topic 8 Flashcards
1
Q
the nervous system (NS) is split into (2)
A
- the central nervous system
- the peripheral nervous system
2
Q
central nervous system (CNS) consists of
A
- brain
- spinal cord
relay nerves
3
Q
the peripheral nervous system consists of
A
- sensory nerves. carrying sensory information from the receptors to the CNS
- motor nerves. carrying the motor commands from the CNS to the effectors
4
Q
the peripheral nervous system is subdivided into
A
- autonomic nervous system
- somatic nervous system
5
Q
autonomic nervous system is
A
involuntary
stimulates smooth muscle, cardiac muscle and glands
6
Q
somatic nervous system is
A
voluntary
stimulates skeletal muscle
7
Q
autonomic nervous system is subdivided into
A
- the sympathetic nervous system
prepares the body for fight or flight response - the parasympathetic nervous system
prepares body for rest and digest
8
Q
What is the difference between a neurone and a nerve
A
a neurone is a single cell
a nerve is a more complex structure containing a bundle of the axons of many neurons surrounded by a protective covering.
9
Q
what are the basic characteristics of a neurone
A
- cell body. consisting the nucleus and cell organelles within the cytoplasm.
- dendrites. very fine. conduct impulses towards the cell body
- axon. transmits impulses away from the cell body
10
Q
what are the 3 types of neurone
A
- sensory neuron
- relay neuron
- motor neuron
11
Q
motor neurones
A
the cell body is situated within the central nervous system (CNS) and the axon extends out conducting impulses from the CNS to effectors ( muscles or glands).
the axons of some motor neurones can be extremely long, such as those that run the full length of the leg.
the dendrites are attached to the cell body.
12
Q
sensory neurones
A
these carry impulses from sensory cell to the CNS
the cell body is branched of the axon.
13
Q
relay neurone
A
these are found mostly within the CNS. they can have a large number of connections with other nerve cells.
relay neurones are also known as connector neurones and interneurones
cell body is in the middle of the axon.
axon –> cell body –> axon
14
Q
myelin sheath
A
fatty insulating area that surrounds the axon.
it is made up of shwann cells wrapped around the axon
the sheath affects how quickly nerve impulses pass along the axon.
not all animals have myelinated axons, they are not found in invertebrates and some vertebrate axons are unmyelinated.
15
Q
what is a reflex arc
A
simple nerve pathways responsible for reflexes which is a rapid, involuntary response to a stimuli
16
Q
what happens in a reflex arc
A
- receptors detect a stimulus and generate a nerve impulse
- sensory neurones conduct a nerve impulse to the CNS along a sensory pathway
- sensory neurone enters the spinal cord through the dorsal route.
- sensory neurone forms a synapse with a relay neurone
- relay neurone forms a synapse with a motor neurone that leaves the spinal cord through the ventral route
- motor neurone carries impulses to an effector which produces a response.
17
Q
how is the brain involved with stimulus response
A
most nerve pathways involve numerous neurones within the central nervous system. a sensory neurone connects to a range of neurones within the CNS and passes impulses to the brain to produce a coordinated response.
even in reflex arcs there are additional connections within the CNS to ensure a coordinated response. some synapses with motor neurones will be inhibited to ensure that the desired response occurs
18
Q
what is the advantage of reflex pathway?
A
they produce rapid response; important for protection and survival
19
Q
how do the muscles of the iris respond to light
A
- the iris controls the size of the pupil
it contains a pair of antagonistic muscles; radial and circular muscles.
these are both controlled by the autonomic nervous system.
the radial muscles are like the spokes of a wheel and are controlled by a sympathetic reflex.
the circular muscles are controlled by a parasympathetic reflex.
one reflex dilates the pupil and the other constricts it.
for the pupil to constrict radial muscles must relax and circular muscles must contract.
for the pupil to dilate the radial muscles must contract and the circular muscles must relax
20
Q
how is pupil size controlled
A
- high levels of light striking photoreceptors in the retina cause nerve impulses to pass along the optic nerve to a number of different sites within the CNS, including a group of coordinating cells in the midbrain.
- impulses from these cells are sent along parasympathetic motor neurones to the circular muscles of the iris, causing them to contract. as the radial muscles relax. this constricts the pupil reducing the amount of light entering the eye
21
Q
what are the purpose of the pupil reflex
A
to prevent damage to the retina from high intensity light; in dim light it ensures maximum light reaches the retina.
22
Q
potential difference
A
the difference in electrical voltage across the cell surface membrane
23
Q
what is the resting potential of a neurone
A
-70 m V (millivolts)
the axon is more negative than the outside
so the membrane is said to be polarised.
24
Q
what causes the potential difference in a neurone
A
the uneven distribution of ions across the cell surface membrane.
there is more potassium ions (K+) inside the cell then extracellular.
more sodium ions (Na+) outside (extracellular) of the cell
there is more calcium ions (Cl-) outside of the cell (extracellular)
this is achieved by the action of sodium-potassium pumps in the cell surface membrane of the axon. these carry Na+ out of the cell and K+ into the cell.
these pumps act against the concentration gradients so is active transport with energy supplied by hydrolysing ATP>
the other organic ions (e.g -ve amino acids) are large and stage within the cell, so Cl- ions move out of the cell to help balance the charge cross the cell surface membrane
25
how is the resting potential maintained
1. Na+ / K+ pump creates concentration gradient across the membrane.
2. K+ diffuse out of the cell down the K+ concentration gradient, making the outside of the membrane +ve and the inside -ve creating a potential difference
3. the potential difference will pull K+ back into the cell as it diffuses down the electrical gradient
4. at 70- mV potential difference, the 2 gradients counteract each other and there is no net movement of K+
26
why is the axon resting potential -70 mV
the 2 forces involved in the movement of potassium ions:
1. the concentration gradient generated by the Na+ / K+ pump
2. the electrical gradient due to the difference in charge on the 2 sides of the membrane resulting from K+ diffusion.
K+ ions diffuse out of the cell due to the concentration gradient.
the more K+ ions that diffuse out of the cell the larger the potential difference across the membrane.
the increased negative charge created inside the cell as a consequence attracts K+ back across the membrane into the cell.
when the potential difference across the membrane is around -70 mV, the electrical gradient exactly balances the chemical gradient.
there is no net movement of K+ and hence a steady state exists, maintaining the potential difference at -70 mV.
an electrochemical equilibrium for K+ is in place and the membrane is polarised
27
what happens when a nerve is stimulated
- neurones are electrically excitable cells, so the potential difference across cell membrane changes when they are conducting.
if an electrical current above a threshold level is applied to the membrane a massive change in potential difference occurs.
the potential difference across the membrane is locally reversed making inside of axon positive and outside negative this is known as depolarisation.
potential difference becomes +40 mV for 3ms before returning to resting state. in order to conduct more impulses.
this is depolarisation.
the large change in voltage across membrane is action potential
28
what causes an action potential
| 1. depolarisation
- neurone is stimulated and some depolarisation occurs
- the change in the potential difference across the membrane causes a change in the shape of the Na+ gate, opening some of the voltage dependent sodium ion channels
- as Na+ flow in, depolarisation increases, triggering more gates to open once a certain potential threshold is reached. the opening of more gates increases depolarisation further. example of positive feedback.
- a change encourages further change of the same sort and it leads to a rapid opening of all the Na+ gates.
- this means there is no way of controlling the degree of depolarisation of the membrane; action potentials are either there or they are not.
- this property is called all nor nothing
the higher conc. of sodium ions outside of the axon, so Na+ flow rapidly inwards through open voltage dependent Na+ channels. causing a build up of +ve charges inside. this reverses the polarity of the membrane. potential difference reaches +40 mV
29
what causes an action potential
stage 2
2. repolarisation
after about 0.5 ms, the voltage dependent Na+ channels spontaneously close and Na+ permeability of the membrane returns to its usual very low level.
voltage dependent K+ channels open due to depolarisation of the membrane. as a result K+ ions move out of the axon down the electrochemical gradient. (down conc gradient and attracted by -ve charge outside cell)
as K+ flow out of the cell, the inside of the cell once again becomes more -ve than the outside.
30
what causes an action potential
stage 3
3. restoring the resting potential
the membrane is now highly permeable to K+ ions and more ions move out than occurs at resting potential, making the potential difference more negative than the normal resting potential.
this is known as hyperpolarisation of the membrane. the resting potential is re-established by closing the voltage dependent K+ channels and K+ diffuse into the axon.
31
action potential
| summarised
1. depolarisation. all nor nothing. voltage dependent Na+ channels open. Na+ flow into axon depolarising the membrane
2. repolarisation. voltage dependent Na+ channels close. voltage dependent K+ channels open. K+ leave the axon, repolarising the membrane
3. restoring resting potential. the membrane is hyperpolarised. voltage dependent K+ channels close. K+ diffuse back into the axon to recreate the resting potential.
32
sodium pump action at restoring and maintaining resting potential
if a lot of action potentials occur in an neurone, the Na+ conc. inside the cell rises significantly.
the sodium potassium pumps start to function, restoring the original ion concentration across the cell membrane.
if a cell is not transmitting many action potentials these pumps will not have to be used very frequently.
At rest there is some slow leakage of Na+ into the axon.
these sodium ions are pumped back out of the cell.
33
is it possible for an action potential to be triggered in a dead axon?
no. (unless ATP was added)
the polarisation of the membrane is maintained by the concentration gradients achieved by the action of energy requiring sodium potassium pumps; membrane integrity is lost in a dead axon.
34
how is the impulse passed along an axon
1. at resting potential there is +ve charge on outside and -ve on inside of membrane with high Na+ conc on outside and high K+ concentration on inside
2. when stimulated, voltage dependent Na+ channels open, Na+ flow into the axon depolarising membrane. localised electric currents are generated in the membrane. Na+ move to the adjacent polarised (resting) region causing a change in the electrical charge (potential difference) across this part of the membrane
3. the change in potential difference in membrane adjacent initiates second action potential. at the site of first action potential the voltage dependent Na+ ions close and voltage dependent K+ channels open K+ ions leave axon polarising membrane becomes hyperpolarised
4. a 3rd action potential is initiated by the second. in this way local electrical currents cause the nerve impulse to move along the axon. at the site of the first action potential, K+ diffuse back into the axon, restoring the resting potential.
35
refractory period
the new action potential cannot be generated in the same selection of membrane for about 5 milliseconds. this is known as the refractory period, which makes sure that the impulses travels in one direction along a nerve fibre.
lasts until all the voltage dependent Na+ and K+ channels have returned to their normal resting state (closed) and the resting potential is restored. the refractory period ensures that impulses only travel in one direction.
36
how does the refractory period ensure that an action potential will not be propagated back the way it came
a new action potential will only be generated at the leading edge of the previous one; because the membrane behind it will be recovering / incapable of transmitting an impulse; the membrane has to be repolarised and return to resting potential before another action potential can be generated.
37
can impulses be different sizes
no.
a stimulus must be above threshold level to generate an action potential. the all or nothing effect for action potentials means that the size of the stimulus, assuming it is above the threshold, has no effect on the size of the action potential.
38
the size of of the stimulus does not effect size of impulses but it does affect
1. the frequency of impulses
2. the number of neurones in a nerve that are conducting impulses
a frequency of firing and the firing of many neurones are usually associated with a strong stimulus.
39
what determines the speed of conduction
- in part determined by the diameter of the axon. the wider the diameter, the faster the impulse travels.
nerve axons of mammals ( 1- 20 um) are much narrower than others but impulses travel along them at up to 120 ms-1 .
40
what determines the speed of conduction of axons in mammals
presence of myelin sheath
saltatory conduction
myelin sheath acts as an electrical insulator along most of the axon, preventing any flow of ions across the membrane
gaps (nodes of ranvier) occur in the myelin sheath at regular intervals and these are the only place where depolarisation can occur.
as ions flow across the membrane at one node during depolarisation, a circuit is set up which reduces the potential difference of the membrane at the next node, triggering an action potential.
in this way, the impulse effectively jumps from one node to the next. this is much faster than a wave of depolarisation along the whole membrane. myelinated axons has a higher impulse velocity.
41
synapse
where 2 neurones meet.
42
synaptic cleft
the space between the 2 neurones
43
stages in synaptic transmission
1. an action potential arrives at the presynaptic membrane
2. the membrane depolarises. calcium (Ca2+) ions channels open. Ca2+ enters the neurone
3. Ca2+ cause synaptic vesicles containing neurotransmitter to fuse wit the presynaptic membrane.
4. neurotransmitter is released into the synaptic cleft (exocytosis) it takes 0.5 ms to diffuse across the synaptic cleft and reach the postsynaptic membrane.
5. neurotransmitter binds with complementary receptors on the postsynaptic membrane. cation channel open. sodium ions Na+ flow through the channels.
6. the membrane depolarises and initiates an action potential.
extent of depolarisation depends on amount of neurotransmitter reaching the postsynaptic membrane. depends on frequency of impulses reaching the presynaptic membrane and the number of functioning receptors in the postsynaptic membrane.
7. when released from the receptor the neurotransmitter will be taken up across the presynaptic membrane (whole or after being broken down) or it can diffuse away and be broken down.
44
what is the role of synapses in nerve pathway
control and coordination
- control of nerve pathways, allowing flexibility of response
- integration of information from different neurones allowing a coordinated response.
the postsynaptic cell is likely to be receiving input from many synapses at the same time.
45
what are the main factors that affect the likelihood that the postsynaptic membrane will depolarise
- the type of synapse
| - the number of impulses received.
46
what are the 2 types of synapses
- excitatory synapses.
| - inhibitory synapses
47
excitatory synapses
make the postsynaptic membrane more permeable to sodium ions.
as single excitatory synapse typically does not depolarise the membrane enough to produce an action potential, but several impulses arriving within a short time produce sufficient depolarisation via the release of neurotransmitter to produce an action potential in the postsynaptic cell.
48
summation
the overall effect of impulses on the postsynaptic membrane
49
what are the 2 types of summation
- spatial summation
| - temporal summation
50
spatial summation
here the impulses are from different synapses, usually from different neurones. the number of different sensory cells stimulated can be reflected in the control of the response.
51
temporal summation
in this case several impulses arrive at a synapse having travelled along a single neurone one after the other. their combined release of neurotransmitter generates an action potential in the postsynaptic membrane.
52
inhibitory synapses
make it less likely that an action potential will result in the postsynaptic cell.
the neurotransmitter from these synapses opens channels for chloride ions and potassium ions in the postsynaptic membrane, and these ions will then move through the channels down their diffusion gradients.
chloride ions will move into the cell carrying a -ve charge and K+ ions will move out carrying a +ve.
greater potential difference across the membrane as the insides become more negative than usual (about -90 mV)
this is called hyperpolarisation.
this makes subsequent depolarisation less likely. more excitatory synapses will be required to depolarise the membrane.
53
how do hormone bring about a change in the activity of its target cell
binds to receptors on target cell surface or within target cell; directly or indirectly via a second messenger molecule, the hormone affects gene expression.
54
what is the differences between nervous control and hormonal control (5)
1. NS - electrical transmission by nerve impulses and chemical transmission at synapses
1. HS - chemical transmission through blood
2. NS- faster acting
2. HS- slower acting
3. NS- usually associated with short term changes
3. HS- can control long term changes
4. NS- action potential carried by neurones with connections to specific cells
4. HS- blood caries the hormones to all cells, but only target cells are able to respond.
5. NS- response is often very local, such as a specific muscle cell or gland
5. HS- response may be widespread, such as growth and development.
55
what are the chemicals that control development and response to environment in plants
plant growth substances
| they are chemicals produced in the plant in very low concentrations and transported to where they cause a response
56
early experiments on auxin
Darwin and son Francis completed experiments on phototropism (bending of plants towards a light source) which are considered to be some of the earliest work on the effects of auxin.
their experiments showed that an oat coleoptile with its tip cut off stops bending towards the light.
replacing the tip starts to growth towards the light again.
they concluded that some influence was transmitted from the shoot top to the lower parts of the seedlings, causing them to bend.
later experiments by researchers Boysen Jensen and Went.
57
Boysen Jensen and went research into phototropism and auxin
showed that a chemical made in the tip passed down the coleoptile.
demonstrated by removing the tip, placing it on a small block of agar jelly and putting the agar on top of the cut end. the coleoptile started to grow again; a chemical produced by the tip had diffused down through the agar jelly.
went provided further evidence by placing the agar blocks on one side of the cut coleoptile tip in the dark; this caused the coleoptile to curve away from the side receiving the chemical messenger from the agar.
the chemical identified as Auxin one its major functions is to stimulate growth.
the growth response is a result of cell elongation.
58
why does the coleoptile curve towards the light when the tip is in place
measured amount of chemical being produced on the shaded an unshaded side of the shoot and found that the total amount produced did not change compared with a shoot illuminated from all sides.
instead more auxin has passed down the shaded side.
the increased conc. of auxin on the shaded side increased cell elongation; the reduced concentration on the illuminated side inhibited cell elongation. as a result the shoot grew towards the light.
59
Cholodny-Went model
explained growth curvatures as resulting from the unequal distribution of axin due to lateral transport of auxin.
critised for small sample sizes and the difficulty of measuring the very small concentrations involved.
research still investigate. new techniques used to study tropisms include the use of genetically modified plants that produce fluorescent proteins in the presence of auxin, making it possible to visualise the location of the auxin
60
where are auxin used in phototropism
indoleacetic acid (IAA)
61
where are auxins such as IAA synthesised
synthesised in actively growing root and shoot tips (meristems) and in developing leaves, seeds and fruits. they are transported from where they are synthesised to sites of action where they bring about a range of responses.
they are transported long distances in the phloem and shorter distances between cells via specific carrier proteins in the cell membrane.
62
auxin's affect on cells
auxin bind to protein receptors in the target cells.
this activates intracellular second messenger signal molecules, which activate transcription factors.
these control the transcription of auxin related genes, and the proteins produced bring about metabolic changes that result in a range of responses through changes in cell expansion, division and differentiation.
the auxin's functions in a similar way to animal hormones (topic 7)
63
how does auxin bring about cell expansion
to bring about cell expansion requires a loosening of the cell wall, it is thought that auxin causes the acidification of the cell wall by stimulating the activity of proton pumps that move H+ ions out of the cytoplasm and into the cell wall.
here, the low pH activates proteins called expansions. these expansins disrupt the bonds that hold the cellulose microfibrils and hemicelluloses together.
there is loosening of the cell wall: there is slippage of the polysaccharides relative to each other, bonds reform in new locations, allowing expansion of the cell.
other plant hormones and non enzymatic proteins are also involved in a complex sequence of extracellular and intracellular changes.
the acidification of the cell wall increases the potential differences across the membrane, this enhances the uptake of ions into the cell. in turn, the presence of these ions causes water uptake by osmosis, causing the cell to swell resulting in cell elongation.
plant growth involves cell division and enlargement. in the meristem, cells are actively dividing, most of these cells then enlarge, forming a region of elongation adjacent to the meristem. these cells go on to mature and differentiate.
64
receptors
receptor cells detect stimuli and send electrical impulses to the central nervous system.
many receptors are spread throughout the body, but some types of receptor cells are grouped together into sense organs.
65
sense organs
groups of receptor cells.
help to protect the receptor cells and improve their efficiency; structures within the sense organ ensure that the receptor cells are able to receive the appropriate stimulus.
66
structure of the eye
- choroid. black layer prevents internal reflection of light
- vitreous humour- transparent jelly
- retina. contains light sensitive cells
- yellow spot (fovea) most sensitive part of the retina located within the macula, the central area of the retina.
- optic nerve
- blind spot. no light sensitive cells where optic nerve leaves the eye
- sclera. protective layer
- iris. controls amount of light entering the eye
- lens. focuses light on retina
- cornea. bends light
- conjunctiva. protects cornea
- ciliary muscle. alters thickness of lens for focusing.
67
what are the 2 types of photoreceptor cells in the human eye
the human retina contains 2 types of photoreceptor cells sensitive to light
- rods
- cones
68
what is the differences and similarities between rods and cones
both are human photo receptor cells
cones allow colour vision in bright light
rods only give black and white vision but work in dim light as well as bright light.
cones are in the centre of the retina. this area allows us to pinpoint accurately the source and detail of what we are looking at.
over the remainder of the retina, rods outnumber cones by a factor of 20 to 1.
both contain photochemical pigments which absorb the light resulting in a chemical change.
rods contain the purplish pigment rhodopsin. these are contained in the membranes of the many layers of flattened vesicles found in the rods outer segment.
69
what doe rods and cones synapse with
synapse with bipolar neurone cells which in turn synapse with ganglion neurones, whose axons together make up the optic nerve.
light hitting the retina has to pass through the layers of neurones before reaching the rods and cones/
70
rod cells in the dark
Na+ flow into the outer segment through non specific cation channels. the Na+ move down the concentration gradient into the inner segment where pumps continuously transport them back out of the cell.
the influx of Na+ produces a slight depolarisation of the cell.
the potential difference across the membrane is about -40 mV, compared with the -70 mV resting potential.
this slight depolarisation triggers the release of a neurotransmitter thought to be glutamate, from rods ells.
in the dark the rod cells release this continuously.
the neurotransmitter then binds to the bipolar cell, stopping it depolarising.
71
rods cells in the light
- when light falls on the rhodopsin molecule, it breaks down into retinal and opsin, non protein and protein components.
- the opsin activates a series of membrane bound reactions, ending in hydrolysis of a cyclic nucleotide molecule attached to the cation channel in the outer segment.
- the breakdown of this molecule results in the closing of the cation channels. the influx of Na+ into the rod decreases, while the inner segment continues to pump Na+ out.
- this makes the inside of the cell more negative. it becomes hyperpolarised and the release of the glutamate neurotransmitter stops.
- the lack of glutamate results in depolarisation of the bipolar cell with which the rod synapses.
- the neurone that make up the optic nerve are also depolarised and respond by producing an action potential
72
dark adaption
the reforming of rhodopsin
rapidly converted back into its original form so that subsequent stimuli can be perceived.
each individual rhodopsin molecule takes a few minutes to do this.
the higher the light intensity, the more rhodopsin molecules are broken down and the longer it can take for all the rodopsin to reform, up to a maximum of 50 minutes.
73
phytochromes
plant's photoreceptors
absorb red and far red light.
consists of a protein component bonded to a non protein light absorbing pigment molecule.
the non protein component exists in 2 forms (isomers):
- Pr phytochrome red; absorbs red light
- Pfr phytochrome far red; absorbs far red light
74
why are the 2 phytochrome isomers photoreversible
plants synthesises phytochromes in the Pr form.
absorption of red light converts Pr into Pfr
absorption of far red light converts Pfr back to Pr.
in sunlight Pr is converted into Pfr more than Pfr into Prr. because more red than far red light is absorbed.
so Pfr accumulates in the light
and in the dark any Pfr present is slowly converted into Pr
75
which phytochrome causes developmental processes
Pfr
76
phytochromes role in the triggering of germination
a flash of red light
converts Pr into Pfr and causes germination
if that flash of red light is followed by a flash of far red light no germination will occur as the Pfr will have turned back into Pr
77
photoperiod
the relative length of day and night, is the environmental cue that determines time of flowering.
78
how does the ratio of Pr to Pfr enable plants to determine length of day and night
lon winter nights give ample time for Pfr to convert back to Pr, so that by sunrise all phytochromes will be Pr
summer nights are shorter and so may not be long enough to convert all Pfr back into Pr so some Pfr may still be presented in the morning
79
long day plants
only flowers when day length exceeds a critial value.
| flower when the period of uninterrupted darkness is less than 12 hours, they need Pfr to stimulate flowering
80
short day plants
flower when period of uninterrupted darkness is greater than 12 hours.
they need long hours of darkness in order to convert all Pfr present at sundown back to Pr.
Pfr inhibits flowering
in most short day plants, a flash of red light in the middle of the dark period negates the effect of the dark period.
81
greening
once a shoot has broken through soil into sunlight, the plant undergoes profound changes in both its form and biochemistry.
once in light, phytochromes promote the development of primary leaves, leaf unrolling and the production of pigments.
they can also inhibit certain processes, such as elongation of internodes (length of stem between leaves)
82
how do phytochromes switch processes on or off
- it is thought that each activated phytochrome then interacts with other proteins
- the phytochromes may bind to the protein or disrupt the binding of a protein complex.
- these signal proteins may act as transcription factors or active transcription factors that bind to DNA to allow transcription of light regulated genes.
- the transcription and translation of proteins result in the plant's response to light.
83
what other environmental cues can plant detect
- gravity
more than a short distance under the soil surface lught cannot be the cue.
- touch and mechanical stress.
84
what is each cerebral hemisphere made up of
- frontal lobe
- parietal lobe
- occipital lobe
- temporal lobe
85
cortex
the grey and highly folded outer layer of the brain.
composed mainly of nerve cell bodies, synapses and dendrites.
this outer layer is known as the grey matter
un- myelinated
86
below the cortex lies white matter.
| why is it called this
white matter is composed of millions of nerve axons that connect neurons in different parts of the brain
the white colour is due to the axon's myelin sheath.
87
corpus callosum
broad band of white matter. that connects the 2 cerebral hemispheres. allows communication between the 2 hemispheres.
88
what are the structures lying directly below the corpus callosum
- thalamus
- hypothalamus
- hippocampus
- basal ganglia
89
thalamus
is responsible for routing all the incoming sensory information to the correct part of the brain, via axons of the white matter
90
hypothalamus
lies below the thalamus
contains the thermoregulatory centre
this monitors core body temperature and skin temperature, and initiates corrective action to restore the body to its optimum temperature. a
also located in the hypothalamus are other centres that control sleep, thirst and hunger.
the hypothalamus also acts as an endocrine gland, secreting hormones such as antidiuretic hormone (controls water re absorption in the kidneys and hence controls blood concentration.
the hypothalamus connects directly to the pituitary gland, which in turn secretes other hormones.
91
hippocampus
is involved in layer down long term memory
92
basal ganglia
collection of neurones that lie deep within each hemispheres and are responsible for selecting and initiating stored programs for movement
93
frontal lobe
concerned with higher brain functions such as decision making, reasoning, planning and consciousness of emotion.
it is also concerned with forming associations (by combining information from the rest of the cortex) and with ideas.
it includes the primary motor cortex which has neurones that connect directly to the spinal cord and brain stem and from there to the muscles.
it sends information to the body via the motor neurones to carry out movements. the motor cortex also stores information about how to carry out different movements
94
parietal lobe
concerned with orientation, movement, sensation, calculation, some types of recognition and memory
95
occipital lobe
visual cortex.
| concerned with processing information from the eyes, including vision, colour, shape recognition and perspective.
96
temporal lobe
concerned with processing auditory information i.e hearing sound recognition and speech (left temporal lobe)
also involved in memory
97
brain stem
in evolutionary terms is the oldest part of the brain and is sometimes referred to as the reptilian brain.
it lies at the top of the spinal column.
the brain stem extends from the midbrain to the medulla oblongata.
98
cerebellum
responsible for balance
coordinates movement as it is being carried out, receiving information from the primary motor cortex, muscles and joints.
constantly checks whether the motor programme being used is the correct one. for example, by referring to incoming information about posture and external circumstances
99
midbrain
relahyes information to the cerebral hemispheres, including auditory information to the temporal love and visual information to the occipital lobe.
100
medulla oblongata
regulates those body processes that we do not conscious control, such as heart rate, breathing and blood pressure.
101
neural plasticity
the potential for neurones to change in structure and function.
the structure of the brain remains flexible even in later life and can respond to changes in the environment.
brain structure and functioning is affected by both nature and nurture.
102
CT scans
Computerised Axial Tomography (CT / CAT) imaging.
thousands of narrow beam X rays rotated around the patient to pass through the tissue from different angles.
each narrow beam is attenuated (reduced in strength) according to the density of the tissue,
X rays are detected and are used to produce an image of a thin slice of the brain in which the different soft tissue within the brain can be distinguished.
- only look a structures rather than functions
- detect brain disease monitor tissue in the brain.
- limited resolution so small structures in the brain cannot be distinguished.
- harmful X rays.
103
MRI
magnetic resonance imaging
uses a magnetic field and radio waves to detect soft tissues.
hydrogen atoms in water are monitored in MRI because of the high water content in the tissues under investigation.
one magnetic field runs down the centre another magnetic field is superimposed on this, which comes from high frequency radio waves.
the combined fields cause the direction and frequency of spin of the hydrogen nuclei to change, taking energy from the radio wave to do so. when the radio waves are turned off the hydrogen nuclei return to their original alignment and release the energy they absorbed.
this energy is detected and a signal is sent to a computer, which analysis it to produce an image.
- diagnose tumours, strokes, brain injuries and infections of the brain and spine.
- produce finely detailed images of brain structures.
better resolution than CT scans for the brain stem and spinal cord.
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fMRI
functional magnetic resonance imaging
is used to look at the functions of different areas of the brain by following the uptake of oxygen in active brain areas.
deoxyhaemoglobin absorbs the radio wave signal
oxyhaemoglobin does not.
with increased neural activity in the brain area, oxygen absorption from the blood increases and so there is a large increase in oxyhaemoglobin levels in the enhanced blood flow, so less signal is absorbed.
the less radio signal absorbed the higher the level of activity.
4 images per second.
images are collected continually while the subject alternates between resting and carrying out some tasks such as object recognition, listening or memorising number sequences.
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PET
positron emission tomography
- used to produced detailed images that allow the structure and functioning of tissues and organs to be evaluated.
cancers, heart disease and brain disorders.
use isotopes with short half lives. e.g Carbon-11 incorporated into compounds such as water or glucose or molecules that bind to receptors, radio tracers
patient injected with radio tracer. as radio tracer decays, emits positrons. when tissue is more active more oxygen and glucose increased blood flow show up as more radio tracer atoms present. positron collides with electron, 2 gamma rays are emitted picked up by detectors. bight spots indicate high levels of neurone activity. once or twice a year for safety and expensive. diagnosis and monitoring of Alzheimers
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Alzheimers
symptoms: memory loss, problems with thinking, problem solving and language. neurone loss
as neurone dies, a piece of beta- amyloid protein found in the myelion sheath clump together and form clusters of sticky plaques blocking signalling at synapses and activate immune cells that trigger inflammatory response. accumulation of beta-amyloid can be detected using a PET scan with an amyloid tracer.
as B-amyloid plaques accumulate and synapses and acetylcholine receptors are destroyed in the brain shows progression.
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how does information from the eyes reach the visual cortex in the brain
axons of the ganglion cells that make up the optic nerve pass out of the eye and extend to several areas of the brain, including the thalamus. impulses are then sent along further neurones to the primary visual cortex where the information is processed. before reaching thalamus some branch to mid brain to connect to motor neurones involved in controlling pupil reflex and movement of the eye.
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axon growth in visual development
axons of the neurones from the retina grow to the thalamus where they form synapses with neurones in the thalamus in a very order arrangement. axon from these thalamus neurones then grow towards the visual cortex in the occipital lobe.
the visual cortex is made up of columns of cells. the same part of the left eye and right eye send information to adjacent cells
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critical period
use to think that these columns of cells formed during a critical period for visual development after birth, the result of nurture
this is not the case
work with ferrets has shown that the columns are formed before the critical period for visual development. newborn baby monkey also have these columns. ext due to nature
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critical windows
times in post natal development. at these times the nervous system must have specific experiences to develop properly.
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evidence of critical period in visual development
medical observations
- baby with eye infection bandaged eyes for 2 week. when removed he was left with permanently impaired vision
- if cataracts are not removed before 10 years child will not be able to perceive shape or forms
but in older people their vision is not affected.
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animal models
are animals that are studied extensively in science
animal models tends to be species that are easy to breed, have short life cycles and a small adult size. kittens and monkeys used to study visual development similarity to humans
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examples of animal studies into the critical period for visual development
- newborn monkeys raised in dark for first 3 - 6 months
another group raised in light but with no patterns
both groups had problem discriminating objects and patterns
- monkeys deprived in one eye (monocular deprivation) monkey was blind in light deprived eye. retinal cells responded but the cells in visual cortex did not respond
- deprivation for just a week in critical period same effect in adults no effect.
- kittens deprived under 3 weeks had no effect. 3 months had no effect. deprivation at 4 weeks had a major effect.
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what happens during the critical period
columns in visual cortex narrower if they do not receive light.
axons compete for target cells in visual cortex. every time a neurone fires onto target cell other synapses weakened. axons that are not used are cut back.
1. there is a lack of visual stimulation in one eye
2. axons from the visually deprived eye do not pass impulses to cells in the visual cortex
3. axons from non deprived eye pass impulses to cells in visual cortex
4. inactive synapses are eliminated
5. synapses made by active axons are strengthened.
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neurones in the visual cortex
called simple cells respond to bars of light
complex cells respond to edges, slits or bars of light that move.
other cells respond to angle of the edge and others to contours, movement or orientation
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visual perception
is not just creating an image of an object
| involves knowledge and experience as the brain interprets the sensory information from the retina
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depth perception
is the visual ability to perceive the world in 3 dimensions and the distance of an object
when we look at any object we can make a judgement about how far away the object is. the brain does this in different ways for close and distant objects
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depth perception close objects
less than 30 m away
we depend on the presence of cells that obtain information from both eyes at once
the visual field is seen from 2 different angles and cells in the visual cortex let us compare the view from one eye with that from the other. stereoscopic vision and allows the relative position of objects to be perceived.
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depth perception distant objects
for objects more than 30 m away the images on both retina's are very similar. this means that visual cues and past experiences is used to interpret the image
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common visual cues
size of objects
lines converging in the distances
overlaps of objects
changes in colour
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cross cultural studies in depth perception
| carpentered world hypothesis
people who live in a world full of straight lines perceive depth cues differently to people living in a circular culture
straight line world (buildings) used to interpreting images with acute and obtuse angles. people living in a circular culture have little experience of straight lines and are not fooled by optical illusions
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genetics as being the reason for different depth perception
not due to experiences.
differences in pigmentation between individuals. individuals who find it harder to detect contours are less susceptible to the illusions.
poor contour detect to higher retinal pigmentation. people with low retinal pigmentation contour detection is good and people are more easily caught out by illusions
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a cross cultural study into depth perception
young children have trouble perceiving images as 3D. by the age 11 almost all European children interpret images as 3D
some Bantu and Ghanaian kids did not nor did non literate adults. less experience of depth cues. they must be learned.
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studies with newborns
some behaviours are present from birth e.g crying and grasping. within 24 hours newborns can distinguish a human face and prefer them. for genes determining hard wiring of the brain before birth.
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the visual cliff
babies encouraged to crawl across a table made of glass. patterns create appearance of steep drop. shows that depth perception may be innate. but babies who can crawl may have already learned depth perception. repeated with animals who walk after birth these animals refused to go other
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where are memories stored
not localised to any one part. distributed throughout cortex. different types of memory controlled by different parts.
demonstrated by case studies HM.
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how are memories stored
making memories is an active process
- the pattern of connections
- the strength of synapses
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habituation
a diminishing of a innate response to a frequently repeated stimulation
gives animals the ability to ignore unimportant repetitive stimuli so that limited sensory, attention and memory resources can be concentrated or more threatening or rewarding stimuli
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sea slugs and habitation
breath through gill located in a cavity on the upper side of its body water is expelled through a siphon tube at one end of cavity. if the siphon is touched the gill is withdrawn into the cavity, this is a protective reflex
because they are frequently buffeted by waves they learn not to withdraw their gills every time a wave hits them.
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what happens in habituation of sea slugs
when siphon is repeatedly stimulated with a jet of water. the response gradually faded away until the gill was not withdrawn any more
the neurones involved in the reflex were identified. found that the amount of neurotransmitter crossing the synapses between the sensory and motor neurones decreased with habitation. with repeated stimulation, fewer calcium ions move into the presynaptic neurone when the presynaptic membrane is depolarised by an action potential; fewer neurotransmitter molecules are then released.
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what happens in habituation
1. with repeated stimulation, Ca2+ channels become less responsive so less Ca2+ crosses the presynaptic membrane
2. less neurotransmitter is released
3. there is less depolarisation of the postsynaptic membrane so no action potential is triggered in the motor neurone.
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ethics of using animals in medical research
- importance of consent.
- animal welfare. not allowed to use vertebrates in medical experiments if there is a non animal alternative.
- animal suffering and experiencing pleasure.
- utilitarianism. belief that the right course of action is the one that maximises the amount of overall happiness or pleasure in the world.
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Parkinson's disease symptoms
- stiffness of muscles
- tremor of the muscles
- slowness of movement
- poor balance
- walking problems
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what causes Parkinson's disease
dopamine a neurotransmitter secreted by neurones including those located in the mid-brain. the axons of which extend throughout the frontal cortex, the brain stem and spinal cord.
dopamine secreting neurones in the basal ganglia die. these neurones normally release dopamine in the motor cortex. the motor cortex receives little dopamine and there is a lost of control of muscular movements.
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treatment for Parkinson's disease (5)
- slowing the loss of dopamine in the brain. MAO inhibitors which inhibits mono-amine oxidase, the enzyme responsible for the breakdown of dopamine. thereby increasing availability of dopamine. MAOA and MAOB.
- treating symptoms with drugs. dopamine cannot be given as it cant cross the blood-brain barrier. L-dopa a precursor to dopamine can cross the barrier where it is converted into dopamine increasing concentration. main therapy.
- dopamine agonists. are drugs that activate dopamine receptors directly and often more than one is gived. drugs mimic role of dopamine binding to receptors and triggering action potentials. they avoid high dopamine levels which has side effects.
- gene therapy. trials in animals and phase 1 in humans show promise. genes for proteins that increase dopamine production, and that promote the growth and survival of nerve cells inserted into the brains.
- deep brain stimulation (DBS) is a type of surgery used to treat symptoms of the disease. reduce medication reducing side effects
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what happens when you have excess dopamine
- major cause of schizophrenia
excess dopamine in the brain can be treated with drugs that block the binding of dopamine to is postsynaptic receptor sites. these drugs look similar in structure to dopamine but unable to stimulate receptors. side effect of these drugs is Parkinson's like symptoms.
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what causes depression
the neurotransmitter serotonin plays important role in mood.
neurones that secreate serotonin are stiuated in the brain stem. their axons extend into the cortex, cerebellum and spinal cord targeting a huge area.
lack of serotonin has been linked
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symptoms of depression
is a common disease that effects 1 in 5 people at some point.
- persistently low mood interfering with everyday life.
sadness, anxiety and hopelessness. loss of interest and reduced energy levels, insomnia, restlessness and suicidal thoughts.
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depression is multifactorial
- several genes confer susceptibility with environmental factors also contributing
traumatic, stressful events, childhood events, bereavement, illness or job or money worries.
gene 5-HTT influence. it codes for transporter protein that controls serotonin re uptake into presynaptic neurones. people with short version likely to develop after stressful event. environmental trigger needed.
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treatment of depression
MAOIs monoamine oxidase inhibitors first type of drug they break down neurotransmitters including serotonin.
selective serotonin inhibitors (SSRI) blocking only the uptake of serotonin. one of the more common drugs is prozac high levels of serotonin
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drugs affect on synaptic transmission
synapses have number of features that can be disrupted.
- chemical with similar molecular structure to neurotransmitter is likely to bind to same receptor sites and stimulate postsynaptic.
- others may prevent the release of neurotransmitter block or open ion channels, or inhibit breakdown enzymes.
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effect of ecstasy (MDMA) affects synapses
MDMA increases the concentration of serotonin in the synaptic cleft. by binding to molecules in the presynaptic membrane that are responsible for transporting serotonin back into the cytoplasm. this prevents the removal from the synaptic cleft. drug may also cause the transporting molecules to work in reverse, further increasing amount of serotonin outside cell. high levels bring about mood changes. MDMA may have similar effect on molecules that transport dopamine as well.
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effect of using MDMA
feelings of euphoria, well being and enhanced senses.
side effects and unpredictable consequences.
clouded thinking, agitation and disturbed behaviour.
sweating, dry moth, increased heart rate, fatigue, muscle spasms and hyperthermia. since MDMA can disrupt ability to regulate body temperature.
high blood pressure, irregular heartbeat, muscle breakdown and kidney failure.
evidence long term effects include insomnia, depression and other psychological problems. effect normal brain activity even after drug is no longer taken. cells cannot synthesis enough to meet demand once i is gone resulting in of depression
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human genome project
intended to produce the complete base sequence of the human genome. in ho;e it will give us better understanding, to avoid risk factors specific to own genetic make up and continue to improve the help given to people with these conditions
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SNPs
single nucleotide polymorphisms.
A SNP is a DNA sequence variation that occurs when a single nucleotide in the genome sequence is altered in at least 1% of the population, with one base substituted for another. may alter the protein formed or may have no effect on cell function, possession of particular SNPs could predispose people to disease or influence their response to a drug.
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genes in Alzheimer's disease
six genes identified. multifactorial.
genetic fault on chromosome 21 in the APP gene for production of the precursor of a particular protein implicated.
possession of alleles of a gene APoE. there are 3 common APoE alleles and having 2 alleles of ApoE4 seems to increase the risk of getting the disease. APoE controls production of a lipoprotein used in the repair of cell membranes in damaged neurones.
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what as the human genome project accomplished
- detailed information about the genome
- identification of new genes. in relation to susceptibility of some diseases
- identification of new drug targets
- personalised medicine. preventative medicine and improved drug treatment
differences in the way people respond to drugs may be due to differences in SNPs. enable to prescription right drug at the correct dose.
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ethical dilemmas of the human genome project
- testing for genetic predisposition and discrimination. insurers to have information of people applying for health insurance
- who should decide about the use of genetic predisposition tests and on whom they should be used
- making and keeping records of individual geneotypes raises acute problems of confidentiality
- many medical treatments made possible through the development of genetic technologies will initially be very expensive. their restricted availability will add considerably to the problems faced by health services
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genetic modification / genetic engineering
the artificial introduction of genetic material from another organism through genetic modification, to produce a transgenic or genetically modified organism.
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genetically modifying microorganisms
- bacteria contain simple DNA structures, plasmids which can be transferred from one cell to another.
- using restriction enzymes, the circular plasmids can be cut and using another set of enzymes a piece of DNA from another species can be inserted into it.
The plasmid is inserted back into the bacteria, which are then allowed to multiply.
- the protein produced is extracted from the culture
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genetic modification in plants
- removal of plasmid from bacterial cell. plasmid is then cut with restriction enzyme.
- identified gene of interest, the foreign gene is cut with the same restriction enzyme and inserted into the DNA plasmid along with a selected antibiotic marker
- the plasmid is then reinserted into the bacterium. the bacterium is now allowed to introduce a plasmid vector with foreign DNA into plant cell. the foreign gene is the incorporated into the plant chromosome transforming the plant cell
- alternatively after the DNA is inserted into the plasmid, it is coated with gold or tungsten and a gene gun is used to fire pellets coated in DNA into the plant cell at high velocity
- the plate cells then put on a growth medium with antibiotic, only transformed cells will be selected
- micropropagation: transformed cells grow in sterile culture medium containing sucrose, amino acids, inorganic ions and plant growth substances.
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marker gene
gene insertion is never 100% successful so in order to screen for cells which actually have the new gene a marker gene for antibiotic resistance is incorporated alongside the desired one. the antibiotic is toxic to plant cells at a high enough does so the plant cells are incubated with the antibiotic, which kills off any cells that have not incorporated the new genes.
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the 3 ways of inserting the new gene into the plant cell
- bacterium that infects plants. when it invades plant cells, genes from plasmid DNA become incorporated into the chromosome of the plant cells. so insert the desired genes into a plasmid, which them carries these genes into the plant DNA
- minute pellets that are covered with DNA carrying the desired genes are shot into plant cells using a particle gun
- viruses are sometimes used. they infect cells by inserting their DNA or RNA. this can be used to transfer the new genes into the cell.
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what are the health concerns of GM plants
- transfer of antibiotic resistance genes to microbes
- formation of harmful products by new genes
- transfer of viruses from animals to humans
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GM plants. antibiotic resistance
the transfer of antibiotic resistance genes to microbes
since antibiotic markers genes are only there to assist in the development is is unnecessary to leave them in products an they are already started to be removed.
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GM plants. environmental issues (3)
- transfer of genes to non target species
- possible breeding of superweeds
- the possibility that GM crops will lead to the increased use of chemicals in agriculture.
