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PCL470 > Introduction to The Central and Peripheral Nervous System > Flashcards

Introduction to The Central and Peripheral Nervous System Flashcards

1
Q

What is the role of CSF and where is it produced?

A
  • prevents mechanical damage and absorbs shock from body movement
  • generated and maintained by choroid plexus in ventricles
  • these are in the centre of the brain and flow through ventricles providing continuous CSF to brain and spinal cord
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2
Q

Why is the CSF useful in pharmacology?

A
  • introduction of drugs to CSF bypasses BBB through hole drilled in skull
  • sampling CSF provides information about drug distribution and PK
  • access point for measuring drug concentration and concentration (changes in ion [ ] in brain causes seizures)
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3
Q

What is contained in the CNS vs PNS?

A

CNS: brain and spinal cord
PNS: nerves that connect to spinal cord or brain
- nerves –> motor or sensory
- cranial nerves go straight into brain (vision, face innervation, etc)
- SNS and ANS

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4
Q

Somatic nervous system

A
  • sensory neurons and motor neurons
  • sensing environment, controlling voluntary movements and reflexes
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5
Q

Autonomic nervous system

A
  • self governing - we are not in control of this and cannot tell it what to do
  • controls body’s physiology along with endocrine system
  • sympathetic ANS: mobilizes body for action
  • parasympathetic ANS: energy conservation
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6
Q

Sympathetic ANS

A
  • adrenaline
  • engaged during crisis (fight or flight)
  • disengaged when parasympathetic is on
  • dilates pupils, inhibits salivation, more oxygen, speeds heartbeat, sweating, constricts blood vessels, inhibits digestion, liver stimulates glucose release, secretion of NE and EP by adrenal medulla, relaxes bladder
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7
Q

Parasympathetic ANS

A
  • acetylcholine
  • homeostatis
  • conserves energy maintaining system
  • disengaged when S-ANS is on
  • constricts pupil, stimulates salivation, constricts airways, slows heartbeat, stimulates digestive system, contracts bladder, stimulates sexual arousal
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8
Q

Forebrain

A
  • more developed in humans
  • cerebral cortex
  • basal ganglia
  • amygdala
  • thalamus
  • hypothalamus
  • hippocampus
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9
Q

Midbrain

A
  • older structures, less connected to conciousness
  • raphe nucleus
  • periaqueducta grey
  • ventral tagmental
  • substantia striata
  • locus ceoruleus
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10
Q

Hindbrain

A
  • controls body’s vital functions
  • reticular formation
  • pons
  • medulla
  • cerebellum
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11
Q

Cerebral cortex

A
  • consciousness
  • perceiving and integrating sensory information
  • storing and retrieving memories
  • self reflection
  • planning
  • decisions and voluntary behaviours
  • higher thought and reasoning
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12
Q

Basal ganglia

A
  • initiating voluntary movement
  • reward system (pleasure) –> addiction
  • decision making based on previous experience
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13
Q

Thalamus

A
  • filters information and relays it between the cortex and subcortical structures
  • consciousness
  • sleep rhythm regulation
  • can be affected for attention disorders
  • drug target for anesthetics and anti epileptics
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14
Q

Hypothalamus

A
  • endocrine system
  • hormone regulation
  • stress response
  • hunger and satiety
  • regulates when to engage the sympathetic nervous system
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15
Q

Limbic system

A
  • mediates emotional responses and memories
  • important in mood and attention disorders (depression and ADHD)
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16
Q

Cingulate gyrus

A
  • memory retrieval and storage of emotional content
  • concept of self and others
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17
Q

Basal ganglia

A
  • predicts what happens next
  • reinforces actions that promote survival
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18
Q

Amygdala

A
  • involved in negative emotions (fear and anger)
  • overactive in anxiety
  • learns what to fear and what is dangerous
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19
Q

Hippocampus

A
  • spatial memory
  • autobiographical memory
  • memory formation and retrieval
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20
Q

How does hippocampal damage affect memory formation?

A

damage to hippocampus can prevent the formation of new memories even if they are able to remember things from before the damage

21
Q

Hypothalamus and pituitary gland

A
  • hypothalamus neurons secrete hormones into the blood stream right away or to the pituitary
  • pituitary releases hormones into the bloodstream from secretory cells
22
Q

What endocrine glands and hormones does the pituitary control

A

Glands: adrenal, ovaries, testes
Hormones: gonadotropin releasing hormone, leuinizing hormone, follicle stimulating homrone, oxytocin, vasopressin, orexin

23
Q

What NTs are midbrain nuclei associated with?

A
  • raphe nucleus: serotonin
  • substantial nigra and ventral tagmental: dopamine
  • locus coeruleus: NE
  • periacqueductal grey: endorphins –> pain and pain management
  • reticular formation: sleep and attention (DA, HIS, NE), conciousness, habituation
24
Q

Cerebellum

A
  • coordinates and refines movements and timing
  • maintains balance and posture
25
Q

What causes someone to stumble when they are drunk?

A
  • alcohol (and other GABAergic drugs) reduces cerebellum activity which is involved in balance
26
Q

Pons

A
  • relay point for spinal neurons and cranial Ns
  • location of monoamine neurons and reticular activating systems
27
Q

Medulla oblongata

A

essential functions
- heart rate, respiration, BP, vomiting in response to toxins, swallowing, sneezing

28
Q

What is the BBB composed of

A
  • epithelial cells with specialized tight junctions and adherence junctions to restrict the movement of charged molecules
29
Q

What molecules can/cannot pass through the BBB

A

Pass
- lipophilic molecules and drugs through the membran
- charged molecules through active transport by transporters or transcytosis

Excluded
- highly charged particles and drugs (will only have peripheral effect)
- large proteins, antibodies
- bacteria and viruses
- blood and plasma cells –> immune system has limited access

30
Q

What regions are not protected by the BBB

A
  • pituitary gland (hormone secretion)
  • pineal gland (melatonin secretion)
  • area postrema (vomiting)
31
Q

Pathological conditions that can affect the BBB

A

stroke, trauma, alzheimer’s, ALS, multiple sclerosis, inflammation

32
Q

How do CNS drugs cross the BBB?

A
  • they are weak acids or weak bases
  • it passes through the BBB in its non ionized form
  • changes to its ionized state after crossing the BBB
  • drugs use charge dresidues to interact with their target
33
Q

Do CNS affect neuron physiology?

A

Yes, they ultimately change the excitability of the neuron (propensity to fire an AP and release NT). They can also affect astrocytes, oligodenstrocytes and microglia

34
Q

What is the difference between classical and non classical NTs?

A

Classical are packaged into vesicles and non-classical are produced by enzymes and freely diffuse across cell membrane to alter local neuron physiology

35
Q

Glutamate

A
  • classical NT
  • an AA
  • every neuron has receptors for it
  • excitatory
36
Q

GABA

A
  • classical NT
  • derivative of glutamate
  • every neuron has receptors for it
  • inhibitory
  • acts as the breaks for the brain by stopping excitation
37
Q

Glycine

A
  • classical NT
  • AA
  • primarily inhibitory
  • important in spinal cord
38
Q

Acetylcholine

A
  • classical
  • made from nutrient choline and is acetylated
  • mostly excitatory
39
Q

Dopamine, norepinephrine, epinephrine, serotonin, histamine

A
  • classical NTs
  • derivatives of AAs
  • bind to GPCRs that can be inhibitory or excitatory
  • Gq - excitatory
  • Gi - inhibitory
  • Gs - excitatory
40
Q

What are examples of non classical NTs?

A
  • nitric oxide
  • endocannabinoids
  • prostaglandins
41
Q

How do drug targets modulate neuron function?

A
  1. AP of presynaptic neuron - drugs can enhance or block this signal
  2. synthesis of NT
  3. storage of NT into vesicles (drugs can make vesicles store less NT so every time there is less NT delivery)
  4. intracellular metabolism of NT
  5. vesicular release of NT
  6. reuptake of NT into presynaptic neuron or glia
  7. degredation of NT in synaptic cleft
  8. binding of NT to post synaptic cleft
  9. receptor-induced change in excitability
  10. retrograde signalling - chemicals produced in post synaptic neuron diffuse to influence presynaptic neuron
42
Q

How do autoreceptors and post synaptic receptors modulate NT release

A
  • autoreceptors on presynaptic terminal
  • they sense the synaptic levels of NT in the cleft
  • report back to presynaptic neuron and attenuate how much NT is released subsequently
  • autoreceptors have a higher affinity for NT than postsynaptic receptor
43
Q

What happens when an agonist or antagoninst bind to D2 receptors?

A

agonist: lower DA neurotransmission

44
Q

How do psychoactive drugs activate ion channels and metabotropic receptors

A
  • most are agonists or antagonists of NT receptors or voltage gated ion channels
  • agonist: holds channel open, antagonist: holds it closed
  • can increase/decrease probability of firing by modulating ion channels directly or indirectly by activating metabotropic receptors that activate the channel through a G protein or signal cascade
45
Q

resting membrane potential

A
  • negative on inside of cell, positive outside
  • bulky ions (-) are inside, cannot leave
  • Cl ions (-) are low inside and high outside to create a concentration gradient
  • Na ions (+) are low inside and high outside to create a concentration gradient and electrostatic pressure
  • K ions (+) are high inside to create concentration gradient
  • Ca (+) are low inside and high outside for CG
46
Q

depolarization and hyperpolarization

A
  • membrane depolarized when sodium rushes into cell
  • this makes the membrane less polarized (less negative) and the neurons fire
  • potassium leaves the cell and the AP occurs
  • after potassium leaves and cholide rushes in
  • this makes the inside very negative (hyperpolarized) and would take even more sodium to make it fire
47
Q

How do ion channels create excitatory or inhibitory postsynaptic potentials?

A

sodium (+)
- influx into cell down gradient
- depolarization
- ESPS
potassium (+)
- efflux out of cell down gradient
- hyperpolarization
- IPSP
chloride (-)
- influx into cell down gradient
- hyperpolarization
- IPSP (resetting)
calcium (+)
- influx down gradient
- acts as second messenger and activates enzyme
- depolarization

48
Q

What does it take for a neuron to fire?

A
  1. NT as synapse cause ligand gated sodium channels to open
  2. Na rushes in and depolarizes membrane
  3. nearby voltage gated Na channels open to propagate signal down axon
  4. at the terminal volatge gated Ca channels allow Ca into the terminal to signla the release of NT vesicles
  5. the membrane opens volatge gated potassium channels to repolarize the neuron before it can fire

PCL470 (14 decks)

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