Title: Psychology / Biopsychology / 10_Attention
Tags: Biopsychology::10_Attention Biopsychology::Semester_2

Q: What is the difference between a covert and an overt shift of attention ?
A: covert: no eye movement
overt: eye movement involved

Q: What is the general finding of Posner tasks?
A: Covert attention shifts improve the reaction time and identification rates of objects present at the cued location and worsen both rt and accuracy on non-cued locations.

Q: How does neural amplification play into (covert) visual attention?
A: The neural activity in the retinotopically corresponding part of the visual cortex is increased, causing stronger and more efficient neural processing in that area.

Q: What is Visuo-Spatial-Neglect?
A: Patients have problems shifting their attention to one side (most commonly left). They do not process things in that part of the visual field consciously.

Q: What is a common cause for Visou-Spatial-Neglect?
A: Lesions in the posterior Parietal Cortex.

Q: What are the 2 jobs of the frontal eye field?
A: Guiding eye saccades
Covert shifts of attention (monkey study)

Q: What part of the brain is strongly connected to the frontal eye field?
A: Posterior brain areas

Q: What 2 kinds of attention networks are there in the brain?
A: The
Dorsal (frontal eye field, superior parietal lobe)
and
Ventral (temporal-parietal junction, ventrolateral frontal cortex)
Network.

Q: How do the 2 attention networks differ in function?
A: dorsal: top-down attention network (deliberate)
ventral: stimulus-driven attention network

Q: What part of the brain is responsible for sustained attention?
A: The ACC - Anterior Cingulate Cortex

Q: What are the 2 manifestations of ADHD?
A: Inattentive
Hyper-impulsive

Q: What three types of changes can you expect in the brain of an ADHD patient?
A: Structural Changes
(reduced grey matter in striatum/basal ganglia)
Functional Changes
(reduced activity in ACC)
Genetic Abnormalities
(Dopamine Receptor Genes)

Q: How does ADHD work on a molecular level?
A: Dopamine receptors a striatal synapses are taking dopamine into the presynapse too quickly -> reduced effect of action potential
presynaptic autoreceptors register low dopamine levels in cleft and leak more dopamine into the cleft for compensation
-> (tonic vs phasic dopamine level) The signal-to-noise-ratio of dopamine is poor, the activation in the prefrontal cortex is inefficient

Q: What is Methylphenidate more commonly known as?
A: Ritalin

Q: How does Ritalin work?
A: The dopamine transporters are blocked -> more dopamine in the cleft -> less leakage by the autoreceptors -> better signal-to-noise-ratio -> more efficient activation of frontal cortex

Q: What does Ritalin do for neurotypical patients with no ADHD?
A: Makes them hyperactive

Q: What is neurofeedback training?
A: A reward is given for certain brain activation patterns, so they are learned via operant conditioning and automatically trigger more often.
This can be used to treat ADHD patients.

Q: What do Ritalin and Selective Serotonin Reuptake Inhibitors have in common?
A: They increase the efficiency of synapses by prolonging the time that neurotransmitters stay in the synaptic cleft.

Q: How did Moore and colleagues prove the relevance of the FEF to visual attention using monkeys?
A: They stimulated the FEF weakly, leading to shifts of visual attention without eye saccades.