Behavioural neuroscience

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  • Created by: benj
  • Created on: 10-05-17 18:39
decreased AMT uptake in Dorsolateral prefrontal cortex and increased uptake in caudate
SPECT studies of SERT using beta-CIT have shown decreased binding potential and transporter density in midbrain, with greater reduction in binding associated with increased tic severity
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Other studies have  however found  no differences between patient and family 5-HT and related metabolites in the CSF compared to controls
erotonergic modulation of dopaminergic neurotransmission, believed to be involved in the regulation of basal ganglia-thalamocortical circuits involved in movement and cognition
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 comorbid  disorders  such as  OCD  having  serotonergic dysfunction
Differences in serotonin levels more marked in those with co-morbid OCD, a suggestion that 5-HT plays a role in obsessive-compulsive behaviors associated with TS
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Preliminary post-mortem brain studies in TS have suggested that serotonin may be globally decreased in the basal ganglia and other areas receiving projections from the dorsal raphe.
However, more recently no differences in relative density of serotonin receptors was found in post-mortem brain tissue from frontal and occipital regions in TS subjects.  
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Modulation of nervous system tone involved in arousal modulation. ​ ​ Group of serotonergic neurons increase firing rate in facial motor activity. (chewing, biting and licking). ​ ​
Motor output, involved in repetitive motor output and central pattern generators. Facilitation of motor output and suppression of activity in sensory systems irrelevant to behavior. ​
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Serotonergic transmission inhibits information processing in afferent  systems. Hypo-Serotonin  leads to  decreased  inhibition of sensory irrelevant  activity.
Dopamine-serotonin interactions have been implicated in TS pathophysiology in  the  striatum and nucleus  accumbens.
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5HT2A receptor activation facilitates phasic release of DA but does not influence tonic, basal release.
5-HT2c  activation inhibits stimulus-induced phasic release of DA  and tonic release.
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Abnormalities  in phasic release of dopamine facilitated by 5HT2A  activation  and  inhibited by 5HT2C. 
 Abnormalities in TS  are a  result of hypo-serotonergic state producing compensatory up-regulation of postsynaptic 5-HT A  receptors and secondary abnormalities in phasic dopamine release
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erotonergic modulation of dopaminergic neurotransmission, believed to be involved in the regulation of basal ganglia-thalamocortical circuits involved in movement and cognition

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Other studies have  however found  no differences between patient and family 5-HT and related metabolites in the CSF compared to controls

Card 3

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Differences in serotonin levels more marked in those with co-morbid OCD, a suggestion that 5-HT plays a role in obsessive-compulsive behaviors associated with TS

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Card 4

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However, more recently no differences in relative density of serotonin receptors was found in post-mortem brain tissue from frontal and occipital regions in TS subjects.  

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Preview of the back of card 4

Card 5

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Motor output, involved in repetitive motor output and central pattern generators. Facilitation of motor output and suppression of activity in sensory systems irrelevant to behavior. ​

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