Physio & Pharma Flashcards
Dopamine
Dopaminergic Pathways
- both excitatory and inhibitory
- movement, personality, mood, sleep
- Parkinson’s disease (low dopamine in substantia nigra), Tourette’s (excessive dopamine in caudate nucleus), Schizophrenia (dopamine hypothesis, high dopamine levels)
Dopaminergic Pathways: - mesolimbic pathway: reward circuit, ventral tegmental area to ventral striatum (nucleus accumbens)
- mesocortical pathway: motivation, emotion, EF; ventral tegmental area area to PFC
- tuberoinfundibular pathway: hormone regulation (prolactic); hypothalamus to pituitary gland
- Nigrostriatal pathway: purposeful movement; substantia nigra to dorsal striatum (caudate nucleus, putamen)
Acetylcholine (ACh)
- both excitatory and inhibitory
- movement, arousal, attention, memory
- Alzheimer’s memory loss assoc with low ACh in entorhinal cortex & hippocampus
- causes muscles to contract, myasthenia gravis destroys ACh receptors at neuromuscular junctions
Glutamate
- excitatory
- movement, emotions, learning, memory
- Gluatamate induced excitotoxicity –> cell death in diseases like stroke, seizures, Huntington’s, Alzheimer’s
Norepinephrine
- excitatory
- arousal, attention, learning, memory, stress, mood
- Chatecholamine hypothesis: depression caused by low norepinephrine, mania by excess norepinephrine
Serotonin (5-HT)
- inhibitory
- arousal, sleep, sexual activity, mood, apetite, pain
- Low serotonin assoc with depression, suicide, bulimia, OCD, migraine
- Anorexia (high serotonin–> anxiety –> lowered by restricting)
- ASD- high blood level serotonin
Gamma Aminobutyric Acid (GABA)
- pimary inhibitory
- mood, memory, arousal, sleep, motor control
- Low GABA-> insomnia, seizures, anxiety; benzos increase GABA
- Low GABA and ACh in basal ganglia assoc with Huntington’s motor x’s
Reticular formation
- neuron network from medulla to midbrain
- regulates muscle tone, controls eye movement, controls pain
- reticular activating system (RAS): consciousness/arousal, sleep/wake cycle, alerts cortex to incoming sensory stimuli. RAS lesions cause coma, electrical stimulation of RAS can wake you up.
Substantia Nigra
- reward-seeking, drug addition, motor control (with basal ganglia connections, nigrostriatal dopamine pathway)
- dopamine degeneration in substantia nigra –> Parkinson’s motor x’s (tremor, slow movement, rigidity)
Hypothalamus & substructures
Hypothalamus
* maintains homeostasis, regulates survival fx’s (body temp, BP, HR, sex, respiration, hunger/thirst, stress response)
* sends hormones to pituitary glad (GnRH for secondary sex dev, oxytocin and vasopressin for social bonding, sex, social recog, etc.)
* HPA axis- mediates stress response
* emotions- bilateral damage can cause aggression/rage, electrical stimulation can cause other emotions (pleasure, fear)
Substructures
* mammillary bodies- memory
* suprachiasmatic nucleus- biological clock; circadian rhythms and sleep/wake cycle
oxytocin has positive emo recog effects for ASD & Schizo. but negative for healthy controls (oversensitive to facial exp)
Thalamus
Korsakoff syndrome
Thalamus- relay station to cortex of all senses except smell, language/speech, declarative memory, coordinates sensory & motor functioning.
Korsakoff syndrome- thiamine deficiency (usually due to alcoholism) damages neurons in thalamus & mammillary bodies, x’s include anterograde & retrograde amnesia, confabulation.
Basal ganglia
- striatum (caudate nucleus, putamen, nucleus accumbens) receives input from cortex, and globus pallidus sends info to thalamus
- motor initiation & control, procedural memory, attention & decision-making, emotions
- Linked to mood, Huntington’s & Parkinson’s, schizophrenia, ADHD, OCD, Tourette’s.
Limbic system
Amygdala
Kluver-Bucy Syndrome
- emotions (especially fear), emotion recognition in facial exprations, evaluating emotional significance of events, emotions linked to memories (flashbulb memories)
- PTSD- hyperactivity of amygdala and hypoactivity of vmPFC (which regulates the amygdala)
- Kluver Bucy Syndrome- bilateral amygdala lesions cause hyperorality, hyperphagia, hypersexuality, reduced fear, visual agnosia.
Limbic system
Cingulate Cortex
- includes cingulate gyrus & sulcus
- emotional reaction to pain, motivation, memory
- Abnormalities linked to depression and bipolar disorder
Limbic system
Hippocampus
- more memory than emotion; transfers declarative memory from STM into LTM, spatial memory
- Damage to hippocampus –> episodic memory & spatial deficits in Alzheimer’s
- Chronic cortisol increases in hippocampus impairs retrieval
- PTSD- severity of trauma and x’s linked to (smaller) size of hippocampus
Broca’s aphasia
slow & labored paraphrase speech (verbs & nouns only), anomia and impaired repetition, intact comprehension (written and spoken)
Role of the dorsolateral prefrontal cortex (dlPFC)?
EF.
Damage causes concrete thinking, impaired judgment/insight, impairments in planning & WM, apathy/disinterest, perseverative responses.
Don’t care (apathy), don’t know (judgment), don’t know how (planning)
Role of the orbitofrontal cortex (OFC)?
Response inhibition, emotion regulation, social behaviors.
Damage causes impulsivity, inappropriate social behaviors, lack of concern for others, aggression, antisocial behaviors, affective lability, distractibility.
AAA, crystal orb (unpredictable)
What is the role of the ventromedial prefrontal cortex (vmPFC)?
Social cognition, decision making, memory, emotion regulation.
Damage causes impaired social cognition (empathy, emotion recognition), lack of insight, impaired decision-making & moral judgment, emotional blunting.
Social cognition, can’t make a decision, blunted emotion.
Supplementary motor cortex vs premotor cortex
Supplementary motor cortex plans & coordinates self-initiated movements.
Premotor cortex plans & coordinates movements in response to external stimuli.
Wernicke’s aphasia
impaired comprehension (spoken & written), impaired repetition, anomia. Speech is fluent but meaningless and with errors/susbtitutions.
Anosognosia vs asomatognosia
Anosognosia- unaware of own illness
Asomatognosia- lack of interest/recognition of own body part
Hemispatial neglect
Caused by damage to right parietal lobe, neglect left side body & stimuli.
Ideomotor apraxia vs ideational apraxia
Ideomotor apraxia- cannot carry out motor action on verbal command (“pretend to brush your hair”)
Ideational apraxia- inability to plan/execute a task with sequential steps
Both usually due to left (dominant) parietal damage
Gerstmann’s Syndrome
Acalculia, agraphia, right-left confusion, finger agnosia. Due to left (dominant) parietal damage.
What is cortical blindness?
What is blindsight?
What is affective blindsight?
Cortical blindness: eyes and optic nerves intact but occipital lobe is damaged, resulting in visual deficits.
Blindsight: Pts with cortical blindness do not consciously see stimulus but respond appropriately to it (ex, reach for object they claim they cannot see).
Affective blindsight: do not consciously see emotional sitmuli but respond appropriately (ex, cannot see picture of angry/happy face but correctly guess what was shown to them)
What causes prosopagnosia?
Bilateral damage to occipitotemporal junction
Types of colorblindness
Red/green colorblindness: genetic (X-linked) or injury/disease (MS, diabetes). Most common.
Blue/yellow colorblindness: rare; autosomal dominant.
Theories of color vision
Trichromatic theory- we have cones for red, blue, and green in retina.
Opponent-process theory- three types of opponent process cells (blue/yellow, red/green, white/black). Accounts for afterimages and types of colorblindness.
