The effect of a single administration of phencyclidine on behavior in the rat over a 21-day period

Haggerty, G. C.; Forney, Robert B.; Johnson, J. M.

doi:10.1016/0041-008x(84)90181-9

Cited by 16 publications

(7 citation statements)

References 11 publications

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“…Prominent circling behavior induced by PCP (Fig 2) is consistent with rotations reported in zebrafish exposed to ketamine (Riehl et al, 2011a; Zakhary et al, 2011) and MK-801 (Chen et al, 2010; Seibt et al, 2010; Swain et al, 2004), and in rodents injected with PCP and other NMDA antagonists (Ali et al, 1994; Ali et al, 1995; Burket et al, 2010; Eshel and Korczyn, 1985; Haggerty et al, 1984; Van Ree and Leys, 1985). No left or right preference was found in the present study (Table 1), in agreement with our earlier zebrafish data on ketamine (Riehl et al, 2011a).…”

Section: Discussionsupporting

confidence: 86%

Effects of hallucinogenic agents mescaline and phencyclidine on zebrafish behavior and physiology

Kyzar

Collins

Gaikwad

et al. 2012

Progress in Neuro-Psychopharmacology and Biological Psychiatry

101

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Mescaline and phencyclidine (PCP) are potent hallucinogenic agents affecting human and animal behavior. As their psychotropic effects remain poorly understood, further research is necessary to characterize phenotypes they evoke in various animal models. Zebrafish (Danio rerio) are rapidly emerging as a new model organism for neuroscience research. Here, we examine the effects of mescaline (5–20 mg/l) and PCP (0.5–3 mg/l) in several zebrafish paradigms, including the novel tank, open field and shoaling tests. Mescaline and PCP dose-dependently increased top activity in the novel tank test, also reducing immobility and disrupting the patterning of zebrafish swimming, as assessed by ethograms. PCP, but not mescaline, evoked circling behavior in the open field test. At the highest doses tested, mescaline increased, while PCP did not affect, zebrafish shoaling behavior. Finally, 20 mg/l mescaline did not alter, and 3 mg/l PCP elevated, whole-body cortisol levels. Overall, our studies indicate high sensitivity of zebrafish models to hallucinogenic compounds with complex behavioral and physiological effects.

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Section: Discussionsupporting

confidence: 86%

Effects of hallucinogenic agents mescaline and phencyclidine on zebrafish behavior and physiology

Kyzar

Collins

Gaikwad

et al. 2012

Progress in Neuro-Psychopharmacology and Biological Psychiatry

101

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“…Studies investigating the effects of phencyclidine and ketamine (noncompetitive antagonists of NMDARs) in human subjects show these drugs induce behaviors similar to the positive and negative symptoms of schizophrenia, along with repetitive orofacial and limb movements, autonomic instability, and seizures (Luby et al, 1959; Bailey, 1978; Castellani et al, 1982; Krystal et al, 1994; Weiner et al, 2000). In rodents, drugs that antagonize NMDAR function induce cataleptic freeze, and locomotor and stereotype behaviors, consistent with schizophrenia-like manifestations (Haggerty et al, 1984; Jentsch and Roth, 1999; Chartoff et al, 2005; Mouri et al, 2007). Furthermore, mice with decreased expression of NR1 have similar behavioral deficits, while mice lacking NR1 develop breathing problems and die in the perinatal period (Mohn et al, 1999).…”

Section: Discussionmentioning

confidence: 84%

Cellular and Synaptic Mechanisms of Anti-NMDA Receptor Encephalitis

Hughes¹,

Peng²,

Gleichman³

et al. 2010

J. Neurosci.

1,014

847

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We recently described a severe, potentially lethal, but treatment-responsive encephalitis that associates with autoantibodies to the NMDA receptor (NMDAR) and results in behavioral symptoms similar to those obtained with models of genetic or pharmacologic attenuation of NMDAR function. Here, we demonstrate that patients' NMDAR antibodies cause a selective and reversible decrease in NMDAR surface density and synaptic localization that correlates with patients' antibody titers. The mechanism of this decrease is selective antibodymediated capping and internalization of surface NMDARs, as Fab fragments prepared from patients' antibodies did not decrease surface receptor density, but subsequent cross-linking with anti-Fab antibodies recapitulated the decrease caused by intact patient NMDAR antibodies. Moreover, whole-cell patch-clamp recordings of miniature EPSCs in cultured rat hippocampal neurons showed that patients' antibodies specifically decreased synaptic NMDAR-mediated currents, without affecting AMPA receptor-mediated currents. In contrast to these profound effects on NMDARs, patients' antibodies did not alter the localization or expression of other glutamate receptors or synaptic proteins, number of synapses, dendritic spines, dendritic complexity, or cell survival. In addition, NMDAR density was dramatically reduced in the hippocampus of female Lewis rats infused with patients' antibodies, similar to the decrease observed in the hippocampus of autopsied patients. These studies establish the cellular mechanisms through which antibodies of patients with anti-NMDAR encephalitis cause a specific, titer-dependent, and reversible loss of NMDARs. The loss of this subtype of glutamate receptors eliminates NMDAR-mediated synaptic function, resulting in the learning, memory, and other behavioral deficits observed in patients with anti-NMDAR encephalitis.

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“…25,72–75 In rodents, drugs that antagonise NMDAR function induce cataleptic freeze and locomotor and stereotypical behaviours. 76–79 Mice with decreased expression of NR1 also have such behavioural deficits, whereas mice that do not express NR1 develop breathing problems and die in the perinatal period. 80 A mouse strain in which 40–50% of NMDARs in cortical and hippocampal neurons were selectively eliminated showed schizophrenia-related symptoms and social and spatial working memory deficits that emerged after sexual maturity.…”

Section: Patients Phenotype Resembles Those Of Genetic or Pharmacologmentioning

confidence: 99%

Clinical experience and laboratory investigations in patients with anti-NMDAR encephalitis

Dalmau

Lancaster

Martínez‐Hernández

et al. 2011

The Lancet Neurology

2,161

2,664

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Since its discovery in 2007, the encephalitis associated with antibodies against the N-methyl-D-aspartate receptor (NMDAR) has entered the mainstream of neurology and other disciplines. Most patients with anti-NMDAR encephalitis develop a multistage illness that progresses from psychosis, memory deficits, seizures, and language disintegration into a state of unresponsiveness with catatonic features often associated with abnormal movements, and autonomic and breathing instability. The disorder predominantly affects children and young adults, occurs with or without tumour association, and responds to treatment but can relapse. The presence of a tumour (usually an ovarian teratoma) is dependent on age, sex, and ethnicity, being more frequent in women older than 18 years, and slightly more predominant in black women than it is in white women. Patients treated with tumour resection and immunotherapy (corticosteroids, intravenous immunoglobulin, or plasma exchange) respond faster to treatment and less frequently need second-line immunotherapy (cyclophosphamide or rituximab, or both) than do patients without a tumour who receive similar initial immunotherapy. More than 75% of all patients have substantial recovery that occurs in inverse order of symptom development and is associated with a decline of antibody titres. Patients’ antibodies cause a titre-dependent, reversible decrease of synaptic NMDAR by a mechanism of crosslinking and internalisation. On the basis of models of pharmacological or genetic disruption of NMDAR, these antibody effects reveal a probable pathogenic relation between the depletion of receptors and the clinical features of anti-NMDAR encephalitis.

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The effect of a single administration of phencyclidine on behavior in the rat over a 21-day period

Cited by 16 publications

References 11 publications

Effects of hallucinogenic agents mescaline and phencyclidine on zebrafish behavior and physiology

Effects of hallucinogenic agents mescaline and phencyclidine on zebrafish behavior and physiology

Cellular and Synaptic Mechanisms of Anti-NMDA Receptor Encephalitis

Clinical experience and laboratory investigations in patients with anti-NMDAR encephalitis

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