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Biological Basis of Behaviour > Chapter 5 > Flashcards

Chapter 5 Flashcards

1
Q

Who discovered epinephrine?

A
  • Lowei identified the chemical that carries the message to speed up heart rate as epinephrine in FROGS
  • Same substance as adrenaline
  • Produced by adrenal glands located on top of kidneys
  • The chemical that accelerates heart rate in HUMANS is norepinephrine
  • Closely related to epinephrine
  • The chemical that inhibits heart rate in HUMANS is acetylcholine
  • The vagus nerve influences heart rate
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2
Q

What are neurotransmitters?

A

Chemical messengers released by a neuron to a target to cause an excitatory or inhibitory response

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3
Q

What are hormones?

A
  • Chemicals outside of the CNS that circulate in the bloodstream
  • Released by the pituitary gland under the control of the hypothalamus
  • Organs in the ANS & Enteric NS get excited/inhibited as a result
  • Actions of hormones is slower than CNS neurotransmitters because they must travel to distant targets
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4
Q

What are some characteristics of Parkinson disease? Who discovered it?

A
  • Jean Charcot
  • Lean forward, walk on balls of feet
  • Difficulty eating/swallowing/drooling
  • Slowing of bowel movements
  • Loss of muscular control & disruptive tremors
  • Due to dopamine levels in basal ganglia falling to less than 10%—> degeneration of substantia nigra
  • Loss has been linked to the flu virus, toxic drugs, insecticides & herbicides

-If you inject 6-hydroxydopamine (neurotoxin) into rats it destroys the neurons containing dopamine & rats get Parkinson symptoms

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5
Q

What are the different parts of a chemical synapse?

A

Presynaptic membrane–> contains transmitter molecules transmitting chemical messages
Postsynaptic membrane–> contains receptor molecules receiving chemical messages
Postsynaptic receptor–> site to which a neurotransmitter molecule binds
Synaptic cleft–> space separating presynaptic terminal & postsynaptic dendritic spine
Microtubule–> pathway for transporting substances to the axon terminal
Mitochondrion–> organelle providing the cell with energy
Storage granule–> large compartment holding synaptic vesicles containing neurotransmitters that travel to the presynaptic membrane in preparation for release–> expelled into the synaptic cleft by exocytosis & binds to receptors on the postsynaptic membrane

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6
Q

What are dark patches on axon terminal vs on dendrite

A

Dark patches on axon terminal–> proteins serving as channels to signal the release of transmitters or as pumps to recapture the transmitter after it’s been released

Dark patches on dendrite–> receptor molecules made out of proteins that receive chemical messages

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7
Q

How do astrocytes surrounding the synapse contribute to chemical neurotransmission?

A

1) Supplying building blocks for neurotransmitter synthesis
2) Confining the movement of neurotransmitters to the synapse
3) Mopping up excess neurotransmitter molecules

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8
Q

What is a tripartite synapse?

A

the integration of pres & postsynaptic membrane & their association with surrounding astrocytes

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9
Q

What is a chemical synapse?

A

The junction where messenger molecules are released from one neuron to interact with the next neuron

  • Here, the presynaptic membrane forms the axon terminal
  • The postsynaptic membrane forms the dendritic spine
  • Space between the two is the cleft
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10
Q

Describe anterograde synaptic transmission

A

1) Synthesis–> neurotransmitters are transported from cell nucleus to terminal button while others made from building blocks are packaged into vesicles there
2) Release–> in response to an action potential, the transmitter is released across the membrane by exocytosis
3) Receptor action–> transmitter crosses the synaptic cleft & binds to a receptor
4) Inactivation–> the transmitter is either taken back into the terminal or inactivated in the synaptic cleft

(Think “Anti sleeping, relaxing, resting individual”)

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11
Q

Describe the first and second step of anterograde transmission in detail

A

Transporters–> protein molecules that move substances across cell membranes & are powered by mitochondria

The 4 classes of transmitters:
1) Peptide–> synthesized in cell body according to neuron’s DNA instructions & are packaged in Golgi bodies

2) Lipid–>can not be packaged/stored in vesicles but are synthesized on demand when an action potential reaches axon terminal
3) Gaseous–> generated within cells by enzymes & are able to permeate cell membranes so they are not stored in the cell
4) Ion–> not biochemically synthesized but are made in the hearts of dying stars. Can still be packaged & stored in vesicles & released to the synaptic cleft

5) Small-molecule–>quick acting & synthesized from dietary nutrients & packed ready for use in axon terminals
- Can be replaced at the presynaptic membrane
- Diet can influence their abundance & activity

Regardless of origin, neurotransmitters packaged into vesicles can be found on granules, attached to microfilaments in the terminal, or attached to the presynaptic membrane

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12
Q

Describe the third step of anterograde transmission in detail

A

1) The release process begins with voltage changes in the membrane after an action potential reaches the presynaptic membrane
2) The presynaptic membrane is rich in calcium channels while the extracellular fluid is rich in calcium–>will rush into axon terminal after-action potential opens the channels
3) Synaptic vesicles that are loaded with neurotransmitters must dock near release sites on the presynaptic membrane
4) Vesicles quickly fuse with the presynaptic membrane & empty their contents into the cleft by exocytosis
5) The vesicles from storage granules & filaments will replace the vesicles that just emptied their contents

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13
Q

Describe the fourth step of anterograde transmission in detail

A

-The neurotransmitter that has just been released from vesicles diffuses across the synaptic cleft–>binds to specialized protein molecules embedded in the postsynaptic membrane (transmitter-activated receptors)

Ionotropic receptors–> have a pore that opens & allows ions to pass through the membrane & change membrane voltage in 2 ways:

1) May allow sodium to enter the neuron & depolarize the postsynaptic membrane (excitation)
2) May allow potassium to leave the neuron, or chlorine to enter the neuron & hyperpolarize the postsynaptic membrane (inhibition)

Metabotropic receptor–> initiate intracellular messenger systems–> opens an ion channel causing excitation/inhibition

Neurotransmitters could also interact with receptors on the presynaptic membrane by influencing the cell that just released it–> have it recieve messages from their own axon terminal (autoreceptors)

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14
Q

Who is Bernard Katz?

A
  • Discovered the quantum–> smallest postsynaptic potential is produced by the release of the contents of just one synaptic vesicle
  • While producing a postsynaptic potential that can initiate a postsynaptic action potential requires the simultaneous release of many quanta
  • The number of quanta released from presynaptic membrane depends on:
    1) amount of Calcium entering the axon terminal in response to the action potential
    2) the number of vesicles docked at the membrane waiting to be released
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15
Q

Describe the fifth step of anterograde transmission in detail

A

-If a neurotransmitter lingered within the synaptic cleft–> the postsynaptic cell could not respond to other messages sent by the presynaptic neuron

  • Inactivation of neurotransmitters is accomplished in 4 ways:A
    1) Diffusion–>Some of the neurotransmitter diffuses away from the synaptic cleft & is no longer available
    2) Degradation–>enzymes in the synaptic cleft break down the transmitter
    3) Reuptake–> transporters bring transmitter back to presynaptic axon terminal for reuse
    4) Astrocyte uptake–> transmitter is taken up by neighbouring astrocytes for storage & re-exportation

An active axon terminal increases the amount of neurotransmitter made & stored, while a less-often-used terminal breaks down excess transmitters using enzymes

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16
Q

Name 7 types of synapses

A

Dendrodendritic–> dendrites sending messages to other dendrites

Axodendritic–> axon terminal synapses with dendritic spine

Axoextracellular–>Terminal secretes transmitter into the extracellular fluid (can modulate the function of tissue or even body)

Axosomatic–> Terminal ends on the cell body

Axosynaptic–> Terminal ends on another terminal (can exert control over another neuron’s input into the cell)

Axoaxonic–> terminal ends on another axon

Axosecretory–> Terminal ends on tiny blood vessel & secretes transmitter directly into the blood (can modulate the function of tissue or even body)

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17
Q

What are electrical synapses?

A
  • 2 neurons’ intracellular fluids can come into direct contact–> influence each other directly through a gap junction (electrical synapse)
  • Proteins in one cell membrane make a hemichannel that connects to the hemichannel of an adjacent cell membrane–> ions pass through them in both directions through a regulated gate that can either be open/closed.
  • Electrical transmission is faster than chemical transmission which is 5 milliseconds per synapse
  • Gap junctions allow groups of neurons to synchronize their firing, allow for substance exchange between glial cells & neurons
  • Large biomolecules (i.e nucleic acids & proteins) cannot fit through gap junctions

Mixed synapses–> gap junctions at axon terminals synapsing on dendrites & cell bodies which allow for dual chem/electrical synaptic transmission

-Unlike chemical synapses, gap junctions are not plastic & are built for speed & efficient communication, not signal altering

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18
Q

Describe neurotransmitter excitation & inhibition

A
  • Despite the variety of synapses, they all convey messages that are either inhibitory or excitatory
  • The ion channel associated with the receptor decides which type, not the neurotransmitters themselves

Excitatory synapses :

  • Are on the spines of dendrites
  • Have round vesicles
  • Denser material on pre & postsynaptic membrane
  • Wider synaptic cleft
  • Larger active zone

Inhibitory synapses:

  • Are on the cell body
  • Have flat vesicles
  • Less dense material on pre & postsynaptic membrane
  • Smaller synaptic cleft
  • Smaller active zone
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19
Q

What are the two models of excitatory-inhibitory interaction?

A

1) Inhibition blocks excitation by using a “cut them off” strategy:
- If the message is to be stopped, it will be by inhibiting the cell body close to the initial segment

2) Inhibition blocks excitation by using an “open the gates” strategy:
- The message is like a racehorse ready to run down the track, but first, the inhibitory starting gate must be removed

20
Q

Describe the evolution of complex neurotransmission systems

A

The exocytosis mechanism for digestion in a single-cell organism (secreting juices onto bacteria to immobilize & prepare them for digestion)–> parallel to release of a neurotransmitter for communication in complex creatures

21
Q

Describe the multitude of varieties in neurotransmitters

A

1) Some are excitatory in one location/ inhibitory at another
2) two or more may team up in a single synapse; one making the other more potent
3) Interact with several receptors with different functions
4) No single neurotransmitter can cause a single behaviour

22
Q

What are the 4 criteria for identifying neurotransmitters?

A

1) Must be synthesized or present in the neuron
2) When released, the transmitter must produce a response in the target cell
3) The same response must be obtained when transmitter is experimentally placed on the receptor
4) Must be a mechanism for removal after transmitter’s work is done

Identifying chemical transmitters in the CNS is not easy–> must use saline baths, staining, stimulating & collecting to identify them

Putative (supposed) transmitter–>Doesn’t meet all the criteria for being a neurotransmitter

23
Q

Describe acetylcholine

A

-First identified CNS neurotransmitter

Renshaw loop–>

  • All motor neuron axons leaving the spinal cord use it as a transmitter
  • Each motor neuron has an axon collateral in the spinal cord that synapses on a nearby CNS interneuron
  • The interneuron, in turn, synapses on the motor neuron’s cell body
  • This loop made by the axon collateral & interneuron in the spinal cord–> forms feedback circuit enabling motor neuron to inhibit itself from overexcitation
  • Toxin strychnine can block the loop–> neurons become overactive causing convulsions, chocking & death
24
Q

Name some well studied small-molecule neurotransmitters

A 
Acetylcholine 
Dopamine
Norepinephrine/Epinephrine
Serotonin
Glutamate
GABA
Glycine
Histamine
Adenosine/Adenosine Triphosphate

(Think “AH triple G, Sands)

25
Q

Describe Acetylcholine synthesis

A
  • Acetylcholine is present at the junction of neurons & muscles (heart & CNS)
  • Choline is among the breakdown products of fats (e.g egg & avocado)
  • Acetate is found in acidic foods (e.g vinegar & lemon juice)
  • Inside the cell, acetyl coenzyme (COA) carries acetate to the synthesis site
  • Choline acetyltransferase (CHAT) transfers acetate to choline to synthesize acetylcholine
  • ACH is released into synaptic cleft & diffuses to receptor sites
  • Acetylcholinesterase (ACHE) reverses the process & breaks down the transmitter by detaching acetate from choline
  • Products are taken back to the presynaptic terminal for reuse
26
Q

Describe amine synthesis

A

-Tyrosine hydroxylase changes tryosine into L-dopa–>dopamine–>norepinephrine–>epinephrine

  • The supply of Tyrosine hydroxylase is limited & so is the rate of the 3 amine production
  • This limit can be bypassed by oral administration of L-Dopa (used in treating Parkinson)
  • Administering other drugs to prevent L-Dopa from being converted into dopamine before it passes through the blood-brain barrier & gets to dopamine neurons in the brain
  • L-Dopa can produce dyskinesias–> involuntary movements (ballistic throwing & choreic dancing)
27
Q

Describe serotonin synthesis

A
  • Serotonin is synthesized from L-tryptophan which is abundant in pork, turkey, milk & bananas
  • Serotonin regulates mood, aggression, appetite, arousal, respiration & pain perception
28
Q

Describe amino acid synthesis

A
  • Glutamate & GABA are closely related
  • GABA is formed by a modification of the glutamate molecule
  • They both are workhorses of the brain because so many synapses use them
  • GABA is the main inhibitory, Glutamate is the main excitatory transmitter in the forebrain & cerebellum
  • Glycine is a much more common inhibitory transmitter in the brainstem & spinal cord acting within the Renshaw loop
  • Histidine is converted by histidine decarboxylase into histamine & controls arousal, waking & constriction of smooth muscles
29
Q

Describe purine synthesis

A
  • Purines are synthesized as nucleotides
  • Adenosine triphosphate (ATP) consists of adenine attaching to sugar molecule & 3 phosphate groups
  • Adenosine emerges from removal of 3 phosphate groups–> promotes sleep, arousal suppression & regulating blood flow
30
Q

Name some peptide transmitters

A 
Opioids
Neurohypohyseals
Secretins
Insulins
Gastrins
Somatostatins
Tachykinins
31
Q

Describe peptide synthesis

A
  • Synthesized through the translation of mRNA
  • Multifunctional chains of amino acids acting as neurotransmitters
  • Either made in the axon terminal or assembled on the neuron’s ribosomes, packaged by Golgi bodies & transported by microtubules to the axon terminals
  • The process of their synthesis & transport is slow compared to the ready-made small molecules
  • Peptides act slowly & not replaced quickly
  • They act as hormones responding to stress
  • Enable parent-child bonding
  • Regulate eating/drinking & pleasure/pain
  • Contribute to learning
  • Opioids produce euphoria & reduce pain
  • Have no direct effects on postsynaptic membrane voltage & instead, activate synaptic receptors to influence cell structure & function
  • Some CNS peptides take part in specific periodic behaviour
  • (e.g neuropeptide transmitters act as hormones which prepare deers for mating season. After the birth of fawn, oxytocin takes over to help her bond & prolactin to help her nurse)
32
Q

Describe lipid synthesis

A
  • Endocannabinoids are predominant among lipid transmitters
  • Include anandamide & 2-AG derived from arachidonic acid & unsaturated fatty acid in poultry & egg
  • Affect many physiological & psychological responses
  • They are lipophilic (fat-loving) molecules–> are not soluble in water & not stored in vesicles but synthesized on demand
  • Calcium activates transacylase to synthesize anandamide–> then it diffuses across synaptic cleft & interacts with its receptor on the presynaptic membrane
  • Both act as retrograde neurotransmitters, reducing the amount of incoming neural signal
33
Q

Describe cannabinoids

A

The CBI receptor is the target for all cannabinoids generated from the body (endocannabinoids) or from plants (phytocannabinoids) or synthetically

  • CBI receptors are found on glutamate & GABA synapses so cannabinoids act as neuromodulators to inhibit the release of glutamate & GABA
  • Canabinoids dampen neuronal exitation & inhibition
34
Q

Describe gaseous synthesis

A

Nitric oxide (NO), carbon monoxide (CO) & hydrogen sulphide (H2S) are water-soluble.

  • They are neither stored b synaptic vesicles nor released from them; they are synthesized on demand
  • After synthesis, each gas diffuses away & crosses cell membrane to become active
  • NO & CO activate metabolic processes in cells (i.e modulating the production of other neurotransmitters)
  • H2S prevents oxygen from binding in the mitochondria–> slowing down metabolism
  • NO & H2S control intestinal wall muscles & dilate blood vessels in active regions, produce penile erections
35
Q

Describe Ion synthesis

A
  • Zinc is not biologically synthesized but formed by fusion reactions in stars
  • Actively transported & packaged in vesicles & released into the synaptic cleft
  • Zinc dysregulation causes cognitive decline & Alzheimer
36
Q

What do the two general classes of receptors do?

A

1) directly change the postsynaptic membrane’s electrical potential
2) Induce cellular change indirectly

  • Ionotropic receptors have 2 parts: a binding site for a neurotransmitter & a pore/channel
  • In Ionotropic receptors, the transmitter binds to the receptor, the pore opens & allows for the influx or efflux of ions
  • Ionotropic receptors bring about rapid changes in membrane voltage & are usually excitatory–> trigger an action potential
  • metabotropic receptors resemble voltage-activated channels & propagate action potential
  • These receptors indirectly produce changes in ion channels or enzyme channels
  • This receptor consists of a single protein spanning the cell membrane
  • Each receptor is coupled to one of a family of G proteins
  • When activated by a neurotransmitter, a G protein binds to other proteins
  • G proteins consist of alpha, beta & gamma subunits
  • The alpha subunit detaches when a neurotransmitter binds to the G protein’s metabotropic receptor
  • The detached alpha can then bind to other proteins
  • If it binds to a nearby ion channel, channel changes & modifies the flow of ions through it
  • The alpha subunit closes/opens the channel which influences the membranes electrical potential

-The alpha subunit can also bind to an enzyme which will activate a second messenger that carries instructions to other cells

  • This second messenger can:
    1) Bind to a channel, change its structure, alter ion flow through the membrane
    2) Initiate a reaction that causes proteins to incorporate into the cell membrane & form new ion channels
    3) Bind to DNA sites & initiate/cease protein production
    4) Allow for amplification cascade
37
Q

What is amplification cascade

A
  • A single neurotransmitter’s binding to a receptor can activate this escalating sequence of events
  • Results in many downstream proteins being activated/deactivated
  • This is caused by metabotropic receptors
38
Q

How is the variety in receptor subtypes achieved?

A
  • Alternative forms of each subunit assembling in unique combinations
  • NDMA receptor can act as an ionotropic receptor for glutamate, and also as a metabotropic receptor
  • Each subtype has different properties & confer different activities:
    a) presence/absence of binding sites for other molecules
    b) how long channels remain open/closed
    c) ability to interact with signalling molecules in the cell
39
Q

What are some rules about neurotransmitter behaviours?

A

1) neurons can use one transmitter at one synapse & a different transmitter at another synapse
2) Different transmitters may coexist in the same terminal/synapse (e.g neuropeptides & small-molecules)
3) More than one transmitter is packaged within a single vesicle

40
Q

How does neurotransmission happen in the somatic nervous system?

A
  • Motor neurons in brain & spinal cord–> send axons to skeletal muscles
  • Cholinergic neurons–> motor neurons are called this because acetylcholine is their main transmitter (excitatory at a skeletal muscle, producing contractions)
  • The nicotinic acetylcholine receptor (nAChr)->The single main receptor & neurotransmitter that serves the SNS
  • ACH binds to the receptor, ions flow in–> depolarization of muscle fibre
  • The NACR pores are big enough to allow simultaneous efflux of potassium & sodium
  • Nicotine found in tobacco acts the same as ACH
  • Gene-related peptide (GGRP)–> neuropeptide that acts through CGRP metabotropic receptors to increase the force with which muscles contract
41
Q

What is the dual activating system of ANS?

A

-Both sympathetic & parasympathetic divisions are controlled by ACH neurons that come from the CNS at two levels of the spinal cord

  • Cholinergic neurons in the CNS synapse with sympathetic norepinephrine neurons to prepare the body for flight-fight
  • Cholinergic neurons in the CNS synapse with parasympathetic ACH neurons to prepare the body for rest & digest
  • During arousal, norepinephrine turns UP HEART rate & DOWN DIGESTION because its receptors on the heart are EXCITATORY whereas its receptors on the gut are INHIBITORY
  • The reverse is true for acetylcholine. Turns DOWN HEART rate & UP DIGESTION because its receptors on the heart are INHIBITORY whereas its receptors on the gut are EXCITATORY
42
Q

Describe the autonomy of the enteric nervous system:

A
  • Can act without input from CNS; second brain
  • Uses more than 30 transmitters from the main class, identical to those employed by CNS
  • Serotonin & dopamine are chiefs
  • Sensory neurons detect mechanical & chemical conditions in the gastrointestinal system
  • Motor neurons control the mixing of intestinal contents
43
Q

What are the 4 activating systems in the CNS?

A

For each of the 4 activating systems, a small number of neurons that grouped together in one or more brainstem nuclei–>send axons to widespread regions–> synchronize activity throughout brain & spinal cord

Cholinergic system (acetylcholine)

  • ACH is dense in basal ganglia
  • Synapses are connections from ACH to the brainstem
  • Active in maintaining attention & waking EEG pattern
  • Role in memory by maintaining neuron excitability
  • Death of cholinergic neurons & decrease in ACH in neocortex–> Alzheimer’s disease (treatment is elevating ACH or increasing nicotine receptors)

Dopaminergic system (dopamine)
Nigrostriatal pathways:
-Active in maintaining normal motor behaviour
-Loss of DA related to muscle rigidity & dyskinesia in Parkinson disease
Mesolimbic pathways:
-DA release causes repetition of behaviours
-Neurotransmitter system most effected by addictive drugs
-Increases in DA activity related to schizophrenia, while decreases related to attention deficits

Noradregenic system (norepinephrine)

  • NE stimulates neurons to change structure–> influence learning
  • Facilitates healthy brain development & organizes movements
  • Active in maintaining emotional tone
  • Decrease in NE related to depression, while increases are related to mania
  • Decreased activity associated with ADHD

serotonergic system (serotonin)

  • Active in maintaining waking EEG pattern
  • Plays a role in learning
  • Changes in serotonin activity are related to OCD, tics & schizophrenia
  • Decrease in serotonin activity are related to depression
  • Abnormalities in brainstem 5-HT neurons linked to sleep apnea & sudden infant death syndrome (SIDS)
44
Q

What is the adaptive role of synapses in learning & memory?

A
  • Experience can alter the synapse due to plasticity
  • Donald Hebb–> cells that fire together wire together
  • A synapse that physically adapts is called a Hebb synapse
45
Q

What is the neural basis of habituation & sensitization?

A
  • Habituation–> response to stimulus weakens with repeated presentation
  • Eric Kandel–> Stroking or shocking the Aplysia slug’s appendages to produce enduring changes in its defensive behaviours

Habituation phase:

  • A jet of water is sprayed repeatedly on siphon & gill movement recorded
  • Gill withdrawal becomes weaker after a few minutes (habituation) & can last as long as 30 mins
  • The sensory neuron stimulates the motor neuron to produce gill withdrawal prior to habituation
  • As habituation develops, the excitatory postsynaptic potentials (ESPs) become smaller in the motor neuron
  • The neural basis of habituation lies in the change in presynaptic calcium channels
  • With habituation, there is a decrease in the influx of calcium ions in response to an action potential–> fewer neurotransmitters released at presynaptic membrane–> less depolarization of the postsynaptic membrane

Sensitization phase:

  • Novel stimuli heighten the slug’s responsiveness to familiar stimulation
  • A small electric show to its tail enhances its gill withdrawal response for a few minutes to a few hours
  • An interneuron receives input from a shocked sensory neuron in the tail–> releases serotonin onto the axon of a siphon sensory neuron
  • Serotonin reduces potassium efflux through potassium channels–> prolongs an action potential on the siphon’s sensory neuron
  • This results in more calcium influx & increased transmitter release–> longer than normal gill withdrawal response
  • this causes greater depolarization of the postsynaptic membrane after sensitization
  • Gill response can also be prolonged if the second messenger cAMP (in the presynaptic membrane of the siphon’s sensory neuron) makes more neurotransmitters ready for release into the sensory-motor synapse
46
Q

Describe learning as a change in synapse number

A
  • Neural changes in learning must last long enough to account for a permanent change in behaviour
  • Longer training periods produce more enduring learning
  • The number & size of synapses decrease in habituated animals & increase in sensitized animals
  • Habituation & sensitization also trigger processes that result in loss or formation of new synapses
  • These processes begin with calcium ions that mobilize second messengers to send instructions to nuclear DNA
  • The transcription & translation of nuclear DNA–> in turn, will initiate structural changes at synapses (formation of new synapses/new dendritic spines
47
Q

What is the role of dendritic spines in learning?

A
  • Protrude from the dendrite’s shaft, 1-3 micrometres
  • Each neuron may have thousands of spines (approx. 1014)
  • Originate in filopodia that bud out of neurons, especially dendrites
  • Filopodia can grow into dendritic spines–> searching for contact from axon terminals to form synapses
  • Dendritic spines mediate lasting learning, including habituation & sensitization
  • They act independently, undergo changes & provide the structural basis for our behaviour, skills & memory
  • Loss of spines leads to Alzheimer’s.
  • cAMP plays an important role in carrying instructions regarding structural changes to nuclear DNA
  • As evidenced by studies of the fruit fly Drosophila
  • Dunce mutation–> lacks enzymes necessary to degrade cAMP–>abnormally high cAMP levels
  • Rutabaga–> reduces levels of cAMP below the normal range
  • These two mutations produce similar learning deficiencies

Biological Basis of Behaviour (4 decks)

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