Exam 4: Mental Functions Flashcards
Executive functions
Management (regulation, control) of basic cognitive processes including attention, working memory, and task flexibility
Personality
Individual differences among people in behavior patterns, cognition, and emotion
Morality
Differentiation of intentions, decisions, and behaviors between those that are good or right and those that are bad or wrong
What lobes carry out executive functions and express personality and morality?
Pre frontal lobes (“silent lobes”)
3 ways to define prefrontal cortex
- Non-motor area
- Granular frontal cortex (layer 4 present)
- Projection zone of DM nucleus of thalamus (gates info to and from prefrontal)
What does the executive system do? (4)
- Forms goals and objectives
- Devises plans of actions
- Selects cognitive skills needed, coordinates and applies skills
- Evaluates our actions as success or failure
What area of the brain forms the plan of action?
DLPFC
What part of the brain is the attention controller?
PPC
What part of the brain signals a need for adjustment
Dorsal anterior cingulate cortex
What does the Wisconsin Card Sorting Test test?
DLPFC- ability to switch gears
What does the Stroop Test test?
dACC- signals need for adjustment
Where is short-term memory (or working memory) and long-term plans processed?
In prefrontal cortex- DLPFC & VLPFC
What areas of the brain are involved in intelligence?
- DLPFC
- Parietal lobe
- Anterior cingular cortex
Big 5 personality traits
- Openness
- Extroversion
- Conscientiousness
- Agreeableness
- Neuroticism
Extraversion associated brain region
Medial orbito-frontal cortex
Conscientiousness associated brain region
Middle frontal gyrus
Neuroticism associated brain regions
- DMPFC
- Cingulate gyrus/caudate
- Medial temporal lobe
Agreeableness associated brain regions
- Superior temporal sulcus
- Posterior cingulate cortex
Brain area for implicit moral issues
Left temporopatietal junction (TPJ)
Brain area for explicit making of moral right and wrong judgments
VMPFC
Frontal lobe syndromes- Dorsolateral (3)
- Perseverative behavior
- Field-dependent behavior
- Mental rigidity
Frontal lobe syndromes- Orbitofrontal
- opposite of DL syndrome
- behaviorally and emotionally disinhibited
- oscillating between euphoria and rage
- poor to no impulse control
Intracranial self-stimulation (ISS)
Brief bursts of weak electrical stimulation to pleasure centers, involved in mesotelencephalic dopamine system
What two midbrain areas of neurons is the mesotelencephalic dopamine system in?
- Substantial nigra
2. Ventral tegmentum
Nigrostriatal pathway
Substantia nigra neurons project to dorsal striatum (degenerate in Parkinson’s)
Mesocorticolimbic pathway
Ventral tegmental area neurons project to cortical and limbic sites, including nucleus accumbens
What type of pleasure is the mesocorticolimbic pathway involved in?
Anticipatory (NOT actual)
Inputs to ventral tegmentum (3)
- Glutamatergic excitatory input (PFC & LH)
- GABAergic inhibitory input (VTA interneurons and NAc)
- Dopaminergic input (from VTA to PFC and NAc)
What 2 structures does the nucleus accumbens excite?
- PFC (via the ventral palladium)
2. DM nucleus of thalamus
Role of NAc
Anticipatory reward pathway, natural reinforcers (ex: food)= increased dopamine
How do psychoactive drugs work?
Cross BBB and alter the way nerve cells send, receive, and process info=affects behavior, overstimulate reward circuit
Tolerance (2)
- Given dose has less effect
- Need larger dose to produce same effect
- Shift in dose-response curve to right, can be metabolic or functional
Tobacco effect on reward circuit
Nicotine binds to acetylcholine receptors on dopaminergic neurons in the VTA. Channels opened, sodium flows in and depolarizes cell–> increased release of dopamine in NAc.
Alcohol effect on reward circuit
Ethanol reduces the activity of voltage-dependent
potassium channels in VTA neurons. As a result, the relative refractory period of VTA dopaminergic neurons is reduced, allowing them to fire more often. High
rates in VTA neurons–> increased release of dopamine in NAc.
Marijuana effect on brain circuit
THC binds to CB1 (anadamide) receptors on GABAergic inputs in the VTA, reducing calcium influx and thus transmitter release. VTA dopaminergic neurons can thus fire more often–> increased release of dopamine in NAc.
Amphetamine effect on reward circuit
Competes with dopamine for “re”uptake in the NAc.
Once inside the terminal button, it causes reuptake transporters to reverse their mode of operation. The net effect is to increase the level of dopamine in the NAc.
Cocaine effect on reward circuit
Cocaine acts as a serotonin-norepinephrine-dopamine
reuptake inhibitor [known as a triple reuptake inhibitor (TRI)]. Cocaine prevents dopamine reuptake in the NAc,
thus high levels of dopamine persist.
Opiate effect on reward circuit
Opiates bind to endogenous opiate receptors on VTA
GABAergic neurons, enhancing potassium efflux and thus reducing transmitter release. VTA dopamine neurons are disinhibited–> increased release of dopamine in NAc
6 basic human emotions
- Anger
- Happiness
- Surprise
- Disgust
- Sadness
- Fear
James-Lang Theory (1884)
Stimulus triggers autonomic and somatic responses which triggers emotion (“I am trembling; therefore, I am scared”)
Cannon-Bard Theory (1915)
Stimulus triggers both autonomic and somatic responses and emotion (physiological responses & emotion are independent)
Modern view of emotions
All factors influence one another
Limbic system and emotions (3)
- Cingulate gyrus
- Amygdala
- Hypothalamus
Anterior Cingulate Cortex (ACC)
- Dorsal: DLPFC & PPC
- Ventral: Amygdala & Hypothalamus
What are lesions of the ACC associated with?
Fear, irritability, and depression
3 nuclei groups of amygdada
- Corticomedial- receive olfactory input
- Basolateral-receive non-olfactory input
- Central nucleus-major output
Lesions to what structures block fear conditioning to simple tones?
MGB and amygdala
What circuits does the amygdala activate? (2)
- Behavioral circuits in periaqueductal gray
2. Sympathetic circuits in hypothalamus
Hypothalamus and aggression (2)
- Posterior hypothalamus-elicits aggression
2. Medial prefrontal cortex-inhibits/directs response
What side of the brain does production and processing of facial expressions happen?
Right hemisphere
Cytokines
Small proteins produced by immune cells that combat infections and communicate with the brain (particularly the hypothalamus) to elicit appropriate behaviors
5 major psychiatric disorders
- Schizophrenia
- ADHD
- Affective disorders
- Anxiety disorders
- Tourette’s syndrome
SZ NT effect
Excess dopamine –> symptoms of SZ
Non-dopamine theories of SZ
- Neuroleptics don’t alleviate symptoms for weeks, only work for some people, only reduce positive symptoms
- Hallucinogens mimic positive symptoms (agonists of SE)
- Anesthetics mimic negative symptoms (agonists of glutamate)
Too much serotonin creates…
Positive symptoms
Too much glutamate creates…
Negative symptoms
Brain area problem in SZ
Enlarged ventricles and fissues, reduced brain volume
ADHD NT effect
Deficient Dopamine and NE
Brain area problem in ADHD
Slow developing prefrontal cortex (and PPC)
Brain area problem in affective disorders
- Reduction in overall brain size (VA Cingulate Cortex)
- Abnormal:
1. Amygdala (causes emotion)
2. Hippocampus (symptoms of emotional problems)
3. Medial prefrontal cortex (watches emotional state)
Affective disorder NT effects
Low monoamines- serotonin and NE
Neuroplastic theory of affective disorders
Depression is caused by reduction in synthesis of neurotrophins in cortical areas and a decrease in adult neurogenesis in hippocampus
5 major anxiety disorders
- Generalized
- Phobic
- Panic
- OCD
- PTSD
Neurobiology of stress and anxiety
- Amygdala assesses emotional significance
- HPA cortex circuit releases cortisol (excited by amygdala and inhibited by hippocampus)
Anxiety disorder NT effects
Low serotonin (b/c of comorbidity of depression)
Brain problems in anxiety disorder
Too much activity in prefrontal cortex and fewer benzodiazepine binding sites, smaller hippocampus (in depression)
Tourette Syndrome NT effect
Abnormality in basal ganglia-thalamus-cortex feedback circuit
Tourette Syndrome NT effect
Abnormality in basal ganglia-thalamus-cortex feedback circuit, too much dopamine- effectiveness of D2 blockers
6 major causes of brain injury
- Tumors
- Vascular disorders (stroke)
- Closed-head injuries
- Infections
- Neurotoxins
- Genetic factors
2 major types of stroke
- Cerebral hemorrhage-caused by aneurysm
2. Cerebral ischemia-disruption of blood supply (usually L cerebral artery)
Infarct
Area of dead tissue
Penumbra
Area of dysfunctional tissue surrounding infarct
Glutamate theory os Ischemia
Glutamate storm= excess glutamate leaves damaged neurons in its wake, little initial damage but substantial neuron loss detected later
Contusions
Injuries that involve damage to the cerebral circulatory system, causes internal bleeding and a hematoma (bruise), can be coup or countrecoup
Concussion
No contusion but a disturbance of consciousness
CSF and closed-head injuries
Run along outside of blood vessels enclosed by end feet from astrocytes, washes brain and carries waste out
2 common types of brain infections
- Bacterial infections-lead to abscesses (ex: syphilis), can inflame meninges
- Viral infections- attack neural tissue (rabies) or have no specific affinity for it (mumps and herpes)
Neurotoxins
Can produce toxic psychosis, some can be endogenous (ex: excessive glutamate, antibodies in autoimmune disorder)
Genetic accident
Causes neuropsychological disorders, Down syndrome- extra chromosome 21
4 neuroplastic responses to brain damage
- Degeneration
- Regeneration
- Reorganization
- Recovery of function
Neuroplasticity degeneration
- Axotomy (cutting axon)
- Anterograde degeneration (degen. of distal segment)
- Retrograde (degen. of proximal segment)
- Transneuronal degeneration (degen. spreads from damaged neurons to neurons linked by synapses)
Neuroplasticity regeneration
Regrowth of damaged neurons, better in lower order vertebrates (accurate axonal growth lost in maturity), nonexistent in CNS of adult mammals (oligodendrocytes prevent growth in CNS)
Neuroplasticity reorganization
Reorganization of primary sensory and motor systems observed in lab animals following damage to peripheral nerves and cortical areas (compensating)
2 mechanisms to account for neural reorganzation
- Strengthening of existing connections through release of inhibition (quick remapping)
- Est. of new connections (magnitude of effect is large)
Neuroplasticity recovery of function: 3 main ways to reduce cognitive dysfunction
- Block neurodegeneration
- Promote recovery
- Rehabilitative training
