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Lecture 5

PSY 2301 Lecture Notes - Lecture 5: Acetylcholinesterase, Frontal Lobe, Auditory Cortex


Department
Psychology
Course Code
PSY 2301
Professor
Andra Smith
Lecture
5

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Direct/simpler
Receptor are proteins embedded in membrane
Have a biding site for neurotransmitter
Eg. Nicotine - nicotinic receptor - allows sodium ions to enter cell (looks
like acetylcholine; therefore binds at that site)
Which will then Core that will open for an influx or eflux of ions
Iontropic receptor
-
Metabolism needs energy to occur
No pore
Also has binding site
Instead linked to G-protein that can effect other properties of the membrane
Neurotransmitter is the 1st messenger
Realizes a second messenger (2nd chemical released to effect cell
altering biochemical process - lead to more responsive pore s iontropic
receptors form new ion channel, help increase synthesis of Protiens
Second messenger
Metabotropic receptors
-
Receptors for direct and indirect effects
Varieties of Neurotrnasmitters
Peripheral
-
Depending on neurotransmitter release and where it is released depends on
behaviour
Acetylcholine is released at muscles
Excitatory neurotransmitter
Ionotropic receptors
Cholineergic neuRon
-
Somatic nervous systems
Acetylcholine reduces heart rate increasing digestion
Parasympathetic
Acetylcholine binds through norepinephrine; and therefore
norepinephrine is released (fight or flight)
Sympathetic
Cholineergic neurons control both divisions
-
Autonomic nervous system
Central
-
Midbrain nuclei that project and send acetylcholine to the rest of
the brain
Acetylcholine is involved with learning and memeory
Degenerative Brian disorder that first appears as progressive
memory loss and later in to he most common cause of
generalized dementia
Secondary source of acetylcholine; where you
see a depletion of acetylcholine; helps with
Loss of cholinergic cells in the basal forebrain
Two principle changes that occur
Plays a role in Alzheimer's
Cholinergic
4 systems
-
Activating systems
Neurotrnasmitter systems and behaviour
Chp 5
Wednesday, October 12, 2016
8:51 AM
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see a depletion of acetylcholine; helps with
neuroplasticity; therefore memory can be
impacted
Build up protein; therefore cannot communicate
In the entorhinal cortex; major input and output
to and from hippocampus; first sign of build up
protein occurs
Presence of neuritic plaques and neurotfibrillary
tangles in t he cerebral cortex
Block that from happening with a acetylcholine
esterase blocker, no breakdown of acetylcholine
there longer time in synapse (eg. Aricept exelon)
Increase acetylcholine in the synapse; most drugs
block acetylcholine esterase
Treatments
Movement; have to have dopamine released to activate basal
ganglia; stimulating motor cortex
Invlves dopamergic system + sertonergic system
Hallucination
Delusions
Disordered thoughts
The voices arise because Broca's
area rangers outputs in to parts of
the brain that receive speech inputs
from the outside (auditory cortex)
Broca's area
Poverty of speech
Postive (added to us)
Emotions
Loss of pleasure
Social withdrawal
Dopamine hypothesis - excels in medial
Negative
Charecteristics
Mesolimbic system - positive
Mesocortical system -negative systems
Nigrostriatal system - substanigra
Tuberoinfudibular system
4 major dopamergic systems
Most effective drugs for schizophrenia has many transmitter
involved - serotonin increases in the frontal cortex; causes
reduction in dopamine
Schizophrenia
Dopamine is the reward neurtansmitter
Dopaminergic
Norepinephrine is in the brain stem
Impacts emotional tone
Decreased in depression
A lot of new antidepressants also increase norepinephrine and
serotonin
Too much norepinephrine in mania
Fine line between too much and too little
Noradrenergic
Multple impacts on behavior
While falling asleep; studying
Maintains waking EEG
Decreased serotonin in depression
Serotonergic
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