Focused cards Flashcards

1
Q
  1. How do genes yield traits (how does genotype become phenotype)? That is, what are the biological processes that lead to synthesis of cell proteins such as receptors and ion channels? If two people differ on a particular trait as adults (e.g., neuroticism, intelligence), what are genetic mechanisms that could explain inherited vs. environmental influences on this particular trait?
A

DNA –> transcription –> mRNA –> Translation –> proteins (receptors, ion channels, some nerve transmitters) –> TRAIT

EX: Dr craft is risk averse (similar to her biological parents), whereas Alfred is bold & fearless (I, E Dr craft is higher than Alfred on neuroticism)

The gene that encodes (leads to the synthesis of) GABA* contributes to neuroticism;

Perhaps Dr craft inherited a type of GABA gene (w/ a particular DNA sequence) that makes only a modest amount of GABA

*GABA= inhibitory neurotransmitter

Alfreds “GABA gene” is very proficient, but craft’s GABA gene is less so

Thus, Alfred’s neurons make a lot of GABA, whereas Crafts makes less.

This results in lower neural firing in Alfreds brain (especially amygdala) than in crafts.

Calmer amygdala=calmer person.

*Amygdala is the brain area highly active during fear.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
  1. Describe two mechanisms at the DNA level that can result in increased or decreased gene expression (i.e., that can turn genes on or off) after conception.
A

Life events can modulate the extent to which genes are activated.

Mechanisms include:

  1. DNA methylation: methyl group binds to a segment of DNA less gene expression (less transcription) – or ^ if demethylation occurs
  2. Histone remodeling: the core around which DNA wraps changes shape >> modulates gene expression or modulates extent of transcription
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  1. Can “selective breeding” be used to improve performance on a maze task in rats? Is the performance of “maze-dull” vs. “maze-bright” rats similarly altered: (a) if they are raised by parents who perform differently on this task? (b) if they are raised in an “enriched environment”?
A

Rearing rats in an enriched enviroment equalized maze performance between the two populations!

Environment altered the gene expression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
  1. What is the genetic basis of PKU (phenylketonuria)? How can environmental (dietary) adjustment compensate for this gene abnormality?
A

Genetic basis at birth?

Gene coding for enzymes that converts phe to tyr is not functional, so little tyr

This the brain cannot synthesize dopamine (DA made from tyr)

Thus abnormal brain development (frontal lobe dopamine activity crucial for cognition)

Can altered diet (envir factor) compensate for gene disorder?

Yes low phenylalanine foods ca help overcome this

Phe > tyresine > low dopamine(5-ht)

Needs low phenyl foods and high tyresine

  • symptoms include vomiting, seizures, hyperactivity, intellectual disability, irritability, and brain damage
  • lack phenylalanine hydroxylase, an enzyme required to convert phenylalanine to tyrosine
  • phenylalanine accumulates in the body; and levels of dopamine, a neurotransmitter normally synthesized from tyrosine, are low
  • Leads to abnormal brain development
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
  1. Why were heritability estimates from early twin studies misleading (i.e., why did early twin studies overestimate trait heritability)? How can epigenetic studies of monozygotic twins be used to help us better understand how environment influences traits/disease as we age?
A

A relatively select (non-diverse) sample of identical twins raised apart vs. together

Comparison of monozygotic twins’ epigenetic differences as they age (periodic DNA sampling to screen for methylations, histone modifications)

Comparison of disease discordant monozygotic twins> epigenetic differences between them may lead to discovery of genes underlying disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  1. Describe the basic divisions of the nervous system (what they’re called, where they’re located, what they do).
A

The central nervous system (CNS) functions as the processing center for the nervous system. It receives information from and sends information to the peripheral nervous system.

The nervous system has three broad functions: sensory input, information processing, and motor output.

The peripheral nervous system (PNS) is the division of the nervous system containing all the nerves that lie outside of the central nervous system (CNS). The primary role of the PNS is to connect the CNS to the organs, limbs, and skin.Jun 4, 2020

The 4 main functions of the nervous system are: Reception of general sensory information (touch, pressure, temperature, pain, vibration) Receiving and perceiving special sensations (taste, smell, vision, sounds) Integration of sensory information from different parts of the body and processing them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
  1. Describe the functions of the sympathetic and parasympathetic nervous systems, including some physiological effects of sympathetic NS activation (and what types of events activate it).
A

Sympathetic vs parasympathetic NS

Fight or flight ie energy expending vs rest and digest (energy conserving)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  1. How well protected is the CNS compared to the PNS (describe protective mechanisms)? Can your CNS and PNS neurons repair themselves if they are damaged? If so, how?
A

NS Protection/injury

CNS is well protected by the skull + meninges

Also the vertebrae.

Cerebrospinal fluid. (CSF)

Cusions brain and spinal cord

CSF produced in ventricles (chambers) of the brain.

PNS not as well protected

… but nerves typically deep within limbs, & PNS neurons regenerate to greater extent (axons regrow, as long as soma intact)

What events cause NS injury?

What determines extent of disability

After peripheral nerve injury? If it can regenerate

After spinal cord injury? Extent and location, lower the better

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  1. What is the blood brain barrier (BBB), physically? What purpose does the BBB serve?
A

Immunological protection:

Blood brain barrier (BBB)

Prevents most large molecules (e.g bacteria) from entering brain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  1. What do the terms dorsal/ventral, lateral/medial, anterior/posterior, and rostral/caudal refer to? [Try describing where different parts of the body/brain are located relative to one another, using these terms]
A

Thus, anterior and posterior indicate front and back; rostral and caudal, toward the head and tail; dorsal and ventral, top and bottom; and medial and lateral, the midline or to the side. Nevertheless, the comparison between these coordinates in the body versus the brain can be confusing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  1. Label the major parts of a neuron and describe the function of each part. Describe the major types of proteins that are embedded in a neuron’s lipid bilayer membrane.
A

Cell membrane

The semipermeable membrane that encloses the neuron `

Cell body

The metabolic center of the neuron; also called the soma

Dendrites

The short processes emanating from the cell body, which receive most of the synaptic contacts from other neurons

Axon hillock

The cone-shaped region at the junction between the axon and the cell body

Axon

The long, narrow process that projects from the cell body

Myelin

The fatty insulation around many axons

Nodes of Ranvier

The gaps between sections of myelin

Buttons

The button-like endings of the axon branches, which release chemicals into synapses

Synapses

The gaps between adjacent neurons across which chemical signals are transmitted

Cell wall= lipid bilayer with proteins embedded in it.

Ion channels: regulate cation+/anion flow in or out of the cell

Receptors: nt bind to them to signal excitation (+, ^ firing) or inhibition (- firing).

Transporters: actively move important molecules in and out of cell (e.g NA+/K+ transporter, nt transporter)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  1. Name and describe the functions of 4 types of glial cells (3 in CNS, 1 in PNS).
A

Glial cells, (Glia)

CNS: all encased in bones

Oligodendrocytes: produce myelin sheath paddles (octopus cns

Microglia: respond to injury, disease (clean up, trigger inflammation); regulate synapse formation and elimination

Astrocytes: part of the BBB; regulates blood flow.

PNS:

Schwann cells: ARE myelin sheath; direct axonal regrowth after injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  1. Name and identify on whole-brain and mid-sagittal views (see below) the major parts of the hindbrain, midbrain and forebrain, and describe at least one function of each structure. What behavior/experience might be changed if each structure was damaged?
A

Hindbrain

  1. Medulla; autonomic, basic life support functions ( breathing, heartbeat, digestion, swallow cough vomit sneeze)
  2. Pons: soma of “reticular activating” neurons, responsible for wakefulness/alertness.
    a. alertness, sleep/wake cycle: locus ceruleus (norepinephrine relasing)

Sleep/wake cycle: raphe (5-HT (serotonin)- releasing)

  1. Cerebellum: motor coordination/balance (execution of learned motor sequences, largely unconcius during execution); some cognitive functions.

Midbrain

  1. Tectum (“roof”, dorsal)
  2. Superior colliculus: visual coordination of movement ( particularly reflexive movement of the head)
  3. Inferior colliculus: sound localization; auditory coordination of movement (includes reflexive movement of the head)
  4. Tegmentum (“floor, ventral)
  5. Periaqueductal Gray (PAG): pain modulation, freezing behavior (opiods bind here)
  6. Ventral Tegmental area (VTA): pleasure/motivated behavior (Dopamine-releasing)
  7. Substantia Nigra: speed of movement ( Dopamine releasing)

Forebrain

  1. Thalamus: sensory motor “relay/coordination station” … Nuclei for vision, audition, somatosensation.
  2. Hypothalamus: 4Fs (sympathetic NS activation starts here)
  3. Basal Ganglia: habitual movement (cannot see this from a whole brain and mid sagittal view) lateral to the thalami. Damage: disease (Tourette’s, OCD also associated with function of basal ganglia
  4. Amygdala: emotion, particularly fear, anger
  5. Hippocampus: episodic, declarative learning/memory (Damage? HM (Anterograde memory formation couldn’t happen) Jimmie G, Alzheimer’s)
  6. Cerebrum (cerebral cortex/Cerebral hemispheres:

Occipital lobe: simple visual perception

Parietal lobe: somatosensory (touch) perception (anterior); Complex visual perception(posterior)

Temporal lobe: complex visual perception; auditory perception

Frontal lobe: decion making/reasoning (prefrontal cortex= PFC; anterior) planning and execution of conscious movement (motor cortex: posterior)

Somatotopic arrangement: Primary motor cortex (frontal lobe) ; primary somatosensory cortex (parietal lobe)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
  1. Motor and sensory systems are said to be mostly “crossed over” – what does this mean?
A

Crossover of motor and sensory pathways

  1. primary motor cortex axons> crossover at medulla> control muscles on other side of body

Somatosensory neurons on one side of body> Axons crossover in spinal cord > ascend to thalamus, somatosensory cortex on other side of the brain

Visual and auditory neurons also mostly crossover to one side of the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  1. Explain how the membrane potential of a neuron is maintained at rest (in a “polarized” state, approx. -70 mV).
A
  1. Resting membrane potential
  2. “potential”=difference in electrical charge from inside to outside of axon (neuron)
  3. At rest, -70 mv, because fewer cations+ inside than outside. (How is this negative state maintained? Pump moves 3+ out for every 2+ in) Cation+ channels closed so cations cant flow back in
  4. What cations are involved?

Na+: more outside than inside axon, so concentration gradient OUT.

K+: more inside than outside axon, so concentration gradient IN

NA+ OUT, K+ IN

Resting potential: neuron is POLARIZED, “poised like a stretched rubber band”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  1. Describe the major ionic events underlying an EPSP, an IPSP, and an action potential (neuron firing), and draw curves that illustrate the changes in membrane potential (y) over time (x), during each of these events.
A
  1. Small changes in membrane potentinial: EPSP, IPSP
  2. EPSP: small positive change in membrane potential (small Depolarization); membrane potential becomes less negative (e.g. -65mV)

What causes this: Na+ channels open briefly> Na+ enters neuron

  1. IPSP: small negative change in membrane potential (small HYPERpolarization); membrane potential> more negative (e.g. -75mV)

What causes this?: K+ channels open more often> k+ flows out (OR cl- channels open briefly > CL- flows in)

Why is electrolyte balance important for nerve cell function? If they get low than your neurons will not work as efficiently.

Action potential (neural firing)

What causes action potentials?

Activation of sensory neuron ending (in skin eye ear tongue nose organs joints muscles

Input from other neurons

17
Q
  1. Describe how an action potential is triggered, and how it is conducted along an axon, both unmyelinated and myelinated.
A

Action potential (neural firing)

What causes action potentials?

Activation of sensory neuron ending (in skin eye ear tongue nose organs joints muscles

Input from other neurons

Ionic basis of action potential: how does the inside of the neuron turn positive relative to the outside

  1. Summation (temporal or spatial) of EPSPs > threshold potential reached (-55mv)

Temporal meaning a whole bunch of inputs from the same area

Spatial is multiple from different areas

  1. This voltage triggers more Na+ channels to open>> Na+ rushes IN.
  2. Then K+ channels open >> K+ starts to flow out.
  3. But large Na+ influx ^ membrane potential to +50mv
  4. Then Na channels close>> membrane potential starts dropping (K+ still flowing out, and NA+/K+ pump working).
  5. Lag in K+ channels closing>> hyperpolarization (refractory period: cell cant fire again because now below resting potential (-85mv)
18
Q
  1. Explain how a local anesthetic like Novocain can prevent action potentials in your sensory nerves, and why a poison like TTX can kill you.
A

Some drugs affect neural activity by blocking ion channels rather than altering chemical transmission

Novocain (local anesthetic) blocks Na+ channels in sensory nerves

TTX (pufferfish) blocks voltage gated Na+ channels> all nerve firing goes down.

19
Q
  1. Explain how a demyelinating disease like multiple sclerosis (MS) leads to slowed movement, or an inability to move.
A
  • The myelin deteriorates which slows down action potential and makes transmission happen slower
  • If you lose all of your myelin then it makes it almost impossible
20
Q
  1. Describe the major steps in chemical neurotransmission (at least 5).
A

Describe step 1 in chemical neurotransmission

Synthesis of a neurotransmitter: packaging in vesicles

Describe step 2 in chemical neurotransmission

  • Action potential arrives at axon terminal and triggers NT release (exocytosis)
  • Ca++ channels open, Ca+ flows IN
  • Ca+ causes vesicle membranes to fuse with axon terminal membrane
  • NT is released into synapse

Describe step 3 in chemical neurotransmission

  • NT molecules cross synapse and bind to receptors on post-synaptic neuron
  • Which receptor the NT binds to determines if the neuron is excited or inhibited

Describe step 4 in chemical neurotransmission

Neurotransmitter goes off the receptor and NT signaling is terminated via: Reuptake of NT

Describe step 5 in chemical neurotransmission

  • Neurotransmitter goes off the receptor and NT signaling is terminated via: Enzymatic degradation
  • Most NTs go back into axon terminal that released them, by the use of a transporter protein, but some are broken down by enzyme in the synapse and thus inactivated
21
Q
  1. What are the similarities and differences between ionotropic vs. metabotropic receptors?
A
  1. Ionotropic receptor: receptor is ON the ion channel> nt binding causes Na+, K+, or Cl- ion channels to open (or close) >> EPSP or IPSP
  2. Metabotropic receptors: receptor is part of a protiein that is INDIRECTLY connected to an ion channel, via a G protein ; activation is slower but longer, and neuron “metabolism” can change (e.g nt or receptor production can change or gene expression can change).
22
Q
  1. When a neurotransmitter binds to its receptor and causes excitation of the post-synaptic neuron, what is the primary ionic event causing this excitation? What are the primary ionic events underlying inhibition?
A
  • Na+ rushes in which causes an epsp and excitation*
  • K+ or Cl- channels open potassium rushes out and chloride rushes in causing an IPSP.*
23
Q
  1. Name 2 neurotransmitters of the amino acid class, and EXPLAIN why one of them is always excitatory and the other is almost always inhibitory.
A
  1. Glutamate
    * 3 glut receptor types: all ionotropic & open Na+ channels s (+) always excitatory (sodium goes in)
  2. GABA
    * 2 GABA recepr types: ionotropic opens Cl- channels ; metabotropic opens K+ channels, so both (-) always inhibitory
24
Q
  1. Name 3 neurotransmitters of the monoamine class. Give an example of a behavior or experience that each type of neurotransmitter is involved in, and give examples of drugs that can alter monoaminergic neurotransmission (and EXPLAIN how the drugs do this).
A

B. Monoamines

  1. Dopamine (DA): movement mood cognition
  2. Norepinephrine (NE) (and epinephrine, E): alertness, mood phe> tyr> Ldopa> DA>NE> E (made in the locus coeruleus)
  3. Serotonin (5-HT): mood, vision, appetite
25
Q
  1. Describe two main functions of acetylcholine (ACh), and EXPLAIN how different drugs can alter cholinergic neurotransmission and thus behavior/experience.
A

2 main functions of acetylcholine (ACh)

  • Chemical that motor neurons release to activate muscles
  • Also used for memory

2 “cholinergic” receptor types of acetylcholine (ACh)

  • One ionotropic: Gates Na+, so +excitation
  • One metabotropic: Gates K+, so -inhibition
26
Q
  1. Describe the circuitry underlying the knee-jerk reflex, including what types of neurons and what neurotransmitters are involved.
A
  • Tap on patellar tendon
  • Sensory neuron fires into spinal cord
  • Excited motor neuron goes back out to quad, releases glutamate, acetylcholine is released and the muscle contracts
  • Sensory neuron activates interneuron and inhibits motor neuron that goes out to the hamstring so the hamstring relaxes

Stretching the patellar tendon activates sensory neurons; these neurons release glutamate, which excites motor neurons that terminate on the quadriceps muscle; the motor neurons release ACh which causes quadriceps muscle contradiction and extension of the lower leg

27
Q
  1. Explain why people who suffer from myasthenia gravis experience “muscle weakness”; what type of medication is used to help them move more normally (how does this drug work)?
A

People with myasthenia gravis experience muscle weakness because the disease results in a loss of acetylcholine receptors

  • Tensilon drug
  • AChE inhibitors prevent AChE from breaking down ACh
  • Increase in ACh
28
Q
  1. What is the difference between an agonist and an antagonist? What are a few examples of specific agonists and antagonists, and how do they work (at what step of neurotransmission does each act, and how)?
A
  1. Agonist vs antagonist: Enhance vs inhibit nt action.

Most psychoactive drugs alter CHEMICHAL neurotransmission (alter nt communication rather than ion channels). Examples, by stage at which they act:

Synthesis: L-dopa ^ synthesis of DA ( parkinsons treatment)

Release:

Amphetemines ^ release of monoamines (DA/NE/5-HT agonist)

Botox reduces release of Ach (antagonist) decreases muscle contraction

Binding: MANY drugs increase nt effect (agonist), or decrease nt effect (antagonist) by binding to receptors of a particular nt

  • Nicotine mimics Ach at 1 type of cholinergic receptor (e.g. motor neuro>muscle)
  • Curare blocks Ach binding at same type of cholinergic receptor > what effect?
  • Paralytic snake venoms by blocking Ach rec neuromusc jxn

Oxycontin, fentanyl mimic endorphin at opiod receptors (decrease pain)

Naltrexone (Trexan, opioid OD antidote) blocks opioid receptors > what effect?

Reuptake: some drugs block reuptake (thereby ^ nt action: agonists)

  • SSRI’s prevent 5-HT reuptake
  • Cocaine prevents reuptake of monoamines>> synaptic DA, NE, 5-HT levels ^

Enzymatic degradation: some drugs inhibit enzyme that breaks down nt (thereby ^ nt action)

  • AChE inhibitory (myasthenia gravis Tx) prevent AChE from breaking down Ach

MAO inhibitors (depression Tx) prevent MAO from breaking down monoamines

29
Q
  1. Describe technologies that are used to examine the structure of the living human brain.
A
  1. To examine structure
  2. Cerebral angiography: inject dye into cerebral artery, then X-ray to localize blood circulation abnormalities like aneurysm
  3. CT scan: X-ray 8-9 horizontal brain sections, then reconstruct as 3d picture (e.g to detect tumor location)
  4. MRI: magnetic field X radiowave scan; higher resolution than CT, so optimal for soft tissue like brain (e.g to precisely localize tumor or stroke)
30
Q
  1. Describe technologies that are used to examine function (and dysfunction) of the living human brain.
A
  1. To examine function (what brain areas active during particular tasks?)
  2. PET: radiolabeled glucose injects into bloodstream> glucose taken up most by active neurons> scan for areas of high radioactivity (=high brain activity)
    * If inject radiolabeled drug that binds to 1 specific receptor (or nt, or transporter), can visualize where those receptors are and whether those are activated
  3. Sex differences in opioid receptor density. Men have a higher density of them
  4. fMRI: measures oxygen utilization (active brain areas take up more oxygenated)
31
Q
  1. Explain what approaches may be used in animals (and sometimes humans) to determine the role of certain brain structures and certain neurotransmitters/receptors/ion channels in particular behaviors or experiences.
A
  1. To more directly link brain structure w/ function, can decrease or increase brain activity, then test performance:
  2. Transcranial stimulation: interrupt or stimulate cerebral cortex neuron activity
  3. Compare functions in people who lack certain brain structures (or w/damage to certain areas) w/ those who have intact brains.
  4. In animals, more invasive approaches:
  • Lesion
  • Deep electrical brain stimulation (only as therapeutic, in humans)
  • Neuron-level electrical recording of action potentials
  • Drug microinjection (agonist or antagonist)