Neuro Sx -neurobiology and pharmacology

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  • Created by: freya_bc
  • Created on: 23-03-18 12:16
Loewi (1921)
Frog heart chambers Elec stim into one chamber made it start to beat This then transferred to heart 2 through the saline Chemical transmission of elec info
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Kim (1980)
discovered reduced glutamate in cerebrospinal fluid in patients with schizophrenia (not replicated, but other enzyme markers for glutamate shown to be reduced)
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Harrison et al., 2003; Moghaddam, 2003).
genes assoc with increase risk sx can influence function of modulatory sites on
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Stefansson et al., 2002
include association with schizophrenia of allelic variants of genes for neuregulin 1
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Egan et al., 2004
NMDA receptors 1 which can influence the expression of NMDA receptors through activation of Erb4 receptors, and GRM3, which encodes the mGlu3 subtype of metabotropic glutamate receptors
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Clinton and Meador-Woodruff, 2004).
Postmortem studies show changes in glutamate receptor binding, transcription, and subunit protein expression in the prefrontal cortex, thalamus, and hippocampus of subjects with schiz e.g. dec in NR1 subunits of the NMDA receptor in hippo&f.cortical
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Klivington (1992)
mesotelencephalic dopamine system in the human brain conssiting of the nigrostriatal pathwya and mesocorticiolimbic pathway - PFC decrease increase in midbrain dopamine
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Weinberger
extended dopamine hypothesis- Sx (+ve symptoms) caused by overactivity of DA synapses likely in the mesolimbic pathway coming from the ventral tegmental area consequent to hypoactivity of dA synapses in prefrontal cortical regions (neg and cog sympt
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Seeman et al.,(1976)
Correl between antipsych drug binding to Da receptors- didn’t know about subtypes at this time- correl between how well drug bound to receptors and their clinical effectiveness If a drug that binds to Da reduce systems maybe caused by da abnorm
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Bay-Richter and O'Callaghan et al., (2013)
when d-amp receptors knocked out still see increase locomotor activity compared to when present an d-amphet admin, also abolishes latent inhibition
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Lubow and Moore, (1959)
Latent inhibition is disrupted by amphetamine, this disruption is reversed by antipsychotic drugs Latent inhibition is enhanced by antipsychotic drugs given alone, prior exp to stim without consequence reduce subsequent learning
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Kapur 2003).
Antipsychotic drugs through their actions on dopamine D2 receptors "dampen the salience" of these abnormal experiences thus alleviating symptoms
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Gray (1991, 1998)
A dysregulated, hyperdopaminergic state leads to faulty assignment of salience to the elements of experience. Symptoms such as delusions arise as a patient tries to make sense of these aberrantly salient exp, hallucin reflect direct exp
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Weiner, 2003)
amphet disrupt LI
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Leng et al., 2003; Timble et al., 2002)
D2 anta enhanced LI
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Warburton et al., 1994, Moran, 1996)
amphet and D2 antag- restore LI after maph disruption
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Trimble et al., 2002)
D1 antag no effect
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Feldon et al., (1991)
D1 agonist no effect
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Kim (1980)

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discovered reduced glutamate in cerebrospinal fluid in patients with schizophrenia (not replicated, but other enzyme markers for glutamate shown to be reduced)

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Harrison et al., 2003; Moghaddam, 2003).

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Card 4

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Stefansson et al., 2002

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Egan et al., 2004

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