little effect by itself. An additional study investigated the effects of chronic intermittent administration of 2.5 mg/kg d- amphetamine. Rats given amphetamine for 8 consecutive days also displayed a loss of prepulse inhibition, with no evidence of tolerance. Finally, prepulse inhibition was examined under high- and low-intensity startle stimulus conditions; apomorphine (1.0 mg/kg) induced a loss of prepulse inhibition under both intensity conditions in approximately equal proportion. The results of these studies suggest a connection between sensorimotor gating, as measured by prepulse > inhibition, and dopaminergic overactivity, supporting suggestions that information processing deficits in schizophrenia may be responsible for some psychotic symptoms and their effective treatment by antipsychotic D2 dopamine antagonists. TI: Psychiatric side effects attributed to phenylpropanolamine. AU: Lake-CR; Masson-EB; Quirk-RS AD: Dept. of Psychiatry, F. Edward Hebert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland. SO: Pharmacopsychiatry. 1988 Jul; 21(4): 171-81 AB: Phenylpropanolamine (PPA) is a sympathomimetic drug similar in structure to amphetamine which, in the United States, is present in over 130 medications, primarily decongestants, cough/cold remedies, and anorectic agents. We have reviewed 37 cases (published in North America and Europe since 1960) that received diagnoses of acute mania, paranoid schizophrenia, and organic psychosis and that were attributed to PPA product ingestion. [... ] TI: Hallucinatory behaviors in primates produced by around-the- clock amphetamine treatment for several days via implanted capsules. AU: Nielsen-EB; Eison-MS; Lyon-M; Iversen-SD SO: Prog- -Clin-Biol-Res. 1983; 131: 79-100 TI: Dextro-amphetamine and schizophrenia [letter] AU: Ostow-M SO: Am-J-Psychiatry. 1983 Apr; 140(4): 517-8 TI: Effect of chronic amphetamine administration on dopaminergic systems in the vervet brain: relationship to findings in the brains of schizophrenics. AU: Owen-F; Baker-HF; Ridley-RM; Cross- AJ; Crow-TJ SO: Biochem-Soc-Trans. 1983 Jan; 11(1): 68-9 TI: Behavioural and biochemical effects of chronic amphetamine treatment in the vervet monkey. AU: Ridley-RM; Baker-HF; Owen-F; Cross-AJ; Crow-TJ SO: Psychopharmacology-Berl. 1982; 78(3): 245- 51 AB: Five vervet monkeys were administered increasing doses (4- -12 mg/kg/day) of d-amphetamine over a period of 35 days. Three phases of behavioural change were discerned: phase 1 during which animals exhibited repetitive stereotyped action sequences with rapid head movements, occasional abnormal grooming, picking at the cage, hand-staring and snatching; phase 2 in which behaviour became progressively more restricted and animals became markedly unresponsive to auditory, visual and tactile stimuli; phase 3 > was characterised by the abrupt development of gross over- responsiveness to environmental stimuli, ataxia and tremor. [...] TI: Comments on "Amphetamine models of paranoid schizophrenia": a precautionary note. AU: Rebec-GV; Bashore-TR SO: Psychol-Bull. 1982 Sep; 92(2): 403-9 TI: Differential effects of microinjections of d-amphetamine into the nucleus accumbens or the caudate putamen on the rat's ability to ignore an irrelevant stimulus. AU: Solomon-PR; Staton-DM SO: Biol-Psychiatry. 1982 Jun; 17(6): 743-56 AB: Latent inhibition is an attentional process by which animals learn to ignore an irrelevant stimulus. Rats received either 0 or 30 preexposures to a tone which was later used as a conditioned stimulus (CS) in a two-way avoidance task. Tone preexposure resulted in retarded conditioning (i.e., latent inhibition) in animals which received microinjections of saline or amphetamine in the caudate-putamen and for those which received microinjections of saline in the nucleus accumbens. This latent inhibition e> ffect, however, was not present in animals which received d-amphetamine microinjections in the nucleus accumbens. The failure of CS preexposure to retard conditioning in these animals was not due to drug-induced changes in either tone or shock sensitivity> . The results are discussed in terms of the role of the mesolimbic dopamine system in learning to ignore an irrelevant stimulus and the use of LI as a possible animal model of the attentional deficit that seems to characterize some subpopulations of schizophrenic humans. TI: Disruption of selective attention in the rat following chronic d-amphetamine administration: relationship to schizophrenic attention disorder. AU: Crider-A; Solomon-PR; McMahon-MA SO: Biol-Psychiatry. 1982 Mar; 17(3): 351-61 AB: In the blocking paradigm, prior training to one conditioned stimulus (CSA) blocks the ability to attend to a second conditioned stimulus (CSB) when the two form a compound (CSAB) in subsequent training. Blocking is an associative process by which anim> als learn to ignore CSB because it contains no new information regarding the reinforcing event. Experiment 1 showed that d- amphetamine disrupted rats' ability to ignore the irrelevant CSB: The animals responded equally to both elements of the CSAB compound following five dialy administrations of 4 mg/kg d- amphetamine. In Experiment 2 the disruption of blocking by d- amphetamine was eliminated by concomitant administration of 0.02 mg/kg haloperidol. These results are consistent with previous research showin> g that d-amphetamine disrupts rats' ability to ignore repeated presentations of a single nonreinforced stimulus in the latent inhibition paradigm. The inability of amphetamine- treated animals to ignore one element of! a dual-element compound bears some resemblance to selective attention deficits seen among schizophrenic patients. TI: Disrupted latent inhibition in the rat with chronic amphetamine or haloperidol-induced supersensitivity: relationship to schizophrenic attention disorder. AU: Solomon-PR; Crider-A; Winkelman-JW; Turi-A; Kamer-RM; Kaplan-LJ SO: Biol-Psychiatry. 1981 Jun; 16(6): 519-37 AB: Latent inhibition (LI) is an attentional process by which animals learn to ignore a stimulus that is repeatedly presented without reinforcement. This ability to tune out a motivationally irrelevant stimulus is disrupted by pharmacological manipulation> s producing hyperdopaminergic states. [...] These data suggest that pharmacological disruption of LI may provide an animal analogue of the defective stimulus filtering thought to characterize at least some forms of schizophrenia. From: verdant@twain.ucs.umass.edu (Sol Lightman) Subject: LSD, the CIA, and Your Brain Date: 24 Jan 1994 20:03:17 GMT PSYOPS- HTTP://WWW.TELEPORT.COM/~WALTER _______________________________________ blast trauma data fer social dissection made available to: realpolitic junkies, info tyros, kultur buzzards & da masses ======================================= FBI-CIA-KGB-NSA-BCCI-DIA-DEA-FEMA-THULE KKK-CONTRA-JFK-RFK-MLK-MKULTRA-LAROUCHE COINTELPRO-ILLUMINATI-P2-CFR-ADL-MOSSAD BLUEBIRD-OSS-ONI-SOE-BIS-AIDS-ARTICHOKE OTO-OCCULT-NEA-BILDERBERGER-40 CTTE-SLA VELIKOVSKY-SDI-INSLAW-TESLA-TSS-CROWLEY JIM JONES-GURDJIEFF-ABWEHR-T4-WACO-BATF EFF-PGP-RHIC/EDOM-PANDORA-CAN-TAVISTOCK ENIGMA-BEARDEN-GEHLEN-SPETZNAZ-EUGENICS MASONS-ODESSA-WFMH-IRS-MI5-FOIA-TRILATS