Studied by 4 people
radial muscles
contract to dilate
sympathetic reflex
circular muscles
contract to contract pupil
parasympathetic reflex
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
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
Na+/K+ pump creates concentration gradients across the membrane
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
the potential difference will pull K+ back into the cell
at -70mV, the two gradients counteract each other and there’s no net movement of K+
as it becomes less negative, voltage gates Na+ channels open and Na+ flows into the axon to depolarise the membrane
at +40mV, voltage-dependent Na+ channels close, voltage-dependent K+ channels open
K+ leave the axon, repolarising the membrane of the neurone and charge the outside
the membrane becomes hyperpolarised as it takes time for the channels to shut (-90mV)
K+ diffuse back until resting potential is restored
part of the membrane becomes depolarised at the site of the action potential
local electrical current is created as Na+ flow between the depolarised part of the membrane and adjacent region
depolarisation spreads to the adjacent region
nearby Na+ gates open to trigger another action potential
repeated along the membrane to cause a wave of depolarisation
depolarised by an action potential
channel membranes open, increase membrane permeability to Ca2+
Ca2+ concentration is greater outside, so diffuses across the membrane into the cytoplasm
increased Ca2+ concentration causes synaptic vesicles to fuse with presynaptic membrane
neurotransmitter is released into the sunaptic cleft by exocytosis
neurotransmitter diffuses across the synaptic cleft and reaches the postsynaptic membrane
binds to complementary shaped receptor
receptor changes shape to open cation channels, making the membrane permeable to Na+
this flow causes depolarisation, the extent of which depends on the amount of neurotransmitter reaching the membrane and number of receptors on it
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
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
frequency of impulses
number of neurones in a nerve conducting impulse
eg strong stimulus → high frequency and many neurones
control of nerve pathways, allowing flexibility of response
integration of information from different neurones to allow a coordinated response
type of synapse
number of impulses received
excitatory synapse
help stimulate an action potential
inhibitory synapse
make it less likely for a postsynaptic membrane to depolarise
a postsynaptic cell can have both types of synapse, generation depends on the balance of the synapses at any one time.
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)
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
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 released by neurones in the midbrain and is involved in movement
these neurones’ axons extend to the spinal cord, brainstem and frontal cortex
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
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
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
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
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
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
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
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
seed germination
stem elongation
leaf expansion
chlorophyll formation
flowering
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
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
controls higher functions
thinking, feeling, seeing and learning
mainly grey matter
folded cortex to give a large surface area
divided into lobes
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
visual information
input from the eyes to deal with vision, shape recognition, colour and perspective
at the back of the brain
memory recognition
ability to calculate
sense of movement and orientation
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
larger structure attached to hypothalamus
routes all incoming sensory information to the correct parts of the brain
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
producing frozen pictures of the brain to identify structures to detect brain disease
monitor tissues over the course of an illness
narrow beam X-rays rotate around the patient
the strength of the beam varies depending on the density of the tissue it is passing through
X-rays are detected to produce an image
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
magnetic fields and radio waves detect soft tissue
in a magnetic field, nuclei of atoms line up with the direction of the magnetic field
H atoms are monitored due to the high water content in the tissues and they line up with the magnetic field
energy absorbed by the H ions is detected and analysed by the computer to produce an image
makes it possible to study human activities
can also be used to follow the sequence of events over a short period of time
increased neural activity results in an increase in O2 absorption from the blood, reducing the signal received by the computer
the less signal absorbed, the higher activity in that area
different ares of the brain light up on the image when they are active
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
patient injected with a radiotracer (short half life isotopes incorporated into glucose or water that will bind to receptors)
as it decays it emits positrons
when a particular area is active, there is increased blood flow, so more radiotracers are present in that area
release of gamma rays as they collide with positrons that are converted into an image on the computer
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