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Bio Basis Final > Oral Final > Flashcards

Oral Final Flashcards

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Biology 101 flashcards
1
Q

What is the HPA Axis

A

The hypothalamic pituitary adrenal (HPA) axis is our central stress response system. The HPA axis is an eloquent and dynamic intertwining of the central nervous system and endocrine system.

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2
Q

What happens during acute stress?

A

Improved attention and memory formation, performance on simple tasks, performance on complex tasks that require cognitive flexibility, enhances immune system

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3
Q

What happens during prolonged stress?

A 
Impaired memory (hippocampus) and immune activity, enlarged adrenal glands, digestive difficulties. 
Long term impacts: heart complications, digestive issues (IBS, Colitis), anxiety, PTSD
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4
Q

What are the components of the stress response system?

A

Amygdala activates hypothalamus.
Hypothalamus releases TRH.
TRH activates Pituitary Gland.
Pituitary Gland releases ACTH.
ACTH activates Thyroid and Adrenal glands
Thyroid and Adrenal glands produce Cortisol.
Cortisol deactivates hypothalamus.

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5
Q

What are the epigenetic implications?

A

Changes in Phenotype not Genotype.

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6
Q

What is the role of Oxytocin?

A

reduction of blood pressure and cortisol levels, increases pain thresholds, promotes growth and healing, non-noxious sensory stimulation, ingestion of food.

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7
Q

How does Cortisol affect memory?

A

Enhances: memory consolidation, simple emotional learning (fear conditioning) and habit learning
Impairs: long term memory retrieval, working memory

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8
Q

What is the GANE theory?

A 
NE release (under arousal) interacts with glutamate receptors, resulting in greater glutamate release, which in turns leads to greater NE release. 
Positive feedback loop between NE and glutamate creates local NE hotspots near the neurons that transmit high-priority information.
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9
Q

What is the natural process of reward?

A

The dopamine neuron on the VTA is activated
DA is released in Nucleus accumbens (NAcc)
Reward is experienced
DA also binds to the GABA neuron in the NAcc
DA activates GABA ne NAcc, which fires
GABA inhibits DA ne VTA, stopping DA release in NAcc

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10
Q

How do Stimulants affect the reward pathway?

A

When all of the DA is released, the enzymes that break down DA are overwhelmed and take a while to do their job, explaining the duration of the high.
Related to both meth and cocaine, reuptake by presynaptic transporters is prevented, making the DA last longer in the synapse, causing increased pleasure.

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11
Q

How do Opiates affect the reward pathway?

A

Opioids provide inhibitory feedback to the GABA negative feedback loop (stopping the brakes).
In addition, opioids provide inhibitory feedback to the GABA interneuron.

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12
Q

Alcohol?

A

Alcohol neutrally blocks the binding of GABA on the DA ne VTA.
Alcohol causes release of enkephalins. Enkephalins neutrally block (aka occupy without activating) GABA receptors. Inhibits GABA interneuron.

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13
Q

Sedatives?

A

When sedative hypnotics and benzodiazepines are present, they neutrally block the postsynaptic GABA receptors (not activating the neuron and blocking transmission of the signal).

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14
Q

MARIJUANA & THC?

A

THC inhibits release of GABA (activating the brakes through activation of the CB1 receptor)

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15
Q

NICOTINE?

A

Dopamine is enhanced by glutamate from the PFC, and ACH.

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16
Q

HALLUCINOGENS?

A

The DA neuron on the VTA (DA ne VTA) is activated. This is enhanced by excitatory input from projections from the raphe nucleus. Since hallucinogens act as serotonin agonists, increased activation of the DA ne VTA occurs.

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17
Q

What is the role of the Anterior Cingulate Cortex

A

Affect and autonomic regulation (connections with amygdala and hypothalamus)
Various aspects of cognition, ranging from decision making to the management of social behavior (impulse control, decision making, cognitive flexibility, adaptability, cooperation)

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18
Q

What is the role of the Subgenual Subregion (SGSR) of the pACC?

A

Autonomic visceromotor regulation
Respiratory rate, heart rate, blood pressure, dilation of pupils, facial flushing, goosebumps, nausea/vomiting, butterflies in stomach, salivation, bowel and bladder evacuation

19
Q

What is the role of the Midcingulate Cortex?

A 
Discrete motor activities (motor task acquisition and performance) 
Cognitive functions (response selection, divided attention (multitasking))
20
Q

What is the role of the Posterior Cingulate Cortex?

A

Visual spatial processing
Topographic and topokinetic memory (memory of spatial positional relationships)
Large visual scene assessment
Recall of autobiographical memories
Helps regulate balance between internally and externally-focused attention (stimulated when daydreaming)

21
Q

What are the impacts of starvation?

A

Malnutrition
Inaccurate or absent hunger cues
Concentration and processing impaired
Body-down regulates
GI system particularly impacted (delayed gastric emptying, damaged absorption, abdominal pain)
Brain and Nerves: Poor concentration, fear of gaining weight, moody, memory issues
Hair: hair thins and is brittle
Heart: low blood pressure, slow heart rate, fluttering of the heart, heart failure
Blood: anemia and other blood issues
Muscles, Joints, and Bones: weak muscles, swollen joints, bone loss, fractures, osteoporosis
Kidneys: kidney stones, kidney failure
Body Fluids: low potassium, magnesium and sodium
Intestines: constipation, bloating
Hormones: periods stop, problems with height, trouble getting pregnant
Skin: bruise easily, dry skin, growth of fine hair all over body, gets cold easily, yellow skin, nails get brittle

22
Q

What are starvation behaviors?

A

Slow pace, tiny bites
Isolation while eating
Hoarding food
Overfocus on food/eating

23
Q

What are the cognitive risk factors for Anorexia?

A

Inflexibility: set-shifting behavior
Impaired global processing with inconsistent evidence of superior local information processing (limits seeing the bigger picture)
Suggested impaired social cognition (other people’s thoughts and feelings)

24
Q

What are the changes in the reward system associated with anorexia?

A

significant decrease in activity for AN
Either sensory or reward/motivation weaker in AN
Hunger in AN – decreased insula response than typically, reduced food reward in AN, paradoxical effect (connection with anxiety signaling)

25
Q

What are the changes in the reward system associated with Bulimia?

A

Increased volume in medial frontal cortex – central striatal volume
Limitations in synaptic purging associated with dysfunction in food-reward processing and self-regulation
Decreased activation in the brain’s reward system in anticipation and after chocolate milkshake
May compensate by overeating
High initial response in reward system to food, then lower subsequent response

26
Q

What are the cognitive risk factors for Bulimia?

A

Inhibitory limitations – not impairment
Modified Stroop tasks used with words to body weight and shape – strong Stroop effect occurs
Attention may be altered
Impulsivity

27
Q

What are the cognitive risk factors for Binge Eating Disorder?

A

Difficulty set-shifting and problem solving
More likely to perform worse on a decision-making task
Self-reported difficulty with executive functioning

28
Q

What are the changes in the reward system associated with Binge Eating Disorder?

A

Consistent with substance abuse disorders (DA and Endogenous Opioids)
When rats are injected with high levels of sugar in prolonged binge-like experiment:
Increased dopaminergic receptor binding occurs in striatum and nucleus accumbens
Striatum: important for food reward, satiety, and pleasure

29
Q

What is the Mirror system?

A

Mirror neurons are activated when observing another person’s behaviors
Found in frontal and parietal lobes
May be important for empathy (e.g. shared enjoyment, seeing people sad, speculation of dysregulation in autism)

30
Q

How do the mesolimbic system relate to Autism and social reward?

A

Anomalous mesolimbic responses to social and nonsocial rewards
Serotonin dysregulation
Endorphin elevations
Cerebral spinal fluid – elevated levels of endorphin in ASD
High pain tolerance and self-injurious behaviors

31
Q

What are the Volumetric and Pruning differences?

A

Volumetric increases
Neuronal overgrowth
Lack of synaptic pruning
Areas such as prefrontal cortex (role in communication, social skills, and executive functioning)
Premature cessation of cerebellum, cerebrum, and overall limbic system

32
Q

What are the positive symptoms of schizophrenia?

A

Delusions and Hallucinations.

33
Q

What are the negative symptoms of schizophrenia?

A

Apathy, Anhedonia, Attention, Alogia, Affective Blunting

34
Q

What are the cognitive symptoms of schizophrenia?

A

Impaired attention and information processing, executive dysfunction.

35
Q

What are the aggressive symptoms of schizophrenia?

A

Overtly Hostile, Arson, Self Injury, Assault

36
Q

What are the affective symptoms of schizophrenia?

A

Depression, Anxiety, Guilt, Tension, Irritability

37
Q

What is the region associated with the affective symptoms?

A

Mesocortical and ventromedial PFC

38
Q

What is the region associated with the cognitive symptoms?

A

Dorsolateral PFC

39
Q

What is the region associated with the negative symptoms?

A

Mesocortical and ventromedial PFC

40
Q

What is the region associated with the positive symptoms?

A

Mesolimbic System

41
Q

What is the region associated with the aggressive symptoms?

A

Orbitofrontal PFC and connections to amygdala

42
Q

What is the dopamine hypothesis?

A

Schizophrenia related to not enough dopamine in cortex, too much in limbic structures
Arose because too much dopamine causes psychosis and medications that reduce dopamine reduce psychosis (Increased dopamine transmission = positive symptoms)

43
Q

What is the glutamate hypothesis?

A

Glutamate driving dopamine
Insufficient glutamate leads to not enough dopamine in cortex
Because of GABA interneurons (inhibitory), end up with dysregulation of dopamine in limbic structures
Hypofunction of glutamate receptors (NMDA receptors)

Bio Basis Final (2 decks)

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