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Biopsych > Midterm 2 > Flashcards

Midterm 2 Flashcards

1
Q

In the central nervous system clusters of cell bodies are called what

A

Nuclei

Singular: nucleus

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2
Q

In the peripheral nervous system clusters of cell bodies are called what

A

Ganglia

Singular: ganglion

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3
Q

In the central nervous system, bundles of axons are called what

A

Tracks

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4
Q

In the peripheral nervous system, bundles of axons are called what

A

Nerves

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5
Q

What is an axon hillock

A

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

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6
Q

What are synapses

A

The gaps between adjacent neurons across which chemical signals are transmitted

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7
Q

What are the two fundamentally different types of cells in the nervous system

A

Neurons and glia cells

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8
Q

What are myelin

A

Fatty insulating substance around many axons, the myelin sheath they form increase the speed and efficiency of axonal conduction.
-saltatory conduction>AP jumps from node to node down axon skipping over myelinated regions

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9
Q

What are oligodendrocytes

A

Type of glial cell with (usually myelin rich) extensions that wrap around the axons of some neurons of the central nervous system.

  • myelination of CNS axons
  • provide several myelin segments, often on more than one axon
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10
Q

What are Schwann cells

A

Another class of glial cells found in the PNS

  • myelination of the PNS axons
  • each Schwann cell constitutes one myelin segment
  • can guide axonal regeneration (regrowth) after damage * this is why axons in brain/spinal cord usually cannot be repaired after damage (Schwann cells are only in the PNS)
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11
Q

What are microglia

A

Class of glial cells that are smaller than other glial cells

  • respond to injury or disease by multiplying, engulfing cellular debris, and triggering inflammatory responses
  • originate in bloodstream and migrate to the brain
  • Phagocyte (removes waste, repairs damage)
  • releases growth factor
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12
Q

What are astrocytes

A
  • largest glial cells that are star shaped
  • some extensions cover the outer surfaces of blood vessels that course through the brain
  • can make contact with neuron cell bodies-allowing the passage of some chemicals in the blood into the CNS neurons and in blocking other chemicals (Control/create the blood brain barrier)
  • provide physical structure to the CNS( helps keep things in place)
  • serves as a bridge from blood to cells (nutrients in, waste out)
  • scar tissue
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13
Q

What are synaptic vesicles

A

spherical cell membrane packages that store neurotransmitter molecules ready for release near synapses

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14
Q

what are neurotransmitters

A

Molecules that are released from active neurons and influence activity of other cells

  • produce either excitation or inhibition, not both; but a few produce excitation under some circumstances and inhibition under others
  • synthesized in the neuron
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15
Q

What are microtubules

A

Tubules responsible for the rapid transport of materials throughout neurons

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16
Q

What is a pyramidal cell

A

Multipolar neuron found in areas of the brain-many found in cerebral cortex
-type of interneuron

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17
Q

What is a purkinje cell

A

Neuron mainly found in cerebellum,

  • elaborate dendritic tree heavily invested with dendritic spines.
  • type of interneuron
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18
Q

What are sensory neurons (Afferent neuron)

A

-don’t have dendrites receive neurotransmitters
-interact with outside world converting physical impulse into electrical impulse
-can be bipolar or unipolar
-has receptors
Ex. Visual and olfactory cells (bipolar)

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19
Q

What are motor neurons (efferent neuron)

A

Release NT’s on muscles or glands

  • has dendrites
  • info flows from brain to muscles or glands
  • usually multipolar
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20
Q

What are Interneurons or relay neurons

A
  • connects neurons together (Connects sensory to motor>reflex arc)
  • most neurons are interneurons
  • in the brain(pyramidal&purkinje cells) and spinal cord
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21
Q

What are ependymal cells?

A

Glial cell along the walls of ventricles and central canal of spinal cord

  • produce CSF
  • shock absorber, brain cooling, Carries particles (nutrient/waste)
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22
Q

Describe multiple sclerosis

A
  • demyelinating disease of glia in CNS
  • oligodendrocytes are attacked. Myelin is damaged/destroyed(breaks down/breaks apart) and axon is exposed
  • can no longer carry out electrical signal down to the end of axon to other cells
  • mostly affects relay neurons/ interneurons
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23
Q

Describe Amyotrophic Lateral Sclerosis (ALS)

A
  • Motor neurone disease (PNS)
  • death of neurons which controls voluntary muscles
  • Target Schwann cells
  • gradual weakening do to shrinking of muscles
  • myelin sheath is rotten away, signal can’t travel to muscles to make them contract> eventually they waste away in leads to cell death
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24
Q

How do Schwann cells aid in neuron regrowth

A

After axon is damaged, Schwann cells first shrink and then divide forming glial cells along the axons former path. The neuron sends out axon sprouts, one of which finds the Schwann cell path and becomes the new axon. Schwann cells envelop the new axon forming new myelin

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25
Q

What is membrane potential

A

The difference in electrical charge between the inside and outside of a cell

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26
Q

What are microelectrodes

A

Intercellular electrodes with tips that are too small to be seen by the naked eye. The tip can pierce the neural membrane without severely damaging it and can record membrane potential

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27
Q

What is a neurons resting potential? Where are the ions distributed?

A

In a neurons resting state, the charge build up across its membrane is -70 mV. The neuron is said to be polarized

  • steady membrane potential of -70mV
  • more Na+ ions outside the cell then inside and more K+ ions inside than outside
  • Na+ ion channels are closed (but some still leak in)
  • K+ ion channels are opened but few exit because they’re largely held inside by the negative resting membrane potential
  • sodium potassium pump’s transport 3 sodium out for every two potassium they transport in
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28
Q

What is an excitatory postsynaptic potential? (EPSP)

A

When the postsynaptic neuron becomes depolarized (less negative/polar) due to excitatory NT’s and increase the likelihood that the neuron will fire

  • type of graded response>amplitude proportional to the intensity of the signals that elicit them
  • transmitted at great speed
  • are decremental: decrease in amplitude as they travel through the neuron
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29
Q

What are Inhibitory postsynaptic potentials (IPSP)?

A
  • postsynaptic hyper polarizations that decrease the likelihood that the neuron will fire
  • type of graded response>amplitude proportional to the intensity of the signals that elicit them
  • transmitted at great speed
  • are decremental: decrease in amplitude as they travel through the neuron
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30
Q

What determines whether or not a neuron fires?

A

Depends on the balance between the excitatory and inhibitory signals reaching its axon

  • AP’s are generated in the axon initial segment where EPSP and IPSP are conducted
  • if the sum of the depolarizations and hyperpolarizations reaching the axon initial segment at any time is sufficient to depolarize the membrane to a level referred to as its threshold of excitation(~65mV) an AP is generated
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31
Q

Describe actions potentials

A
  • massive but momentary(1ms) reversal of the membrane potential from about -70mV to ~+50mV
  • all or none responses
  • each multipolar neuron adds together(integrates) all the graded excitatory and inhibitory postsynaptic potentials reaching its axon and decides to fire or not to fire on the basis of their sum
  • they do not grow weaker as they travel across the axonal membrane (except in myelinated axon)
  • conducted more slowly than PSPs
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32
Q

What are the two ways that neurons integrate incoming signals?

A

-over space and time

  1. Spatial summation: local EPSPs produced simultaneously on different parts of the receptive membrane sum to form a greater EPSP and vice versa for IPSPs. EPSPs and IPSPs can also sum to cancel each other out
    * Grade potential’s that occur closer to the axon hillock have a larger effect
  2. Temporal summation: postsynaptic potentials produced in rapid succession at the same synapse sum to form a greater signal
    - if two great potential to happen closer together, they are more likely to reach threshold and if they happened further apart
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33
Q

What happens during an action potential in unmylinated axon

A

When the threshold of excitation is reached by an EPSP, the membrane potential is depolarized. Voltage activated Sodium channels open and Na+ ions rush in causing the membrane potential to suddenly change from about -70 to about +50 mV. This activates voltage activated potassium channels to open and K+ ions near the membrane are driven out of the cell to repolarize the neuron. Once the neuron is re-polarized potassium channels gradually close and the neuron is left hyperpolarized for a brief period of time. Sodium potassium pump’s reestablish resting potential. (depolarized, repolarized, hyperpolarized)

  • each sodium stores energy by holding back Na+ ions which are under pressure to move down their concentration and electrostatic gradients into the neuron> once one channel opens it triggers adjacent channels to open all the way to end of axon to axon terminals
  • expenda a lot of energy
  • requires pumps
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34
Q

What is the absolute refractory period

A

Brief period after the initiation of an action potential during which is impossible to elicit a second one

  • during repolarization
  • followed by the relative refractory period
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35
Q

What is the relative refractory period

A

Period during which it is possible to fire the neuron again only by applying higher than normal levels of stimulation

  • during hyperpolarization
  • K+ channels are still open
  • occurs after the absolute refractory period.
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36
Q

What two important characteristics of neural activity is the refractory period responsible for?

A
  1. APs travel across axons in one direction(cannot reverse direction)
    - section axon cannot fire again until it has been repolarized
  2. The rate of neural firing is related to the intensity of the stimulation (intermediate levels of stimulation produce intermediate rates of neural firing)
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37
Q

What is antidromic conduction

A

Action potential generated in the direction from the terminal buttons to the cell body

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38
Q

What is orthodromic conduction

A

Axonal conduction in the natural direction> from the cell body to the terminal buttons

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39
Q

What is a concentration gradient and a voltage gradient (both are forces that act on neurons)

A

Concentration gradient: the tendency of substances to move (diffuse) from area of high concentration to an area of low concentration

voltage gradient: ions tend to move from areas of high(away from 0) charge to areas of lower charge
-opposite charges attract each other, similar charges repel each other

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40
Q

What are the four kinds of ions in resting potential? where they found?

A

1 anions: negative charged ions that stay inside cell but want to go outside cell (attracted to positive forces outside the cell)

2 sodium: positive charged ions mostly outside the cell and want to be inside the cell (leak in)

3 potassium: positive charged ions mostly inside the cell but want to go outside of cell (few leak out through channels)

4 chloride: negative charged ions in abundance that stay outside of cell, little on inside (want to move inside the cell but do not)

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41
Q

What is a graded potential or graded response?

A

Post synaptic potentials

  • Small short lived voltage fluctuations between inside and outside of cell. Restricted to small area. Cell either gets more positive or more negative.
  • can either be excited toilet or Vittori
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42
Q

Describe action potential in myelinated axon

A
  • not a proper AP
  • no exchange of ions
  • faster conduction
  • let energy expended (no pumps)
  • however, strength of signal gradually decreases due to the fact that there is no ion exchange
  • nodes of Ranvier replenish action potential and allows it to continue traveling across atonal membrane jumping from node to node
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43
Q

What are some differences in APs in different neurons

A
  • some are longer or shorter
  • threshold may very
  • some fire faster than others
  • some dendrites can conduct action potentials
  • some neurons don’t display APs
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44
Q

What is the advantage of presynaptic facilitation and inhibition

A

Axoaxonic synapses selectively influence single synapses, rather than the entire neuron

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45
Q

What is a directed synapse

A

A synapse at which the site of neurotransmitter release and the site of neurotransmitter reception are in close proximity

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46
Q

Describe the two basic categories of neurotransmitter molecules

A

Small-molecule NTs: typically synthesized in the cytoplasm of the terminal button and packaged in synaptic vesicles by golgi complex. Once vesicles are filled with neurotransmitters they are stored in clusters next to the presynaptic membrane
-tend to be released into directed synapses and activate either ionotropic or metabotropic receptors that act directly on Ion channels

Large-molecule NTs(Neuropeptides): short proteins or chains of amino acids that are synthesized in cytoplasm of the cell body on ribosomes. They are packaged in vesicles by Golgi complex and transported by microtubules to the terminal buttons
-tend to be released diffusely(further away from receptor binding site) and bind to metabotropic receptors that act through second messengers

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47
Q

What is exocytosis

A

The process of neurotransmitter release into the synaptic cleft by the fusion of synaptic vesicles to the presynaptic membrane
-vesicles fuse to the membrane due to voltage activated calcium channels opening and calcium ions enter the button

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48
Q

What are receptor subtypes?

A

The different types of receptors to which a particular neurotransmitter can bind are called receptor subtypesfor that neurotransmitter

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49
Q

What is an ionotropic receptor?

A
  • easy/simple kind of receptor
  • binding site for neurotransmitter(receptor) is on ion channels
  • changes are direct and fast
  • when a NT molecule binds to an ionotropic receptor, the associated ion channel opens or closes immediately, inducing an immediate post synaptic potential by altering the flow of ions into or out of the neuron
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50
Q

What is a metabotropic receptor?

A
  • more complex
  • associated with signal proteins and G proteins
  • affects are slower to develop, longer-lasting and more varied
  • it is attached to a serpentine signal protein that winds its way back-and-forth through the cell membrane seven times
  • The metabotropic receptor is attached to this signal protein outside the neuron, the G protein is attached to a portion of the signal protein inside the neuron
  • changes or indirect and slow
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51
Q

What happens when a neurotransmitter binds metabotropic receptor

A

-A subunit of the associated G protein breaks away and it may bind to an ion channel inducing a posted synaptic potential or may trigger the synthesis of a second messenger

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52
Q

What is a second messenger

A

Once it is created, a second messenger diffuses through the cytoplasm and may influence activities of neuron in a variety of ways
* neurotransmitters are considered to be first messengers

53
Q

What are autoreceptors

A

One type of metabotropic receptor

  • located on presynaptic membrane
  • The blind to their neuron’s own neurotransmitter molecules
  • Monitor the number of NT molecules in the synapse
  • signals the presynaptic cell to stop releasing neurotransmitters or to continue releasing them
54
Q

Describe reuptake

A

The majority of neurotransmitters, once released, are almost immediately drawn back into the presynaptic buttons by transporter mechanisms to be reused

55
Q

Describe enzymatic degradation

A

Once released, neurotransmitters are degraded or broken apart in the synapse by the action of enzymes

56
Q

There are many types of synaptic communication name several

A

-axoaxonic, denrodendritic, axodendritic

57
Q

The Amino acids, the monoamines, and acetylcholine are all what

A

Conventional small molecule neurotransmitters

58
Q

What are the four most widely studied amino acid neurotransmitters

A

Glutamate, aspartate , glycine and GABA

59
Q

Describe glutamate

A

Most prevalent excitatory neurotransmitter are in the CNS (for humans)
-all over the place… many different pathways
>cortico-cortical, cortical-strial, thalamus-cortical
-amino acid neurotransmitter
-has both ionotropic(NMDA, AMPA, Kainate) and metabotropic(1) receptors
-AMPA and Kainate are relatively simple as they only require glutamate binding to open ion channel
-NMDA has more complex activity>receptor channel for Na+ and Ca++ has 4 receptors on the outside(only one for glutamate, glycine, zinc& polyamine) and 2 sites on the inside(for magnesium & PCP)
> glycine is required to bind to open channel
-if magnesium is binded, channel will not open

60
Q

Describe GABA

A

-main inhibitory neurotransmitter in the brain
-widespread distribution in brain and spinal cord
-two types of receptors
>GABAa(ionotropic) and GABAb(metabotropic)
-this is a chloride channel and therefore hyperpolarizes
_receptor has 5 binding sites

61
Q

What are the four monoamine neurotransmitters

A

Dopamine, epinephrine, norepinephrine, and serotonin

62
Q

Which monoamine neurotransmitters are classified as catecholamines

A

dopamine norepinephrine and epinephrin
-each synthesized from the amino acid tyrosine. Tyrosine is converted to l-dopa which in turn is converted into dopamine, dopamine is converted into norepinephrine and norepinephrine is converted into epinephrine

63
Q

Describe dopamine and its 4 main pathways

A

-inhibitory or excitatory neurotransmitter
-metabotropic receptors only
1. Nigrostriantal system
Origin: substantia nigra
Terminals: striatum (caudate and putamen)
Function: control of movement -Parkinson’s disease
2. Mesolimbic system
Origin: Ventral tegmental area
Terminals: limbic system & nucleus accumbens
Functions: memory formation, motivation and *rewarding effects of drugs
3. Mesocortical system
Origin: ventral tegmental area
Terminals: frontal lobe
Functions: organization -schizophrenia
4. Tuberoinfundibular system (long name short path)
Origin: hypothalamus
Terminals: pituitary
Function: secretion of hormones

64
Q

Describe norepinephrine and its pathway

A

Its a monoamine neurotransmitter that has all metabotropic receptors and can be excitatory or inhibitory
-receptors respond to both epinephrin and norepinephrine
Origin: locus ceruleus
Terminals: most of the brain
Function:
>vigilance-ready to respond/aware of surroundings
>emotions-depressed people may have low levels of norepinephrine

65
Q

What are axon varicosities

A

Bead like swellings along the axon

66
Q

Describe serotonin

A

Monoamine neurotransmitter that can be excitatory or inhibitory
-indolamine
-has ionotropic receptors
> triggered reaction to get rid of toxins, involved in nausea and vomiting
Two origins:
Dorsal Raphe(thin axons, slow AP conduction)-projects to basil ganglia
Medial raphe(thick axons, fast AP conduction)- projects to hippocampus
*in general, both terminate in the cortex
Function: depression (at low levels), anxiety, appetite and many more

67
Q

Describe acetylcholine

A

Small molecule neurotransmitter that is in a class by itself
-main impact is excitatory
-at neuromuscular junctions and many synapses of the PNS and several synapses of the CNS
-broken down in the synapse by enzyme
-synthesis in the dorsal lateral pons
-in CNS
>facilitates learning
> involved in R.E.M. sleep and triggering dreams
-used in Botox >prevents Ach release (prevent wrinkles by inhibiting muscular contraction- nicotinic antagonist)
-black widow spider venom stimulates Ach release (start twitching, convulsions, cardiac arrest)

68
Q

Describe the 2 acetylcholine receptors (receptor subtypes)

A
  1. Nicotinic:
    Ionotropic receptor found on muscle fibres(some in the brain too)
    -stimulated by nicotine>generate muscle twitches
    -many occur at the junctions between motor neurons and muscle fibres
  2. Muscarinic:
    Metabotropic receptor predominant in the CNS
    -found on axoaxonic synapses>presynaptic facilitation
    -stimulated by muscarine (found in mushrooms)
    -many located in the autonomic nervous system
69
Q

What is nitric oxide

A

Unconventional Soluble gas neurotransmitter

  • neutral of soft muscles in intestines and blood vessels, penile erection
  • if uses out of cell as soon as it is produced, no vesicles
  • no receptors: goes directly into other cells
  • activates metabolic activity of cells: production of NTs
70
Q

What are endocannabinoids?

A

Unconventional Neurotransmitters that are similar to THC
-produced immediately before they are released and synthesized from fatty components in the sun membrane
Ex. Anandamide

71
Q

What are endogenous opioids

A 
-natural ligand for receptors that bind to opiate drugs(pain killers) 
Effects of opioid receptors:
-analgesia 
-inhibition of defensive response 
-reinforcement (reward)
72
Q

What are antagonist and agonist drugs?

A

Agonist: enhance or facilitate the effects of a particular NT-provide more activity

Antagonist: impede the effect of a neurotransmitter
-Less activity

73
Q

What are some ways that drug action affects neurotransmitters

A
  • drug can block(PCPA decreases serotonin)or increase(ex. L-dopa) NT synthesis by destroying synthesizing enzymes or increasing the amount of precursor
  • drug can prevent storage of NTs by causing them to leak out and get destroyed by degrading enzymes(reserpine on monoamines) or drug can increase NT by destroying degrading enzymes
  • drug can stimulate NT release(black widow spider venom-Ach) or block release(Botox-Ach)
  • drug can block or activate autoreceptors to influence their inhibitory effect
  • drug can bind to postsynaptic receptor and either activate(nicotine on Ach) it or block it(curare on Ach-stops muscle contractions)
  • drug can block reuptake( cocaine on DA) or degradation(MAO inhibitors increase monoamine activity) so NT stays in synaptic cleft and can continue binding to receptors
74
Q

What is atropine

A

It is the main active ingredient of belladonna plant, it is a receptor blocker that exerts its antagonist effect by binding to muscarinic receptors thereby blocking the effects of acetylcholine on them

75
Q

What are endogenous opioids and give to examples

A

Opioids that are naturally occurring within the body
Ex. Enkephalins
Ex. Endorphins-contraction of “endogenous morphine’”

  • all endogenous opioid transmitters are neuropeptides and have metabotropic receptors
76
Q

What is a drug and what are its two types of effects

A

Exogenous substance (not produced in our body) that is not necessary for normal function(not needed for a healthy person), which alters the functions of cells

  1. Behavioural changes:ex increased attention
  2. Physiology changes: ex blocks reuptake of the dopamine
77
Q

What are sites of action (drugs)

A

Location where drug interacts with molecules/cells in the body
-there are specific sites of action where drugs are more effective

78
Q

What is the role of the blood brain barrier and what three regions is the BBB weakened/opened

A

Protects the brain from “foreign substances” in the blood that may injure the brain.
Protects the brain from hormones and neurotransmitters in the rest of the body.
Maintains a constant environment for the brain.

  1. Pineal gland: Allows entry of chemicals that affect day night cycles-associated with circadian rhythms.
  2. posterior pituitary: Releases neurohormones like oxytocin and vasopressin into the blood and allows entry of chemicals the influence pituitary hormones
  3. Area postrema: “Vomiting center”: when a toxic substance enters the bloodstream it will get to the area postrema and may cause the animal to throw up. In this way, the animal protects itself by eliminating the toxic substance from its stomach before more harm can be done.
79
Q

Describe effectiveness of drugs

A

Effectiveness refers to the strength of the drug

  • low-dose = not a high effect
  • high dose = a higher effect but levels out at a certain point)
  • in general, the higher dose the higher effect

> plotting the dose of drugs versus effect of drugs shows that some drugs don’t take as much to get a large effect

80
Q

What is potency

A

potency is a measure of drug activity expressed in terms of the amount required to produce an effect of given intensity.[1] A highly potent drug (e.g., fentanyl, alprazolam, risperidone) evokes a given response at low concentrations, while a drug of lower potency (codeine, diazepam, ziprasidone) evokes the same response only at higher concentrations. The potency depends on both the affinity and efficacy.

81
Q

What is the therapeutic index

A

The therapeutic index = the margin of safety

  • it is the difference of dose between wanted(analgesic) effect and unwanted(depressive-heart) effect
  • you want as wide of a region as possible to prevent overdose
82
Q

What is the placebo

A

It is an inert substance-no physiological effect on it own without any context

  • if a person believes that a substance will have an effect, it may be produced
  • certain colours or prices of placebos may be seen as more a less effective
83
Q

What is drug sensitization

A

Increasing sensitivity to a drug

84
Q

What is tolerance

A

Decreased effectiveness of a drug

  • it can be a problem for therapeutic effects but not toxic
  • many kinds of adaptive changes occur in the body to reduce or compensate the drugs effects
  • you get use to a drug so you need more of it to get the same effect
85
Q

What is metabolic tolerance and functional tolerance

A

Metabolic tolerance: result from changes that reduce the amount of drug getting to its sides of action

Functional tolerance: results from changes that reduce the reactivity of the sites of action to the drug (more common)
-can reduce number of receptors for it
-decrease the efficiency with which it binds to the receptors
* can have functional tolerance to some effects of the drug but not all
Ex. Could be tolerant to sedation but not depressed breathing from Anastasia

86
Q

What is cross tolerance

A

Tolerance to one drug can spread to other drugs that rely on the same mechanism

87
Q

What is withdrawal syndrome

A

Sudden elimination of a drug can trigger an adverse physiological reaction called a withdrawal syndrome

  • with no drug to counteract them, the neural adaptations produce withdraw effects virtually always opposite the initial effects of the drug
  • withdrawal is associated with physical dependence
  • in general longer exposure to greater doses followed by more rapid elimination produces greater withdrawal effects
  • ex. The withdrawal of sleeping pills often produces insomnia
88
Q

What is physical dependence

A
  • physiological need for a drug, that reveals itself through unpleasant withdrawal symptoms when the drug is discontinued
  • Individuals who suffer withdrawal reactions when they stop taking the drug are said to be physically dependent on that drug
  • physical dependence occurs when physical changes take place due to the repeated intake of the drug
89
Q

What are drug addicts

A

Habitual drug users who continue to use a drug despite its adverse effects on their health and social life and despite the repeated efforts to stop using it

90
Q

What is contingent drug tolerance

A

Refers to demonstrations that tolerance develops only to drug effects that are actually experienced (you need to experience effect to develop tolerance)

91
Q

What is psychological dependence

A

Psychological need to continue using a drug or complete an activity to relieve negative emotions and obtain a pleasurable state
-marked by cravings

92
Q

What is conditioned drug tolerance

A

refers to demonstrations that tolerance effects are maximally expressed only when a drug is it administered in the same situation in which it has previously been administered

  • The tolerance they developed is specific to the location where they take the drug
  • it is associated with OD when taking drug in new location(ex. vacation)
93
Q

What is the conditioned compensatory response

A

Occurs when conditional stimuli that predict drug administration come to elicit conditional responses opposite to the unconditional effects of the drug

94
Q

What is direct and indirect action

A

Direct action: drug attaches to the binding site of a neurotransmitter (same place)

  • competitive binding
  • makes a big difference for antagonist drugs

Indirect action: drug attaches to the receptor at a location not used by the NT (different place)
-non-competitive binding

95
Q

Describe nicotine:

  • it’s neurological, physiological and behavioural effects
  • its withdrawal symptoms
A
  • nicotine is a stimulant in the major psychoactive ingredient of tobacco

Physiological: increase heart rate/blood pressure, constricts blood vessels in the skin(age faster/wrinkles due to lack of blood flow), lowers skin temperature, inhibits stomach secretion, stimulates bowels (unable to properly get nutrients out of food resulting in weight loss)

Neurological: Acetylcholine agonist-binds to the same receptor as Ach (stimulates nicotinic receptors) also DA agonist (more DA in the NA)

Behavioural: affects Ach receptors at neuromuscular junction and therefore may result in muscle tremors, inhibition of some reflexes

Withdrawal: anxiety, restlessness, insomnia, irritability, also due to the sudden decrease in dopamine in the NA cravings and relapse may occur

96
Q

What is drug craving

A

An affective state in which there is a strong desire for the drug, which is a major defining feature of addiction
Ex. Readily apparent in any habitual smoker who has run out of cigarettes

97
Q

What is a teratogen

A

An agent that can disturb the normal development of the fetus
-nicotine is a teratogen

98
Q

Describe Alcohol:

  • it’s neurological, physiological and behavioural effects
  • its withdrawal symptoms
A

*It is a depressant because at moderate to high doses it depresses neural firing (at low doses it can stimulate neural firing and facilitate social interaction)
-Physiological: dilates blood vessels in the skin resulting in skin turning red & feeling warm as heat is lost from body(lowering body temp), increases production of urine(diuretic)
-Neurological: indirect GABA agonist leads to increased neuronal inhibition also increases DA in NA (related to reinforcing effects)
> Depresses the sympathetic NS, slows down breathing and heart rate and also interrupts REM sleep
-Behavioural: slows reaction time by about 10%, decreases hand-eye coordination (driving limit), poor judgment/decision making skills
-Withdrawal: causes serious health problems (can be fatal), headaches, vomiting, hallucinations, delirium tremens, convulsions and seizures

99
Q

What are stimulants and What are the four most common stimulants

A

speed up the body function: increase heart rate/breathing, energy rises, self-confidence rises
-primary effect is to produce generally increases in neural and behaviour activity
withdrawal(in general): fatigue, headache, irritability, depression
-Caffeine nicotine cocaine and ecstasy (differ in their potency)

100
Q

Describe Marijuana(Cannabis sativa):

  • it’s neurological, physiological and behavioural effects
  • its withdrawal symptoms
A

It is a hallucinogen with THC as its main hallucinogenic ingredient. However, THC serves as a depressant and a hallucinogen

  • Depending on which cannabinoid receptors these chemical compounds activate in the brain and spinal cord, using marijuana can produce stimulant, depressant, and hallucinogenic effects.
  • social doses of marijuana are subtle, high doses do impair psychological functioning

Physiological: elevate heart rate, Bloodshot eyes, Dry mouth,

Neurological: over-stimulating the release of neurotransmitters and disrupting communications between nerve cells. THC has stimulating effect on DA in the NA but not in the VTA

Behavioural: increased sense of well-being: initial restlessness followed by a dreamy, carefree state of relaxation. feeling of hunger, especially a craving for sweets. Slowed cognition and motor functions (feeling “stoned”), hallucinations . At high doses short term memory is impaired and speech becomes slurred

Withdrawal: 
Anxiety
Depression
Mood changes
Irritability
Stomach pains
Loss of appetite
Nausea
Insomnia
101
Q

What are some therapeutic effects to marijuana

A
  • Suppressed nausea and vomiting in cancer patients
  • stimulates the appetite of AIDS patients
  • can serve as an analgesic(pain killer)for chronic pain
  • blocks seizures
  • reducing anxiety
  • reduce symptoms of multiple sclerosis
102
Q

How does THC bind

A 
THC has two receptors for it, CB1 and CB2
Cannabinoid receptors(opiates use the same receptors)
103
Q

Describe cocaine& amphetamines:

  • it’s neurological, physiological and behavioural effects
  • its withdrawal symptoms
A
  • both are stimulants that result in large increases in DA within the NA -extremely potent

Physiological: dry nasal passage, dilate pupils, constricts arteries increases heart rate and blood pressure, makes you feel warm,

Neurological:
C-acts on DA receptors, blocks reuptake- more DA left in synaptic cleft
A-increases DA release

Behavioural: self-confident, alert, energetic, friendly, fidgety, talkative, less desire for food and sleep, high(euphoria), suspiciousness, convulsions, cardiac arrest and respiratory failure
-can induce psychotic behaviour (schizophrenia like symptoms)

Withdrawal: Relatively mild- negative mood swings and insomnia

104
Q

What are some potential long-term effects of amphetamine abuse

A

Make calls problems with dopamine transporters in the caudate and putamen which may lead to Parkinson disease later in life

105
Q

Describe ecstasy

A
  • stimulant and mild hallucinogen& potent relative of amphetamines
  • considered to be a empathogen(psychoactive drug that produces feelings of empathy)
  • releases enormous amount of serotonin resulting in euphoria, increased happiness and feeling social, however the body destroys more serotonin than usual because there is so much there so when your Brain is functioning normally again, there is not enough serotonin to make you feel good for normal events.

Neurological effects: serotonin agonist – blocks reabsorption and flushes out serotonin in neurons

Long term effects: serotonin depletion, long term memory problems(medial raphe-projects to hippocampus), depression(both dorsal/medial raphe-project to cortex)
Withdrawal: feeling extra tired, irritability, depression

106
Q

Describe LSD(acid)

A

It is a hallucinogen

  • acts on serotonin receptors (and others)
  • behaviour affect: emotional experience can vary depending on the person’s mood at the time. amplifies whatever you are feeling in the moment
  • hallucinations and flashbacks and euphoria(high)
107
Q

Describe opiates

  • it’s neurological, physiological and behavioural effects
  • its withdrawal symptoms
A

-wide category of drugs including morphine and codeine and heroin -stimulates easily

Physiological: constricts pupils, constipation, reduce sex hormones/sex drive, disrupts coronation of digestive activity (slow digestion)

Neurological: bind to endogenous opioid receptors-endorphin agonist (mimic naturally occurring endorphins). Stimulates the VTA – reinforcement

Behavioural: analgesic effect(reduce pain), rush, wave of intense abdominal orgasmic pleasure, evolves into a state of serene drowsy euphoria (good and positive)
-heroin can kill in high doses by dressing breathing

Withdrawal: can be very addictive-cravings, restlessness, watery eyes, running nose,yawning and sweating, vomiting, diarrhea, leg spasms

108
Q

What are two common misconceptions about drug addiction and give evidence against them

A
  1. “Addictive drugs quickly corrupt”
  • people typically don’t get addicted when taking drugs medically ex. Morphine
  • not everyone develops an addiction after using drugs
  • if you try a drug you’re actually not likely to develop an addiction (addiction to drugs may be more prominent in some families than others)
  1. “addictions can’t be overcome voluntarily” (you can’t do it on your own)
  • people often the cover on their own (although therapy benefits others)
  • people who recover on their own are less likely to relapse (therapy can lead one to believe that addiction is a disease and out of their control)
109
Q

What is light

A

Waves of electromagnetic energy that travel through space in different frequencies(ups and downs)
-we only respond to/see wavelengths in between 400nm-700nm(visible light)

110
Q

What are the 3 dimensions of light?

A
  1. Hue(color):
    - dominant wavelength (is what you see)
    - length of wave (red is long, blue is short)
  2. Saturation:
    - purity (how much of the colour is actually present in the patch of light-how much colour can you see? Is it faint?
  3. Brightness:
    - intensity (light/dark)
    - related to height of wave (high waves=bright light)
111
Q

What are s sensitivity and acuity

A

Sensitivity: the ability to detect the presence of dimly lit objects
Acuity: the ability to see the details of objects

112
Q

When would pupils dilate

A

When level of illumination is too low to adequately activate receptors(trigger AP), the pupils dilate to let in more light, thereby sacrificing acuity and depth of focus (image is sharper when pupils are constructed)

113
Q

What is accommodation, how does it work

A

The process of adjusting the configuration of the lens to bring images into focus on the retina

  • lens thickens when looking at up close things
  • lens flattens when looking at distant objects
  • lens isn’t as flexible as you get older and accommodate as well
114
Q

What is the cornea

A

First layer of the eye that focuses light on the back of the eye

115
Q

What is the blind spot?

A

Place where all retinal ganglion axons come together to go to the brain forming optic nerve ( no photoreceptors here)
-gap in receptor layer

116
Q

What is binocular disparity?

A

The difference in the position of the same image on the two retinas-is greater for close objects than for distant objects

117
Q

What is myopia and hyperopia

A

Myopia:

  • eye is longer
  • image focuses in front of the retina
  • shortsightedness
  • the worser the myopia, the thicker the glasses😉

Hyperopia:

  • eye is shorter
  • image focuses behind the retina
  • farsightedness
118
Q

What is the retina

A

5 layers of cells that rest against the back of the eye. The retina converts light waves into neural signals conducting them toward the CNS, and participates in the processing of the signals
-it extracts key information about an object- primary information about its edges and location-and conducts that information to the cortex, where a perception of the entire image is created from that partial information

119
Q

What are the 5 layers of the retina in order from the back to the front? What layers are more important

A

Photoreceptors(rods and cones), bipolar cells, retinal ganglion cells, horizontal cells, amacrine cells
*horizonal and amacrine cells are specialized for lateral communication (not as important)

120
Q

What is the fovea?

A

Indentation at the centre of the retina inline with the pupil which is very rich in cones (no rods)

  • specialized for high acuity vision(for seeing fine details and colours)
  • the thinning of the retinal ganglion cells at the fovea reduces the distortion of incoming light
121
Q

Compare the two photoreceptors

A

Rods:
Only allow you to see light (black or white/ dark or light) and no colours
-rod shaped
-only in the periphery
-high convergence to a single RGC
-low acuity (can’t see details)
-high sensitivity (can detect image in dimly lit settings)
-most rods on either side on fovea and decrease the further away from fovea you go

Cones:

  • cone shaped and in high abundance in the fovea and low abundance in the periphery
  • allows you to see details/colours, makes images sharp and focused
  • low convergence to retinal ganglion cells
  • high acuity
  • low sensitivity
  • 3 types, blue, green and red cones - each one reacts to a different wavelength and is responsive to one colour

*single retinal ganglion cells receive input from several hundred rods (brain can’t tell which individual rods have become activated-can’t tell detail, just shape and brightness)
whereas only a few cones converge on each retina ganglion cell(receive input from only a few cones)
-both receptors filled with overlaying discs

122
Q

What is protanopia, deuteranopia and tritanopia

A
  1. Protanopia(most common) is a deficit in long wavelength cone pigment and lack those long wavelength cones that detect red light, instead those red cones are filled with green cones.
  2. deuteranopia-is a reduced sensitivity to green light. Deficit in middle wavelength length(green) cone pigment. Green cones are filled with red

Red-green color blindness is split into two different types: Whereas people affected by protan color blindness(protanopia) are less sensitive to red light, deuteranopia (the second type of red-green color blindness) is related to sensitiveness on green light..

  1. Tritanopia(lest common) is a condition where a person cannot distinguish between blue and yellow colors. … Tritanopia is often referred to as color blindness. It is a deficit in short wavelength cone pigment leading to loss of blue cones. tritanomaly is a reduced sensitivity to blue light and is extremely rare.
123
Q

What is the duplexity theory

A

Theory that cones and rods mediate different kinds of vision

124
Q

What is prototypic and scotopic vision

A

Photopic: cone mediated vision
-predominates in good lighting and provides high acuity(finely detailed) coloured perceptions of the world

Scotopic: more sensitive rod mediated vision

  • predominates in dim illumination where there is not enough light to excite the cones .
  • lacks both the colour and detail of photopic vision
125
Q

Compare transduction of rods in the dark to to light

A

Dark:

  • rhodopsin molecules are inactive
  • sodium channels are kept open
  • sodium ions flow into the rods, partially depolarizing the rods
  • rods continually release glutamate(with the absence of light stimuli) which inhibit the bipolar cells *only time glutamate is an inhibitory NT

Light:

  • light hits lamellae and separates photopigment(rhodopsin) into rod opsin and trans-retinal -bleaches rhodopsin molecules
  • this separation activates transducin(G-protein) which is associated with rhodopsin and in turn activates phosphodiesterase to destroy cyclic GMP which is binded to sodium channels
  • as a result, sodium channels are closed
  • therefore because positive sodium cannot enter the rods, the rods become hyperpolarized
  • and glutamate release is reduced which turns on bipolar cell/depolarizes it and then also the retinal ganglion cell
  • rod is turned off/hyperpolarized when in the light which turns on other cells letting brain know that there is light here and makes sense of it
126
Q

What is rhodopsin

A 
Red pigment(substance that absorbs light) that is red but becomes belched when exposed to light
-rhodopsin is a G-protein-coupled receptor that responds to light rather than NT molecules (closes sodium channels when bleached inhibiting the release of glutamate) 
Rhodopsin = rod opsin + retinal
127
Q

What are the two pathways in which light neural signals travel from eye to the cortex ?

A
  1. Geniculostriate pathway

2. Tectopulvinar pathway

128
Q

Describe the geniculostriate pathway of visual information

A

Information from your right visual field is carried in your left optic tract and vice versa
….. you know the rest Jess;)

Biopsych (2 decks)

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