module 1 Flashcards
what are the steps in exocytosis ?
1) secretory vesicle formation
2)budding of the Golgi
3) uncoating
4)docking at the plasma membrane
exocytosis happens
why are intra cellular and extra cellular environments are different ?
difference in ion concentrations which creates an electrical charge , and creates a membrane potential
anion
negative charge
cation
positive charge
what is ohms law ?
The relationship between membrane potential and ionic currents V=I*R
ion channels
large transmembrane proteins that open up to allow ions to enter or exit the cell , down their concentration gradient
voltage gated
open and close in response to changes in membrane potential
chemically gated
open with a specific chemical messenger( found in dendrites )
mechanically gated
open in response to mechanical deformations such as stretch
thermally gated
response to changes in temperature, present in specialzed neurons, act as temperature detectors
step 1: voltage gated channels
ion channels are closed , ions cannot freely move across the membrane , membrane has high resistance (R), and Ion movement is low (I).
step 2: voltage gated channels
If membrane potential changes to a voltage that causes the voltage sensor to open, the channels pores will decrease the membrane resistance to ion movement (becomes smaller )and the current will increase( I) or V?
step 3: voltage gated channels
at any given voltage, when resistance increases , current decreases
and when resistance decrease, current will increase
Concentration gradient
ions want to move down concentration gradient ( diffusions from high concentration to low concentration
ICF pushes potassium out of the cell into extra cellular fluid
electrical gradient
inside the cell is more negative due to the presence of non permeable anions.. This negative charge creates an inward electrical gradient or driving force that tries to prevent positively changed K from leaving the cell
the right and left hemisphere is connected by what ?
corpus callosum
the cerebral cortex is made up of?
grey matter
function of occipital lobe
initial process of vision
function of temporal lobe
vision and hearing
function of frontal lobe
voluntary motor activity, speech and elaboration of thought
parietal lobe function ?
responsible for receiving and processing sensory input
hyper polarization
magnitude of polarization moves even more negative than the resting membrane potential
graded potentials
local changes in membrane potential that are used for short distance signalling ( different than action potentials)
spread of depolarization
charge movement travels along membrane not across
action potentials
caused by triggering event or stimulus that results in a localized depolarization. It will conduct or propagate throughout the entire membrane and doesn’t lose its strength
when the membrane is depolarized, there is a rapid influx of ?
Na+ enters the cell to cause depolarization
input zone
part of neutron where the the incoming signals are received contains the dendrites and cell body
the trigger zone
part where the action potential is initiated contains the axon hillock( where the axon leaves the cells body)
Conduct zone
part of the neuron where the action potential is initiated contains the axon
output zone
part of neuron that releases chemical messengers contains axon terminals
dendrites
numerous projections from the cell body that receives electrical chemical
axon
extension that conducts the action potential away from the cell body
conduction
the result of an action potential down the axon is initiated , triggering a new action potential in an adjacent area
explain the transmission down the axon
1) action potential is triggered at the axon hillock
2) causes inside of membrane to become more positive , and causes adjacent areas from resting to threshold potential
refractory period
caused by the sodium channels remaining inactive after depolarization , which prevents the action potential going in the opposite direction
why can a refractory period be absolute or relative ?
absolute : under no circumstances can an action potential be triggered
relative : if triggering stimulus is strong enough, an action potential may be triggered
what does a strong signal mean ?
the firing rate of the action potential, not meaning that it is stronger signal
Mylein
formed by specialized Schwann cells and oligodendrocytes in the PNS and nerves leaving the spinal cord
Lipid rich regions that provide extra insulation to maintain the Current
describe the Nodes of Ranvier
regions where there is exposed fibre , action potential can be formulated here due to exposure to extra cellular fluid
dense area of Na + channels
saltatory conduction
in myelinated fibres the wave of excitation moves from one node of ranvier to the next which allows impulses to move faster
what are synapses
neuron to neuron junctions , the junction between a presynaptic neuron and a post synaptic neuron which includes the synaptic cleft between the 2
Neurontransmitters
chemicals released into the synaptic cleft which activate ion channels on the post synaptic neurons membrane
synaptic cleft
area of extracellular fluid between pre and post synaptic neurons
what are the mechanisms of synaptic transmission
1) electrical action potential reaches the axon terminal in the pre synaptic neuron
receptor adaptation
receptors have the ability to regulate their response , meaning a stimulus of same intensity does not always bring about the same magnitude of potential
tonic receptors
generally slower and do not adapt at all, important in situations where near constant signal from stimulus is necessary
phasic receptors
rapidly adapting, upon initiation of stimulus
ex) mechanoreceptors known as pacinian corpuscles
watch example , realize the watch is there and then sensation fades
Nociception or nocireceptors
also known as pain: alerts the CNS. can take the form of internal and external events , nocirecptors are found throughout the body
Pain receptors do no adapt
Mechanical nocireceptors
respond to physical damage such as cutting or crushing
thermal nocireceptors
respond to temperature
chemical nocireceptors
respond to noxious chemicals which are both external and internal to the body
Fast Pain fibres
A delta , covered in mylein and are wider in diameter they are responsible for responding to temp nd chemical and mechanical stimuli.( Sensation of quick intense pain, sharp, stabbing )
Slow Pain fibres
C fibres , not myelinated and respond to temp, chemical and mechanical stimuli. They can activate.
Slow pain fibres can activate what ?
Polymodal fibres ( receptors that respond to multiple stimuli. Associated with the burning, aching or throbbing feeling with pain
Bradykinin
chemical that is activated and associated with slow pain pathway. Released from damaged cells and stimulates nocireceptors . explains long lasting pain.
How does the brain process pain ?
1) action potential reaches the end of an afferent pain fibre axon, triggers the realize of neurotransmitters ( Substance P and Glutamate ). Both which help activate the ascending pathways and transmit signals for higher processing
Reticular formation role in processing pain ?
Increases the level of alertness and awareness of a painful stimulus
Hypothalamus/ limbic system
receives information from the thalamus and the reticular formation and allows for behavioural and emotional responses to the pain stimuli
Thalamus
processing here allows for the perception of pain
Cortex
Cortical Somatosensory processing localizes the pain to discrete body region
Glutamate
Released by nocireceptive afferent nerve fibres to activate post synaptic glutamate receptors on neutrons of the dorsal horn and spinal cord
What are the 2 actions of glutamate ?
Activates either AMPA or NMDA receptors
What happens when AMPA receptors are activated ?
leads to permeability changes that can generate action potentials in the dorsal horn neuron and send the signal to higher brain regions
what happens when NMDA receptors are activated ?-
Only happens when certain level of depolarization has taken place with AMPA receptor. Allow calcium to enter neuron, which leads to the activation of a second messenger pathway that results in neuron being more excitable than normal( why injured areas are more sensitive to stimuli
How is a pain signal stopped ?
through the built in endogenous analgesic system which allows for the release of endogenous opioids ( substances released from the body hat have pain killing effects and suppresses the neurotransmitters being released from the afferent pain fibres
Exogenous opioids
substances that have pin killing effect but are not produced int he body
explain what would happen if you stepped on a piece of lego
1) pain would be fist percieved in the delta A fibres, which would then travel to the end of the fibre, glutamate would be released
2) glutamate would allow for the activation of AMPA receptors at the dorsal horn ,
3) the signal would then travel to the reticular formation
4) then to the thalamus to perceive pain and to the cortex to localize the pain to the foot .
5) the hypothalamus would allow for an emotional or behavioural response
Pupillary constriction
caused by the parasympathetic stimulation. One set of muscles is organized in a circular fashion and constrict to make the pupil smaller
Pupillary dilation
caused by parasympathetic stimulation. set of muscles is organized radially ( from the pupil to edge of iris ). Contract to allow more light in
what happens when light passes through a transparent media with density different from air ?
1) the wavelength decreases
2) unless it enters the media perpendicularly its direction will change (known as refraction )
refraction
the bending of light when it passes one medium to another
cornea
contributes the most to the refractive abilities because foe the density difference at the air / cornea boundary
Uneven surface of cornea= astigmatism
Lens
convex structure located behind the pupil that is able to focus light rays onto the retina . The lens is adjustable
Accommodation
eyes ability to adjust the lens to maintain focus on something.
what muscles control accommodation ?
The ciliary muscle and the suspensory ligaments . When muscle is relaxed , the ligaments pull the lens flatter, less convex shape
When muscle contracts, it reduces the tension of the ligaments and the lens becomes more convex
Ciliary muscle contraction is controlled by ?
the ANS with eh sympathetic stimulation causing relaxation and parasympathetic stimulation causing contraction
When the light source is closer what happens ?
Light rays are diverging when the are entering the eye so a stronger more convex( greater ability to bend the light ) lens is needed to bring the light to focus
what happens when a light source is farther away ?
light rays are parallel to one another ( less convex lens needed ).
retinal visual pathway
extends from the photoreceptor cells( cones and rods) to the bipolar cells and then to the ganglion cells
( direction of light moves in the opposite direction of the visual processing )
rods and cones
cones for colour, rods for vision in low lighting
Bipolar cells
involved in the transmission of signals from rods and cones to the ganglion cells
Ganglion cells
The neutrons located at the inner surface of the retina its axons make up the optic nerve
location of blind spot ?
optic disc ( where the ganglion cells bundle together to form the optic nerve.
what is the visual pathway?
transmitted to the visual pathway to the thalamus and relays information to each different area of the cortex( color, form depth movement. Vision takes up 30 % of the cortex processing
what side of the brain processes the the right visual field ?
The left side
what would happen the left optic nerve was cut ?
lose vision in both the left and right side of left eye
what would happen if the optic chiasm was cut ?
loss of vision in the right visual field in right eye and the left visual field in left eye
cut of left optic tract ?
loss of right field of vision in both eyes
what is a sound wave ?
a vibration of air that travel outward from the source . Transfer energy from molecule to molecule ( lose energy much faster
Pitch ( tone )
determined by the frequencuy of vibrations . the greater the frequency the higher the pitch
Intensity ( loudness )
depends of the amplitude of the sounds waves and the greater the amplitude, the louder the sounds
Timbre ( quality of sound)
overtones that are superimposed on the pitch. Allows one to locate the source of the sound as each sound has different overtones
external ears composed of ?
The pinna , the tympanic membrane and the ear canal. Its job is to channel sound waves to the middle ear
Pinna
are essential for the location of sound and collects sound waves
ear canal
sends the waves to the tympanic membrane. Contains hairs and earwax to guide against bacteria ( make the environment more acidic ).
Tympanic membrane
vibrates when sound waves hit it. Stretches across entrance to middle ear. Air pressure must be similar to atmospheric pressure for it to work efficiently.
Middle ear
composed of the malleus incus and stapes. transfer the vibrations and amplify the sound to the inner ear fluid. via the oval window
Inner ear
Cochlea, Organ of Corti, inner hair cells and outer hair cells
what happens at the oval window
sound waves get converted to mechanical energy and then past on into the inner ear
The Cochlea
Fluid filled , responsible for the perception of hearing . Important in the ability to determine pitch
organ of Corti
located inside the cochlea , supposed by the basilar membrane and contains hair cells. known as the sense organ
Inner hair cells
transform the cochlear fluid vibrations into action potentials , and propagates auditory messages to the cortex
Outer hair cells
Do not transmit sound signals to the brain. Instead these hair cells function to modify the electrical signalling of the inner hair cells. They enhance the response of the inner hair cells making them more sensitive to sound intensity and pitch
how is pitch determined ?
depends on the shape of the basilar membrane. Rnage of pitch is heard in different parts of the cohlea
Higher pitches ( 2000hz) are detected at which end of the cochlea? and Lower pitches ?
At the narrow end ( higher ) and lower pitches ( and the wider end
Hair cells send what type of signals ?
auditory signals are picked up from the hair cells and then sent to the auditory nerve. and pass through brainstem( alertness and arousal and then to the thalamus for higher processing
Vestibular apparatus
In the inner ear, contains fluid ad hair cells that are able to detect changes in movement in the fluid. contains the information needed to maintain equilibrium, balance and coordination by detecting changes in head movement
how does the vestibular system help maintain equilibrium ( pathway )
signals of the vestibular system are sent to the vestibular nuclei in the brainstem and then to the cerebellum
The 3 functions of the vestibular system are :
- Maintain balance and posture
- allow the eyes to remain fixed when turning the head
- Perceive motion with orientation
Chemo receptors
both taste and smell rly on these, generate electrical signals after binding to a specific chemical
taste
known as Gustation, sensation produced when. substance reacts with a taste receptor in the oral cavity
Tongue, oral cavity and throat
location of chemo receptor s
Taste buds
the tongue is covered with bumps called papillae. Clusters of nerve ending on the tongue and lining of the mouth and each one contains about 50 taste receptor cells. limited life span of about 10 days
Taste receptor cells
when a tastent ( any chemical that stimulates the sensory cell in a taste bud ) binds to receptors. Ion channels create depolarizing potential which can imitate action potential
How is taste experienced in the brain ?
afferent neurons send signals to the brainstem and thalamus before going to the cortical gustatory area in parental lobe
salty taste
cells are stimulated by salts , these cells have special NA = Channels that allow for direct entry into the cell
Sour taste
stimulated by acids, the free H+ of acids blocks K channels in these cells which reduces the outward flow of K ( depolarizing potential )
sweet taste
Stimulated by glucose, binding of glucose activates a G protein and generate cAMP hat inhibit certain K + channels
Bitter taste ( protective mechanism)
cells are more diverse and are stimulated by a wide variety of compounds such as alkaline, caffeine, nicotine,, morphine etc. Most poisonous substances have a bitter taste
what is the olfactory mucosa ?
located on the ceiling of the nasal cavity , contains the olfactory receptor cells , the supporting cells and the basal cells
supporting cells
secrete mucous
basal cells
pre cursor for new olfactory receptor cell
olfactory nerve
formed from the axons of the olfactory receptor cells
explain the process of olfaction
1) odorants dissolve in the mucous layer and Interact with cilia on the olfactory receptor cells
2) binding of odourant activates G protein and mobilizes cAMP that leads to the opening of NA+ to initiate depolarization
where does the output of the ANS come from
the hypothalamus, the brainstem and the spinal cord
the autonomic nervous system is composed of?
The sympathetic nervous system and the parasympathetic nervous system
sympathetic nervous system
primary role is to stimulate fight or flight response
parasympathetic nervous system
responsible for the body rest and digest activities ( digestion , urination and salivation
two neuron chain
connects the CNS to the effector . The cell body of the first neuron is located within the CNS and its first axon
where do the fibres of the SNS originate ?
the thoracic and lumbar regions of the spinal cord , the preganglionic fibres are short and terminate on the ganglia on spinal cord
Long post ganglionic fibres of THE SNS ?
terminate on the effector organs
preganglionic fibres of PNS?
arise from the brink or lower spinal cord , the pre ganglionic fibres are long and terminate in the ganglia located close to the effector organ
Pre ganglionic fibres of both the PNS and SNS use which neurotransmitter ?
ACh( Acetylcholine )
postganglionic fibre PNS
Use ACh, and are called cholinergic fibres
post ganglionic fibre SNS
use Norepinephrine(noradrenaline) and are adrenergic fibres
Dual innervation
almost all effector organs receive input from both the sympathetic and parasympathetic systems ( not kidneys and adrenal glands)
Effect of the heart of SNS and PNS
SNS: increased heart rate, increased force of contraction
PNS: decreased heart rate
Effect of the eye of SNS and PNS
SNS: dilation of pupil ( far vision)
PNS: adjustment of eye for near vision
Effect of Digestive track for PNS and SNS
SNS: decreased motility( movement contraction of sphincters , inhibition of digestive secretions
PNS increased motility , relaxation of sphincter
Effect of blood vessels for PNS and SNS
SNS: constriction
PNS: dilation of vessels supplying the penis and clitoris only
Lungs effect of PNS AND SNS
SNS: dilation of bronchioles( airways ( inhibiton of mucous secretion
PNS: constriction of Bronchioles
PNS ans SNS effect on bladder
SNS: relaxation PNS contraction ( emptying)
sympathetic dominance
fight or flight, parasympathetic system is diminished while the sympathetic system is in full force
parasympathetic dominance
rest and digest, after you’ve had a stressful encounter when the sympathetic division had to work hard , the parasympathetic division takes over to calm the body down
what are the dual innervation exceptions
1) most arterioles and veins receive sympathetic stimulation only ( exception, penis and clitoris
2) most sweat glands only receive sympathetic stimulation ( release ACh instead
3) the salivery glands receive dual innervation however but both systems can stimulate salivery secretion
What does the adrenal gals release with stimulation
sympathetic stimulation , releases hormones norepinephrine( associated with sympathetic post ganglionic fibres and 80% epinephrine. Acts as an amplifier of the sympathetic system
Cholinergic receptor
a receptor on the membrane of cells that responds to acetylcholine
Adrenergic receptor
A G protein coupled receptor the membrane of cells that responds to catecholamines( epinephrine and norepinephrine
Muscarinic receptors ( cholinergic )
activated by the mushroom poison muscarine
where are muscarinic receptors found ?
on the effector cell membranes, they respond to ACh released by PNS post gangilonic fibres . triggers a G protein reaction , results in the opening of Cation channels
Nicotinic receptors (cholinergic )
activated by the tobacco plant
where are nicotinic receptors found ?
on cell bodies of postganglionic cells in all autonomic ganglia and bind to ACh
Norepinephrine is released from what 2 places?
both as a neurotransmitter from sympathetic post ganglionic fibres and as a hormone from the adrenal medulla
alpha receptors ( adrenergic )
A1 and A2 receptors have greater sensitivity for norepinephrine and epinephrine
all adrenergic receptors do what ?
activate G proteins
A2 activation
surpasses the cAMP pathway
A1 activation
activates the CA+ second messenger system
Beta receptor
B2 receptors have greater affinity for epinephrine than B1 . B1 respond equally to norepinephrine and epinephrine. Both enhance the cAMP pathway
A1 receptors are almost always ?
excitatory and are expressed in smooth muscle cells of blood vessels , stimulation cause contraction
A2 ?
decrease of contraction
B1 is almost always?
excitatory and are primarily found in the heart
B2 is almost always ?
generally inhibitory , and primarily found in smooth muscle cells of arterioles and respiratory airway
Somatic nervous system
comprised of the axons that innervate skeletal muscle under voluntary control
where are cell bodies of motor neurons located ?
located in the ventral horn of the spinal cord and heir axons terminate directly on their effector
motor neurons release what from being stimulated ?
acetylcholine - result is most contraction
relaxation only occurs in the somatic nervous system through ?
by decreasing the excitability of the motor neurons
Upper motor neurons
originate in the brain stem or the motor region of cerebral cortex
what is the role of the upper motor neurons ?
carry motor information from the upper motor neurons down to the lower ones. Upper motor neurons descend in the spinal cord
what parts of the brain send info to the upper neurons?
the cortex, the basal nuclei, the cerebellum and the brainstem
motor neurons accept what ?
collection of both excitatory and inhibitory signals to decide whether or not to generate action potentials and contract the muscles through the lower neurons
Lower motor neurons
located in the anterior grey column, anterior nerve root or the cranial nerve nuclei of brainstem
Neuromuscular junctions
small space between the terminal end of a motor neuron and muscle fibre, this is where neurotransmitter from the neuron stimulates the muscle fibres
explain the release of neurotransmitters for the neuromuscular junction
an action potential in a motor neuron is propogated to the axon terminal ( terminal button)
2)the an action potential reaches the terminal button, voltage gated Cachannels open allowing Ca to enter in the terminal button which triggers exocytotic release of vesicles containing ACh into cleft
3) release of ACh bind to nicotinic receptors on the motor end plate and open cation channels . Net influx of positive charge , membrane potential depolarizes ( known as end plate potential ) which are graded
4) initation of action potential end plate is sufficiently depolarized , the muscle membrane gets influenced and NA+ channels begin to open
When sufficient Na channels are open, the muscle fibres reaches threshold and the wave of excitation radiates out from the motor end plate causing muscle contraction
\5 inactivation of ACh through the enzyme acetylcholinesterase , need to deactivate ACh otherwise muscle would always stay in excited state How
How would venom from a spider effect the neuromuscular junction
causes an explosive release of ACh from all cholinergic sites. This release overwhelms the the ability of acetylcholinesterase to rapidly inactivate it which results in prolonged depolarization
Botulinum Toxin
blocks the release of ACh from the terminal button meaning the skeletal muscle cannot be excited and paralysis occurs
Curare
action occurs on the motor end plate where it binds to the same receptor as ACh however does not cause and end plate potential and blocking ACh from binding to them which causes muscle weakness and paralysis
