biology: topic 8

function of a sensory neurone

carry impulses from receptors to the central nervous system

function of a motor neurone

conducts impulses from the central nervous system to the effectors

function of a relay neurone

transmit impulses from sensory neurones to motor neurones

located within the central nervous system

draw a sensory neurone

draw a motor neurone

draw a relay neurone

cell body

contains nucleus and cell organelles within cytoplasm

very fine dendrites

conduct impulses toward the cell body, collected from other neurones

axon

transmit impulse away from the cell body

fatty insulated layer

aka myelin sheath

made up of schwann cels wrapped around the axon

stimulus

the change in environment

receptor

detects the stimulus

eg photoreceptors, thermoreceptors, chemoreceptors

effector

muscles or glands that carry out the response

response

what happens in response to the stimuli

co-ordinated response

stimulus → receptor → sensory neurone → spine → brain → spine → motor neurone → effector → response

reflex arc

skips the spine and brain, instead goes through the relay neurone

which part of the nervous system controls the pupil reflex?

autonomic nervous system

antagonistic muscles in the iris

* radial muscles

contract to dilate

sympathetic reflex

* circular muscles

contract to contract pupil

parasympathetic reflex

pupil reflex in high light levels

* high light levels hit the photoreceptors in the retina
* causes nerve impulses to pass along the optic nerve
* sends an impulse to nerve sites within the CNS (including coordinating cells in the midbrain)
* impulses sent along parasympathetic motor neurones to the circular muscles
* radial muscles relax to constrict the pupil and reduce the light entering the eye

pupil reflex in low light levels

* low light levels detected by photoreceptors in the retina
* impulses sent down sensory neurone in the optic nerve in the midbrain
* impulses sent along sympathetic motor neurones to radial muscles
* contract to widen the pupil

resting potential of an axon

\-70mV

due to the ion distribution

more X- ions inside, X+ outside

what causes an uneven distribution of ions?

sodium-potassium pumps

K+ → cell

cell → Na+

work against the concentration gradient, requiring energy from ATP

chlorine ions move out of the cell to balance the charge, though not actively BY the cell

how is resting potential generated?

1. Na+/K+ pump creates concentration gradients across the membrane
2. K+ diffuse outside of the cell down the K+ concentration gradient, making the outside of the membrane positive and inside negative to create a potential difference
3. the potential difference will pull K+ back into the cell
4. at -70mV, the two gradients counteract each other and there’s no net movement of K+

how is an action potential produced

1. as it becomes less negative, voltage gates Na+ channels open and Na+ flows into the axon to depolarise the membrane
2. at +40mV, voltage-dependent Na+ channels close, voltage-dependent K+ channels open
3. K+ leave the axon, repolarising the membrane of the neurone and charge the outside
4. the membrane becomes hyperpolarised as it takes time for the channels to shut (-90mV)
5. K+ diffuse back until resting potential is restored

passing impulses across a neuron

1. part of the membrane becomes depolarised at the site of the action potential
2. local electrical current is created as Na+ flow between the depolarised part of the membrane and adjacent region
3. depolarisation spreads to the adjacent region
4. nearby Na+ gates open to trigger another action potential
5. repeated along the membrane to cause a wave of depolarisation

what is the refractory period and why does it occur?

due to hyperpolarisation at the end of an action potential, there is a refractory period

a new action potential cannot be generated as there’s too great a difference in charge (-90mV instead of -70mV

this ensures an impulse only travels in one direction

what happens at the presynaptic neurone?

1. depolarised by an action potential
2. channel membranes open, increase membrane permeability to Ca2+
3. Ca2+ concentration is greater outside, so diffuses across the membrane into the cytoplasm
4. increased Ca2+ concentration causes synaptic vesicles to fuse with presynaptic membrane
5. neurotransmitter is released into the sunaptic cleft by exocytosis

what happens at the postsynaptic neurone?

1. neurotransmitter diffuses across the synaptic cleft and reaches the postsynaptic membrane
2. binds to complementary shaped receptor
3. receptor changes shape to open cation channels, making the membrane permeable to Na+
4. this flow causes depolarisation, the extent of which depends on the amount of neurotransmitter reaching the membrane and number of receptors on it

what happens to the neurotransmitters after synaptic transmission?

* some neurotransmitters are actively taken up and reused by the presynaptic membrane
* others rapidly diffuse away from the synaptic cleft
* some are taken up by other cells or broken down by enzymes so can no longer bind to receptors

impact of axon diameter on speed of conduction

the wider the diameter, the faster the impulse travels

saltatory conduction

* due to myelination with schwann cells, there are gaps along the axon called nodes of ranvier
* depolarisation can only occur at these places
* the impulse jumps from one node to the next
* this is much quicker than depolarising along the whole membrane

does impulse strength vary by the strength of the stimulus?

no

the stimulus must be at or above the threshold level to generate an action potential

* as long as it is at or above, the size of impulse generated is the exact same regardless of stimulus size

what does the size of the stimulus affect?

* frequency of impulses
* number of neurones in a nerve conducting impulse

eg strong stimulus → high frequency and many neurones

roles of synapses

* control of nerve pathways, allowing flexibility of response
* integration of information from different neurones to allow a coordinated response

factors impacting the chance of depolarisation:

* type of synapse
* number of impulses received

types of synapse

* excitatory synapse

help stimulate an action potential

* inhibitory synapse

make it less likely for a postsynaptic membrane to depolarise

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a postsynaptic cell can have both types of synapse, generation depends on the balance of the synapses at any one time.

excitatory synapses

* make the membrane more permeable to Na+
* a single synapse does not depolarise the membrane enough for an action potential
* several impulses arriving within a short amount of time will do, however
* this happens either through spatial summation (many from diff. neurones) or temporal summation (lots from the same neurone)

inhibitory synapses

open Cl- and K+ ion channels, allowing the ions to move down their concentration gradients

* produces hyperpolarisation of -90mV
* action potential is NOT generated as it can’t in a hyperpolarised area

problems with synapses and the blood brain barrier

endothelial cells of capillaries are more tightly packed together

* forms blood brain barrier
* aimed to protect it from changes in ionic composition and toxic molecules
* problems occur with an imbalance in chemicalc crossing the barrier

dopamine release

* dopamine released by neurones in the midbrain and is involved in movement
* these neurones’ axons extend to the spinal cord, brainstem and frontal cortex

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dopamine and parkinson’s

the dopamine-releasing neurones die, so little dopamine is released into the motor cortex

* resulting in a loss of motor control
* and symptoms such as:
* muscle stiffness and tremors
* slowness of movement
* poor balance and walking problems

treatments for parkinsons

* slow the loss of dopamine by protecting dopamine secreting neurones
* treat symptoms with L-DOPA drugs
* dopamine agonists (trigger the same neural pathway)
* gene therapy (does not always accept or retain the new gene)
* deep brain stimluation
* electrodes placed into the brain and connected to a battery pack in the chest that applies a voltage to trigger the neural pathway

condition associated with excess dopamine

schizophrenia

* hallucinations, delusions

treatment for schizophrenia

antagonist drugs that block dopamine binding sites on postsynaptic receptors, NOT stimulating them

* can cause side effects of symptoms of parkinson’s
* NOT parkinson’s itself as the neural cells are still alive

seratonin

neurotransmitter that plays a role in determining mood

the neurones that secrete it are found in the brain stem

* axons extend into the cortex, spinal cord and cerebellum

low seratonin and depression

linked to depression, along with noradrenaline

fewer nerve impulses than normal are transmitted around the brain, so lower levels of neurotransmitter released

* molecules needed for seratonin synthesis are present in only low concentrations
* seratonin binding sites are more numerous to compensate for the low levels of the molecules

treatments for depression

* monoamine oxidase inhibitors (MAOIs)

enzymes that break down neurotransmitters are inhibited, maintaining seratonin levels

(rarely used now)

* selective seratonin reuptake inhibitors (SSRIs)

inhibits reuptake of seratonin from synaptic clefts

maintain higher levels of seratonin, increasing the rate of nerve impulses

genes and depression

there may be a gene known to increase susceptibility that may be triggered by environmental factors

→ twin studies

→ epigenetic causes

how do drugs interact with synapses?

chemicals with similar molecular structure to a particular neurotransmitter is likely to bind to the same receptor site

* from this it could stimulate the postsynaptic neurone
* the chemicals may also prevent the release of a neurotransmitter, block or open ion channels or inhibit the breakdown of enzymes

ecstasy and seratonin

MDMA impacts thinking, mood and memory

* increases seratonin concentration in the synaptic cleft by binding to the molecules in the presynaptic membrane
* prevents the reuptake of seratonin into the membrane

effects of MDMA

* euphoria and enhanced senses
* clouded thinking and agitation
* sweating
* fatigue
* rapid heart rate
* insomnia and depression
* as cells cannot meet the seratonin demand that MDMA increases

what is acetylcholine

neurotransmitter that binds to postsynaptic neurone to change their shape, allowing sodium ions so diffuse in via the newly opened sodium ion channel

auxins

eg IAA

responsible for phototropisms, geotropisms and growth responses

produce in low concenrations, then transported to produce the response

* root tip → inhibits elongation
* shoot tip → promotes elongation

auxin effect on shoot in term of light

moves towards shaded side

promoted elongation of cells on shaded side

curves towards the light

positively phototropic

auxin effect on shoot in terms of gravity

promotes elongation of cells

auxin moves down with the pull of gravity

promotes elongation of cells downward

negatively geotropic

auxin effect on root in terms of light

auxin moved to the shaded side

inhibits elongation

root moves away from the light

negatively phototropic

auxin effect on root in terms of gravity

auxin moves away from the gravitational pull

inhibiting elongation

root grows down

positively geotropic

phytochromes

absorb red and far-red light

consists of a protein component, bonded to a non protein light absorbing pigment molecule

Pr

phytochrome red (660nm)

Pr + red light → Pfr

Pfr

phytochrome far red (730nm)

Pfr + far red light → Pr

which pigment dominates in sunlight?

Pfr

hence overnight it reverts to Pr

what plant responses do phytochromes regulate

* seed germination
* stem elongation
* leaf expansion
* chlorophyll formation
* flowering

germination and phytochromes

when exposed to far red light, Pfr converts to Pr and germination is inhibited

red light triggers germination

if flashed with f.r light, germination is inhibited

if flashed again, germination is re-triggered, proving that the effects are reversible

photoperiods

relative day/night length and environmental cue determining time of flowering

* the Pr:Pfr ratio in plant allows it to internally determine the length of days and nights
* short days give enough time for Pfr → Pr

long day plants

eg strawberries

associated with the summer

when there is darkness less than 12 hours

reqiure Pfr to flower, therefore not enough time for it to convert to Pr

short day plants

eg poinsettias

requires uninterrupted darkness greater than 12 hours to give enough time for all Pfr → Pr

Pfr inhibits flowering

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greening

* shoots undergo greening once the shoot breaks through the soil into sunlight
* once in the light, phytochromes promote development of primary leaves and pigment
* need Pfr for chlorophyll production

phytochromes and switching on and off

each activated phytochrome interacts with other proteins, causing either binding to the protein or disrupting binding of a protein complex

what does Pfr inhibit?

short day plants

no flowering

what does Pfr enable?

germination

long day plants

chlorophyll formation

it is a signal protein that acts as a transcription factors to enable the usual transciption pathway

grey matter

neurone cell bodies

white matter

neurone fibres

cerebral hemispheres

* controls higher functions
* thinking, feeling, seeing and learning
* mainly grey matter
* folded cortex to give a large surface area
* divided into lobes

how to the left and right cerebral hemispheres communicate

joined at the centre with a band of axons called the corpus callosum

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frontal lobe

* emotional response, planning ahead, reasoning and decision making
* the ‘conscious’ area of the brain
* last to be fully developed
* primary motor cortex, controlling body movements via motor neurones passing through the hindbrain and spinal cord

temporal lobes

* auditory information
* near to the ears

occipital lobe

* visual information
* input from the eyes to deal with vision, shape recognition, colour and perspective
* at the back of the brain

parietal lobe

* memory recognition
* ability to calculate
* sense of movement and orientation

hypothalamus

* controls the autonomic nervous system
* thermoregulation
* right in the centre of the brain
* monitors:
* blood chemistry
* hormone secretions of the pituitary gland
* basic drives → thirst, hunger, aggression and reproductive behaviour

thalamus

* larger structure attached to hypothalamus
* routes all incoming sensory information to the correct parts of the brain

hippocampus

* lays down long term memory
* underneath the hypothalamus

cerebellum

* coordinates smooth motor movements
* uses info from muscles and ears for posture and balance

medulla oblongata

* the most primitive part of the brain
* controls reflex centres:
* heart rate
* blood pressure
* sneezing
* digestive muscles
* maintains basic life responses even where major areas of the brain are damaged
* bottom of the skull, down the back of the neck
* will not be considered ‘dead’ until the medulla is no longer functioning

what is a CAT/CT scan used for?

* producing frozen pictures of the brain to identify structures to detect brain disease
* monitor tissues over the course of an illness

how does a CAT/CT scan work?

1. narrow beam X-rays rotate around the patient
2. the strength of the beam varies depending on the density of the tissue it is passing through
3. X-rays are detected to produce an image

what are MRIs used for?

* diagnosis of tumors, brain injuries, strokes and infections
* MRIs have better resolutions than CT scans so more detailed images of the brain can be produced

how do MRIs work?

1. magnetic fields and radio waves detect soft tissue
2. in a magnetic field, nuclei of atoms line up with the direction of the magnetic field
3. H atoms are monitored due to the high water content in the tissues and they line up with the magnetic field
4. energy absorbed by the H ions is detected and analysed by the computer to produce an image

what is a functional MRI used for?

* makes it possible to study human activities
* can also be used to follow the sequence of events over a short period of time

how does a functional MRI work?

1. increased neural activity results in an increase in O2 absorption from the blood, reducing the signal received by the computer
2. the less signal absorbed, the higher activity in that area
3. different ares of the brain light up on the image when they are active

what is a PET scan used for?

* evaluate the structures and functions of tissues and organs
* diagnosis of cancers, heart disease, brain disorders
* monitors spread of cancers and observe the effect of treatment

how does a PET scan work?

1. patient injected with a radiotracer (short half life isotopes incorporated into glucose or water that will bind to receptors)
2. as it decays it emits positrons
3. when a particular area is active, there is increased blood flow, so more radiotracers are present in that area
4. release of gamma rays as they collide with positrons that are converted into an image on the computer