Textbook Sections (Midterm 1)

Question 1

What are the three broad categories of anesthesia?

Answer 1

Local anesthesia, regional anesthesia (larger region than local like epidural during child birth), and general anesthesia

Question 2

How do local anesthetics like lidocaine work?

Answer 2

Block Na+ channels → inhibit action potentials → numb sensation

Question 3

When are sedatives used?

Answer 3

Sedatives are often used alongside anesthesia to reduce anxiety or induce sleep

Question 4

What is the role of GABA receptor agonists in sedation?

Answer 4

They enhance inhibitory synaptic transmission, reducing neuronal activity

Question 5

How does general anesthesia typically affect neurons?

Answer 5

General anesthetics often work on GABA receptors or block glutamate NMDA receptors (e.g., ketamine)

Question 6

What does the Goldman equation account for that the Nernst equation does not?

Answer 6

The Goldman equation accounts for the permeability of multiple ions across the membrane

Question 7

What happens to membrane potential if only Na+ is permeable?

Answer 7

ENa (around +60 mV)

Question 8

How does membrane permeability change during an action potential?

Answer 8

During an action potential, Na+ permeability increases, causing depolarization, and later K+ permeability increases causing hyperpolarization

Question 9

Why are squid giant axons important in neuroscience research?

Answer 9

Their large size allows for easy experimental manipulation and was crucial in the study of action potentials (helped Hodgkin and Huxley observe changes in Na+ and K+ conductance)

Question 10

What evolutionary advantage do giant axons provide squid?

Answer 10

Can conduct APs quicker, making it easier to escape prey

Question 11

What do Tetrodotoxin (pufferfish) and saxitoxin (dinoflagellates) do to Na⁺ channels?

Answer 11

They block Na⁺ channels, leading to paralysis by preventing action potential generation

Question 12

What is the effect of μ-conotoxins from cone snails on Na⁺ channels?

Answer 12

They block Na⁺ channels, paralyzing prey

Question 13

How do α-toxins from scorpions affect Na⁺ channels?

Answer 13

They prolong Na⁺ channel inactivation, increasing the duration of action potentials and disrupting normal neuronal function

Question 14

What do β-toxins from scorpions do to Na⁺ channels?

Answer 14

They shift the voltage dependence of Na⁺ channel activation, causing channels to open at more negative potentials and inducing uncontrolled action potential firing

Question 15

How does batrachotoxin from frogs affect Na⁺ channels

Answer 15

It removes inactivation of Na⁺ channels, causing continuous neuronal firing

Question 16

Which toxins block K⁺ channels, and what is their effect

Answer 16

Dendrotoxin (wasps), apamin (bees), and charybdotoxin (scorpions) block K⁺ channels

Question 17

What are channelopathies?

Answer 17

Genetic diseases caused by mutations in ion channel genes, affecting voltage-gated or ligand-gated ion channels

Question 18

What is the main characteristic of epilepsy and how are ion channels involved?

Answer 18

Recurring seizures linked to mutations in Na⁺, K⁺, and Ca²⁺ channel genes

Question 19

What ion channel mutation is associated with Severe Myoclonic Epilepsy of Infancy?

Answer 19

Reduced Na⁺ channel function due to mutations in SCNAs

Question 20

How does a mutation in KCN genes cause Benign Familial Neonatal Convulsion?

Answer 20

Mutations in K⁺ channels cause brief seizures in newborns

Question 21

What is ataxia and which ion channel mutations are involved?

Answer 21

Ataxia is the loss of voluntary motor movement, often caused by mutations in K⁺ or Ca²⁺ channels

Question 22

How does a mutation in CACNA1A cause Spinocerebellar Ataxia Type 6?

Answer 22

Polyglutamine expansions in this Ca²⁺ channel gene lead to degeneration of cerebellar cells

Question 23

What mutation is associated with Familial Hemiplegic Migraine Type 1?

Answer 23

Gain-of-function mutations in CACNA1A, increasing Ca²⁺ current and causing severe headaches and ataxia

Question 24

How do mutations in the SCN9A gene affect pain perception?

Answer 24

Mutations lead to conditions like Inherited Erythromelalgia (IEM), where Na⁺ channels are more excitable, increasing pain sensitivity

Question 25

What is Sinoatrial Node Dysfunction and Deafness (SANDD) caused by?

Answer 25

A mutation in CACNA1D that disrupts Ca²⁺ influx, leading to congenital deafness and cardiac dysfunction

Question 26

What ion channel mutation is linked to X-linked Congenital Stationary Night Blindness (CSNB)?

Answer 26

Mutations in CACNA1F reduce Ca²⁺ currents in retinal cells, impairing night vision

Question 27

How does latrotoxin cause excessive neurotransmitter release?

Answer 27

It bypasses the usual Ca²⁺ requirement for vesicle fusion, leading to painful muscle cramping

Question 28

What is the effect of botulinum toxin on neuromuscular transmission?

Answer 28

It blocks neurotransmitter release at neuromuscular junctions, leading to paralysis by cleaving SNARE proteins

Question 29

How does tetanus toxin affect the spinal cord?

Answer 29

It blocks inhibitory neurotransmitter release, leading to uncontrolled muscle contractions (tetany)

Question 30

What are myasthenic syndromes, and what do they cause?

Answer 30

Myasthenic syndromes cause weakness and fatigue due to defective neuromuscular transmission

Question 31

What is Lambert-Eaton Myasthenic Syndrome (LEMS) and its cause?

Answer 31

LEMS is an autoimmune disorder where antibodies target and reduce the number of voltage-gated Ca²⁺ channels in motor neuron terminals, decreasing neurotransmitter release and causing muscle weakness

Question 32

What are congenital myasthenic syndromes?

Answer 32

Congenital myasthenic syndromes are genetic disorders affecting presynaptic proteins (e.g., SNAP-25, synaptotagmin) or vesicle size, resulting in reduced acetylcholine release and muscle weakness

Question 33

What causes color blindness?

Answer 33

Mutations in the genes for cone photopigments

Question 34

How does the brain distinguish color?

Answer 34

Compares the activity levels of different cone types (ex: green light activates both M and L cones, but the M cones are more strongly activated, signaling green to the brain)

Question 35

What happens if the three types of cones overlap?

Answer 35

The overlap in their absorption spectra allows us to perceive various colors

Question 36

What are the three types of cones?

Answer 36

Short- (S), medium- (M), and long-wavelength (L)

Question 37

What is Protanopia?

Answer 37

Loss of long-wavelength-sensitive cones (L cones); difficulty perceiving reds

Question 38

What is Deuteranopia?

Answer 38

Loss of medium-wavelength-sensitive cones (M cones); difficulty perceiving greens

Question 39

Where are color blindness conditions most common?

Answer 39

These deficiencies are more common in males because the genes for the L and M pigments are located on the X chromosome

Question 40

What is color contrast?

Answer 40

The perception of a color changes based on its surrounding colors

Question 41

What is color consistency?

Answer 41

Despite changes in lighting, an object’s color can appear constant, allowing us to recognize objects under different lighting conditions (e.g., a tennis ball looking the same in sunlight and at dusk)

Question 42

Besides wavelength, what two other things help with perceiving colors?

Answer 42

1. Context
2. Past experiences

Question 43

What neurotransmitter receptors are affected by toxins from plants and animals?

Answer 43

Many toxins affect neurotransmitter receptors, particularly acetylcholine (ACh) receptors, glutamate receptors, GABA receptors, and glycine receptors

Question 44

What are nicotinic and muscarinic ACh receptors named after?

Answer 44

Nicotinic ACh receptors are named after nicotine (from tobacco), and muscarinic ACh receptors are named after muscarine (from the mushroom Amanita muscaria)

Question 45

What are the symptoms of nicotine and muscarine poisoning?

Answer 45

Symptoms include nausea, convulsions, and, in the case of muscarine poisoning, potentially death

Question 46

Name three toxins that block nicotinic ACh receptors and their sources

Answer 46

α-bungarotoxin from the banded krait snake
Curare (δ-tubocurarine) used by South American natives
α-conotoxin from cone snails

Question 47

What are atropine and scopolamine, and what do they block?

Answer 47

Atropine (from deadly nightshade) and scopolamine (from henbane) are plant toxins that block muscarinic ACh receptors

Question 48

What receptor does the betel nut toxin arecoline target, and what is its effect?

Answer 48

Arecoline from betel nuts targets nicotinic ACh receptors and acts as a stimulant

Question 49

Name two toxins that target glutamate receptors and their sources

Answer 49

Kainate and quisqualate from mushrooms and seaweeds target glutamate receptors, causing excitotoxicity

Question 50

What does strychnine block, and what is its effect?

Answer 50

Strychnine blocks glycine receptors, leading to seizures

Question 51

What do bicuculline and picrotoxin block, and what is their effect?

Answer 51

Bicuculline (from Dutchman’s breeches) and picrotoxin block GABA receptors, causing overstimulation of the CNS

Question 52

What is muscimol, and what does it activate?

Answer 52

Muscimol is a hallucinogen from mushrooms that activates GABA receptors

Question 53

How does baclofen function and what is it used for?

Answer 53

Baclofen is a synthetic GABA receptor agonist used to treat muscle spasms

Question 54

What are the key toxins to remember that block nicotinic ACh receptors?

Answer 54

α-bungarotoxin, curare (δ-tubocurarine), and α-conotoxin

Question 55

How does GABA function in the developing brain compared to the mature brain?

Answer 55

In the developing brain, GABA acts as an excitatory neurotransmitter, while in the mature brain, it functions as an inhibitory neurotransmitter

Question 56

What causes GABA’s shift from excitatory to inhibitory during brain development?

Answer 56

The shift is due to changes in intracellular Cl⁻ concentration, driven by the Na⁺/K⁺/Cl⁻ co-transporter in immature neurons and the K⁺/Cl⁻ co-transporter in mature neurons

Question 57

What is the role of NKCC1 and KCC2 in the function of GABA?

Answer 57

NKCC1 increases intracellular Cl⁻ in immature neurons, making GABA excitatory. KCC2 removes Cl⁻ from cells in mature neurons, making GABA inhibitory

Question 58

Why is early depolarizing GABA important during brain development?

Answer 58

Early depolarizing GABA responses help control neuronal growth, migration, and synaptic development