cns Flashcards
CNS basics
CNS = brain + spinal cord
* protected by bony structures (vertebrae) + 3 layers membranes = meninges
* receive afferent from PNS, analyse, sompare w past, + integrate to gen motor output to PNS
brain regions
forebrain = cerebrum + diencephalon w pit gland, limbic sys + olfactory bulb
midbrain = midbrain
hindbrain = pons + medulla oblongata + cerebellum
cerebrum has longitudinal fissure => L + R hemispheres
spinal cord
out brain @ foramen magnum, down vertebral canal
* each spinal seg gives off pair segmental spinal nerves to supply diff region of bod
* at caudal end canal cord peters out + spinal nerves for caudal structures form cauda equine
timeline brain development
- dorsal ectoderm thickens form neural plate
- other development processes overlap + continue well into adulthood
neurulation
- notochord = cylinder mesodermal cells + secr chem signals inc prot sonic hedgehog induce formation neural plate
- chem signals also stim other mesodermal cells develop -> vertebral bods + intervertebral discs of spinal column (form protective structures)
- plate indented along midline = neural groove
- groove deepens + ectodermal walls thicken @ dorsal lips = neural folds
- folds fuse to close tube, starting cervical region + moving both rostral + caudal
- rostral/caudal neuropore = pt closed to (hole) - get smaller + smaller + close last
- dorsally either side superficial ectoderm proliferates -> cells -> pinch off + form neural crest
which parts from neurulation form what
CNS from neural tube
PNS from tube + neural crest
what happens after neurulation
rostral neural tube forms vesicles bc its hollow
* first 3 primary vesicles develop
* these differentiate into secondary vesicles
* these develop to adult brain structures
which mols control patterning which parts CNS
- patterning ventral structures controlled by sonic hedgehog prot from notochord
- patterning dorsal structures controlled morphogenetic prot signals frojm superficial ectoderm
names of diff vesicle structures + development path
all early in gestation
differential growth means diff outpockets form
brain flexures at vesicle stage
important to orient structures
cerebrospinal fluid is + why
bathes inside (w/in tube) + out (its in meninges) of CNS for nourishment, waste removal, protect brain
spina bifida occulta
incomplete rostral or caudal fusion of neural folds = tube open = vertebral arches can’t form + fuse = neural v close outside world
* caudally common tailless breeds
grey matter + white matter
grey = cell bodies, dendrites + synapses
white = axons - white bc of fat in myelin
glial cells
supporting cells in CNS
nuclei + tracts w/in contect CNS
nuclei = clusters of cell bodies in CNS (ganglia in PNS)
tracts = bundles of axins in CNS (nerves in PNS)
decussation of tracts
many CNS functions cross over bet 2 hemispheres cerebrum
== info from/output to R side bod handled by L side brain
cross section spinal cord vs cerebrum
spinal cord = grey matter inside, white out
cerebrum = white + basal nuclei in deep parts w grey formed over
corpus callosum
white matter tract connecting cerebrum hemispheres, allowing exchange info
corpus striatum
basal nuclei in cerebrum interwoven w white matter tracts = stripy appearance
* involved planning + executing (esp habitual) movements (motor function)
* input from motor cortex + integrate w other inputs (thalamus, limbic sys)
* important animals, e.g. birds, w/o developed cerebral cortex (instead of motor cortex)
lining neural tube
initially pseudostratified columnar then diffs 3 layers:
1. inner ventricular zone = germinal = ependymal = gen new cells (divide into)
2. mantle = neuroblasts migrated here + diff into neurones/glia (+ mitotic in interphase)
3. marginal = axons of neurones w cell bods in mantle = white matter
diagram cell types lining neural tube life cycle
lining -> ciliated to move CSF
surface cerebellum compared cerebrum
cerebellum = smaller folds tiss called folia (as opposed sulci/gyri)
important sulci/gyri to remember
- cruciate sulcus crosses longitudinal fissure at right angle w motor cortex controlling movement sat there
- sylvian gyrus involved in processing auditory info (looks like ear)
brain lobes
named after bone section sits under (ish)
what does frontal lobe control
- thinking
- speaking
- memory
- movement
== personality
what does parietal lobe do
- language
- touch
- taste
- smell
what does occipital lobe do
- vision
- colour
- letters
- L/R
what does temporal lobe do
- hearing
- learning
- feelings
- fear
cortexes: where + what
- motor cortex just rostral cruciate sulcus = conscious movement
- somato-sensory cortex just caudal = conscious sensation
- visual = caudal occ lobe (sight)
- auditory = ventral to cruciate sulcus, dorsal temp lobe (hearing)
- association cortex = rest, linking together, e.g. memory
developing cerebrum
- internal cavity telencephalic forms lateral ventricles
- cell bods form from mantle layer
- SHH + BMP drive arrangement of regions
interconnected ventricles comm w central canal (remnants central cavity) in spinal cord
lat ventr comms rest of tube via 4th ventr
how are brain ventricles connected
lat ventr in each hemisphere, CSF flows thru interventricukar foramen in to 3rd ventr, thru mesencephalic aqueduct -> 4th ventr -> central canal
CSF is circulating around interconnected spaces then down canal
holoprosencephaly
failure in patterning vesicles as prosencephalon (forebrain) fails divide = single-lobed brain + single central eye
* can be caused by corn lily ingestion (cyclopamine toxin) - interferes w SHH signal recog
rhinencephalon is?
= olfactory bulb + olfactory tracts + olfactory peduncle + piriform lobe + hippocampus + fornix ==> olfaction for survival
* comms w higher centres affect emotion, behaviour, comms
* size reflects importance olfaction to species
how does rhinencephalon work
- olfactory bulb receives nerve fibres of olfactory nerve as run thru nasal cavity (via cribriform plate)
- down olfactory tracts
- **piriform lobe ** is part cerebral cortex where olfactory info processed
development brain stem general
midbrain from mesencephalon
pons from metencephalon
medulla oblongata from myelencephalon
mantle layers diff parts organise into dorsolateral alar plates + ventrolateral basal plates
* sepped by central roof + floor plates (no cont neuroblasts)
development myelencephalon/metencephalon
- alar mantle lamina stretches + move laterally over roof (made ependymal cells) to flatten
- form rhimbic lips that join in middle form cerebellum
- thickening develops ventrally form pons + medulla oblongata
cerebellum structure
- central vermis
- 3 peduncles either side connects it to brainstem
- v folded cortex (-> folia) w central nuclei = grey matter
- white matter branches = arbor vitae
cerebrllum development
2 lateral hemispheres formed from rhombic lips metencephalon
* joining of lips forms narrow central vermis
what is frontal cortex involved w
- decision-making
- planning
- motivation
- judgement
pre-frontal cortex
most rostral cerebrum
* personality + social behaviour
what does cerebral cortex do
allows conscious perception sensory input, movement muscs + conscious thought
limbic sys
series tracts + nuclei deep w/in cerebrum key to emotion, learning + memory
* species driven by instincts w less control over emotions + behaviours have relatively larger
thalamus
sensory info to brain synapses here b4 going -> cerebral cortex (except olfactory)
* also involved sleep + wakefulness
hypothalamus
connects endocrine + nervous sys + forms part limbic sys (= role in behaviour)
function brain stem
- cont key CV, resp, GI control centres
- cont nuclei for cranial nerves except I + II
- route comms bet higher structures + spinal cord
- tectum in midbrain involved orienting head + body in response sights + sounds
cerebellum functions
- organises + refines motor activity
- coordinates gait, control musc tone + voluntary musc activity
- compares intended movement w outcome = integrating sensory inputs
- balance + coordination - dysfunction = loss inhibitory component = loss coord
cant initiate musc contraction, can only refine
how does degree folding cerebral cortex vary
varies bet species mainly depending on how much space available in skull (also correlation w intelligence but less important)
how does association cortex vary bet species
amount incr w complexity of species + degree to which use prior experiences + memories to govern functions
layers meninges
- dura mater (outside)
- arachnoid mater
- pia mater
functions of meninges
- physical protection central nervous tiss
- facilitate flow cerebrospinal fluid (CSF)
- provide framework for bvs supplying CN tiss
dura mater
- thick fibrous layer made collagen + elastic fibres
- only CN tiss that’s pain sensitive (trigem innerv)
- own blood supply
2 layers: outer periosteal + inner meningeal - usually indistinguishable except seps as goes into 2 fissures, forming venous sinuses:
1. falx cerebri in longitudinal fissure
2. tentorium cerebelli in transverse fissure
fused to endosteum
where is transverse fissure
bet cerebellum + cerebral hemispheres
arachnoid mater
thin transparent mem w fibres forming web structure in subarachnoid space
* avascular, v lil innerv
subdural space
potential space = dura + arachnoid mater v closely associated, not much space, just a lil lymph-like fluid
subarachnoid space
true space, criss-crossed by fine collagen trabeculae + filaments (connect mems)
* conts CSF + bvs (supply nervous tiss)
pia mater
thin mem
* v vascular w dense innerv
* v adherent underlying tiss to nurture
* follows bvs into tiss + merges w tunica adventitia
denticulate ligaments
given off by pia mater, extend across subarach space + arach mater to join w dura mater
* act as sling to support spinal cord so no vibrate, bounce (= protect it)
how do meninges develop
from mesenchymal tiss around meninges
1. axial mesoderm -> mesenchyme -> ectomeninx -> dura mater (= pachymeninx)
2. neural crest cells from ectoderm -> mesenchyme -> endomeninx -> arach + pia mater (= leptomeninges)
3. spaces in mesenchyme coalesce -> subarach space
epidural space
dura seps from vertebrae w/in vertebral canal, creating epidural space
* -> filled w fat + CT = extra protection
=> dura mater only of spinal cord only attached to bone at foramen magnum + caudal end
filum terminale
beyond end spinal cord dura mater narrows form cord-like ligament that inserts on vertebra
cuff zones
formed from meninges around roots cranial + spinal nerves
* => grape-like structures where arach coming to end
dura mater most perm drugs, arach resistant but arach ending = more perm so these regions allow drugs to more easily enter CNS
cererbrospinal fluid (CSF) composition
- cell-free
- prot-free
- low aas (bc they function as NTs in CNS)
- low stable K+ (or would affect elec activity neurones)
- lower gluc than plasma
function CSF
- physical protection CNS tiss
- circulate nutrients + NTs to CNS tiss
- make stable environ for neurones so random a pots no triggered
- vol buffer - can decr to accomodate small CNS swelling
all works bc comms w ISF of neural tiss freely thru pia mater + ventr lining
how keep CSF stable
caps in CNS low permeability = blood brain barrier (BBB)
* tight junctions bet endothelial cells
* thick basement mem
* specialised connecting glial cells (astrocytes) have foot processes that decr permeability
where find CSF
circs subarach space, brain ventrs + central spinal canal
* constant prod + drainage = press grad, helps circ
* ventr + canal lined ependymal cells w cilia = help circ + joined loose desmosones = CSF can exchange w ISF of neural tiss
where do ventricles develop from
- laterals = telencephalic vesicles
- 3rd = central cavity of telencephalon + diencephalon
- mesencephalic aqueduct = mesencephalic vesicle
- 4th = rhombencephalon
where is CSF proded
mostly choroid plexi + small amount = ultrafiltrate pial bvs
1. bet lateral + 3rd ventr, pumping into ventr
2. in roof 4th - pumping into ventr + subarachnoid space
how is CSF proded
- transporting ependymal cells covering choroid plexi pump solutes (inc Na+) -> CSF
- draws water in by osmosis
- lipid soluble substances pass readily into CSF, e.g. O2, CO2
- cells + large mols like aas can’t pass across
- water soluble mats have be actively transported in, e.g. gluc
varies abt drugs passing in - some diseases affect perm of BBB
where does CSF drain
- out small holes in 4th ventr = bilateral apertures -> subarach space
- arach mat extensions arachnoid granulation/villi push thru dura into sinus -> venous circ
also via veins + lymph vessels around roots spinal nerves
press grad = flow 1 way, but can’t flow other even if press grad flipped
how does pia mater adhere underlying tiss
- choroid plexi
- reticular + elastic fibres
- cytoplasmic process of astrocytes in neural tiss
what is choroid plexus
tiss tufts v vascular w network bvs in covered transporting ependymal cells in ventr
how do choroid plexi develop
- grooves form in ventromedial cerebral hemispheres = choroid fissures + pia mater covering it invags into lat ventrs
- tela choroidea = region pia mater that adheres underlying ependyma (neuroepithelial lining) invaginates in fold into roof 4th ventr in myelencephalon + trapped
how sample CSF
from subarach space:
1. where enlarged form cerebellomedullary cistern @ atlanto-occipital junction
2. where widens beyond end spinal cord form lumbar cistern (L5-6 space)
via cisternal puncture
atlas
C1 bone
why sample CSF
give idea of health - does it have prots in, less gluc than plasma etc
arterial supply CNS
centred round cerebral arterial circle on ventral aspect surrounding hypothalamus
* basilar + internal carotid arteries supply circle
* rostral/middle/caudal cerebral + rostral/caudal cerebellar arteries move to cerebral hemispheres + cerebellum
forebrain receives more than other areas
parenchyma
functional tiss of organ (distinguished from CT + supporting tiss)
possible arterial sources to circle
combo internal carotid, basilar, maxillary + vertebral
* varies bet species - important for humane slaughter to lose lots blood + lose consciousness quick = minimal pain (position of animal has effect)
circle arterial supply horse/dog
from internal carotid + basilar arteries
circle arterial supply cow
maxillary + vertebral artery via 2 retia (net small vessels)
* decr press b4 brain + blood cooled down
circle arterial supply sheep/cat
mainly maxillary artery via rete mirabile
* internal carotids obliterated after birth
* basilar flows caudal so only blood -> caudal medulla oblong
collateral circ in brain
v few interarterial anastomoses = v lil collat circ = lots functional end arteries = occlusion/rupture => ischaemia + infarction of tiss supplies
brain venous drainage
low press sys = accoms changes in blod vol to maintain preload
slow, bidirectional, intermittent bloodflow w thin walls = potential seeding tumour or infection
variation bet species
what part does dorsal sagittal sinus drain
veins of cerebral hemispheres (dorsal part brain)
what part do cavernous sinuses drain
rostral forebrain, nasal cavity, orbit face = easy for infection -> blood supply
internal carotids traverse sinuses = cool blood in species w/o rete
spinal cord blood supply
branches aorta (caudal) + vertebral artery (cranial)
aorta enters thru intervertebral foramina -> 2 branches
1. small dorsal branch
2. ventral spinal art from coalescing large ventral branches
venous drainage spinal cord
bilateral venous plexi in epidural space w loads anastomoses -> segemntal vertebral veins at intervertebral foramina
-> vertebral vein/azygous vein/cranial caudal vena cava depending where in bod
eye =?
- organ of sight - turns light -> a pots in retina (so need light -> there unhindered), optic nerve takes a pots -> visual cortex
- develops from optic cup of embryonic diencephalon
- in bony orbit surrounding supporting soft tiss structures (= adnexa)
eyeball layers
- outer fibrous sclera
- middle vascular uvea
- inner neural retina
shape layers maintained by internal support from humours
eye anatomy
canine/feline
aqueous humour
- transparent, colourless, water-like ~ low-prot plasma
- proded ciliary process (constant w constant drainage)
- maintains intraocular press (= HP) to maintain spherical eyeball
- provides nutrients to avascular structures (cornea + lens)
vitreous humour
transparent, colourless hydrogel to maintain retina against choroid (support globe) + provide nutrients
* lamellar arrangement prot fibrils maintains transparency (trap hyaluronic acid)
* cont phagocytes to remove unwanted cellular debris
* cont hyalocytes to turn over hyaluronic acid
* attached caudal lens capsule, ciliary body + periphery optic disc
same over lifetime so old = more fluidy, affecting vision
fibrous tunic
opaque sclera caudally + transparent cornea rostrally
* junction bet them = limbus = drainage pt for aqueous humour of anterior chamber
* support + structure globe
cornea general
rostral 1/4, avascular
* transmits + refracts light = has be transparent + smooth (also nutrition)
* v sensitive w nerve endings - opthalmic branch trigem => corneal reflex (touch + blink)
layers cornea
- epithelium (squamous outer -> columnar) - protect stroma + decr water entry
- Bowman’s mem - thick, organised collagen fibres keep transparent, supporting keratocytes
- stroma
- Descemet’s mem - proded endothel to sep from stroma, thicker as older bc prod constant
- endothelium - actively pumps water from stroma to maintain transparent (can’t replicate = thins as cells spread to cover damage)
fluorescein stains stroma, not Descemet’s mem - know level of ulcer
sclera
dense fibrous CT + elastic fibres
* protects internal eye structures + maintains globe shape
* vascular w attachment extrinsic muscs
* axons from retina pass thru at lamina cribrosa to form optic nerve
dull white colour
uvea
== choroid (posterior uvea) + ciliary bod + iris (anterior) + suspensory ligament
vascular + pigmented to stop light out back eye
* firmly attached sclera at exit of optic nerve, less firm elsewhere
iris
sphincter w dilator + constrictor muscs to alter size pupil (= opening in centre)
* radial + circular sm musc fibres
* pigmented cells give range colours (lack pigment = light blue)
* ANS occulomotor n. - symp dil (= mydriasis), para constr (= miosis)
* seps anterior + posterior chambers
regs amount light entering eye
rostral continuation ciliary bod
choroid
eye lining (all of uvea behind lens, 2/3)
* vascular: bvs to all internal eyeball structures
* darkly pigmented to prevent light rays escaping out back eyeball
bet sclera + retina
tapetum lucidum
triangular yellow-green iridescent area light-reflecting cells w/in choroid dorsal to where optic nerve leaves
* reflects light back to photoreceptor cells = pass thru again = improve night vision
well developed carnis, present most mammals but humans + pigs
ciliary body
thickened continuation of choroid
1. ciliary musc = sm fibres to control thickness + shape lens
2. ciliary process secr aqueous humour into posterior chamber
also anchors lens
pathway outflow aqueous humour
posterior chamber, thru pupil + drained @ iridocorneal angle = venous plexus so humour can return circ
-> via trabecular meshwork -> Schlemm’s canal -> episcleral veins
iridocorneal angle
junction bet corneal limbus, root iris + anterior ciliary bod
glaucoma
iridocorneal angle blocked = drainage stopped = intraocular press builds up = red eye
serious
suspensory ligament of uvea
continuation of ciliary bod, forming circular support round lens perimeter (zonular fibres)
* connect bod (musc) to lens, all around lens’ circumference
lens
transparent biconcave disc sepping aqueous + vitreous compartments
* suspended by ciliary bod
* cont outer capsule, regular arrangement lens fibres (from around equator to meet anteriorly + posteriorly) + central nucleus
* concentric layers allow eye to focus
contr/relax ciliary musc w suspensory ligs alter shape + change depth of focus = lens accomodation
distance vs close focus
distance = relax musc, tight lig = lens stretched, longer, thinner, less refraction light
close = contr musc, slack lig = lens thicker + refracts light more
cataract
lens opacity due disruption arrangement lens fibres
retina
innermost eye layer of caudal wall
1. light focused onto photoreceptors (light sensitive) by lens
2. converts light -> a pots -> brain by optic nerve
nutrition from choroidal bvs externally + retinal bvs internally (run from optic disc)
layers retina
from closest to choroid (where light hits last)
1. retinal pigment epithelium (no pigment over tapetum lucidum)
2. photoreceptor cells (rods + cones)
3. bipolar neurons
4. multipolar ganglion cells
pigmented layer retina
prevent light leaking out eyeball, augmenting effect pigment cells in choroid (work together)
photoreceptor cells
- rods - sensitive low light levels but not colour = black + white + night vision
- cones - sensitive bright light, provide colour vision
dogs + cats = 95% cones = light + shade but colour poorly developed
bipolar neurons of retina
gather info from rods/cones + transmit to next layer
ganglion cells of retina
axons run across surface retina -> leave at optic disc form optic n.
* unmyelinated so light thru -> photoreceptors
* at optic nerve attachment no rods or cones = blind spot
ocular fundus
structures of posterior eye visible on opthalmic exam
* optic disc
* retina w pigmented epithelium
* retinal bvs
* choroid inc tapetum - where visible = tapetal fundus (rest = non-tapetal fundus)
* sometimes sclera
how are dog + cat fundus diff
dogs = white bc nerves becoming myelinated b4 leave eye
cats = no myelinated until leave eye => black
how is rabbit fundus diff
bvs only medial + lateral + band not circle of myelination
how is horse fundus diff
dots of vessels thru choroid layer (= stars of Winslow)
* abnormal other species that have large clear retinal bvs from optic disc
how does field of vision vary
- predatory species, e.g. cat = eyes pt forward, wide area binocular vision (fields of eyes overlap) = pinpt position accurately
- prey = eyes side head, mostly monocular/uniocular vision - less detail but greater field view to be able see where is to run away
cilia on eyelids
angled away from eye for further protection entry foreign mat
resemble human eyelashes
palpebral ligaments
give palpebral fissure its shape + hold canthi in place
* medial + lateral ligs
conjunctiva
v vascular mucous mem lining inside eyelid front eye except cornea
1. on eyelid = palpebral
2. on globe = bulbar
- lots lymphoid tiss to protect against infection
- conts goblet cells prod mucin component tear film (stabilise it)
covers nictitating mem
tears
keep corneal surface moist bc dry = cornea damaged = loss vision; cont:
1. mucin stabilise tears + keep tear film on eye surface (de goblet cells conjunctiva)
2. lipid reduce evap tears (de Meibomian/tarsal glands)
3. aqueous component = hydrating for eye health (de lacrimal gland + gland of 3rd eyelid @ base)
Meibomian glands
== tarsal glands
* sebaceous, in eyelids, proding oily (lipid) secr so tear film no evap from cornea
Harderian gland
under 3rd eyelid, proding 1/3 aqueous component tear film
* cherry eye = enlarged + protrudes from under nic mem (brachycephalics common) - surgery push back behind
cranial nerves to eye
- optic = sensory, transmit visual info retina -> brain
- trigem - mixed, inc sensory to structures surrounding eye + intraocular surfaces
diffs bet species w eyelid
cat = eyelids well atached to outside eye (narrow palperal fissure)
rabbit = structures looser = less good at moving tear film over eye
horse = prominent lacrimal caruncle (corner eye w oil/sweat glands)
lacrimal puncta
opening that pumps tears out eyes
* most have dorsal + ventral, rabbit just ventral
species diffs w cornea
- ungulates = horizontal oval shaped
- rabbits retain ability replicate corneal endothelium into adulthood
species diffs iris + pupil
cat constr = slit, dil = circle
dog/pig = circular pupil
ungular = horizontal oval shape for max. horizontal field vision (constricts on horizontal plane)
where do optic nerve + retina develop from
outgrowth of wall of wall of diencephalon (optic cup)
fovea
notch in retina w bipolar + ganglion cells displaced so easier for light thru
* 1:1 synaptic contact
* area greatest visual clarity
* only cones then rods round outside of eye
photopigment in rods
rhodopsin
* converts light E -> electrical E to interpret as vision
== opsin prot + small mol ‘retinal’ (~vit A)
why does vit A deficiency cause night blindness
vit A has be converted -> retinal to make rhodopsin (all animals can do)
* night vision = most sensitive = lost 1st
* dogs/apes/horses can convert β-carotene -> retinol but cats can’t = need consume vit A in diet
photopigments in cones
diff opsins in diff colour cones as tuned pick up diff colours
1. ‘blue rhodopsin’ = opsin S + retinal
2. ‘green rhodopsin’ = opsin M + retinal
3. ‘red rhodopsin’ = opsin L + retinal
trichromats
= have 3 diff opsin containing cones - most primates, most other animals can’t see in 3 colours
other mammals inc ungulates, cats = 2 diff opsin-cont cones = dichromats
birds = tetrachromats as have UV asw
night vision
rods more sensitive light than rods so deer have more cones = better light sensitivity = better night vision
just diff adaptations: colour, night vision etc
photoreceptor signal transduction in darkness
high cyclic GMP (cGMP) = special Na+ channs open = Na+ thru -> cell = photoreceptor cells active = release glutamate (NT)
cellular anatomy photoreceptor
lamina of discs stacked to pick up as much light as poss w/in mem
* light detecting prot (e.g. rhodopsin in rods) + cGMP-gated Na+ chann embedded in disc mem together
* transducins (G prots) embedded in disc mem too
what happens when light falls on photopigment
- light E ‘trapped’ by cis-retinal => changes conformation -> trans-retinal
- no longer fits in large opsin = ‘falls out’ = opsin undergoes conform change = active
- active opsin causes α subunit of transducin to activate cGMP phosphodiesterase
- cleaves cGMP = decr cGMP conc (incr GMP) = Na+ channs close = cell hyperpolarises = no release glutamate
== photoreceptors deactivates by light == no glutamate
analagous to NT acting via G-prot receptor
role of glutamate in photoreceptor signal transduction
have ‘on’ + ‘off’ bipolar cells where glutamate inhibitory/excitatory so turned on/off by light
1. ‘on’ activates ganglion cell w light
2. ‘off’ activates ganglion cell in darkness
then axons of ganglion cells form optic nerve so having ‘on’ + ‘off’ means more info to brain to work out what image is
other retinal neurones
horizontal + amacrine cells involved in processing image
visual pathway
- some neurones cross to other side brain, some don’t = partial decussation
lateral geniculate nucleus = lateral part thalamus for more visual processing
* some neurones peel off b4 here -> hypothalamus for reg day/night syscle
* some neurones peel off b4 here to travel to colliculus = involved visual reflexes
pupillary light reflex
circular muscs of iris constr pupil
radial muscs of iris dil pupil
consensual constr if healthy = light in one but both constr
visual cortex
vision processed hierarchically = processed at incr complex levels as go thru
amblyopia
blindness w good eyes = nowt wrong w eye but can’t see
* if hide eye young animal then at 4mo expose - brain parts to eye never developed
==> early stim v important
also if covered adult eye for long time
role spinal cord
- sensory = pass signals from sense receptors round bod -> brain
- motor = pass signals brain -> diff parts bod
- coord local reflexes for quick response to outside stim
basically coord bet barin + bod
important spinal cord structures
intumescences = thickened regions leading brachial + lumbar plexi to supply FL + HL
* thick bc FL/HL have more to control = more neurones + neural tiss needed
vertebral column longer than spinal cord
positioning foramen magnum
diff depending standing/walking position head relative to neck + bod
conus medullaris
region at terminal end spinal cord = naturally tapers (cone shape)
* caudal to lumbosacral intumescence
filum terminale
fine filament neural tiss (glial + ependymal cells)
* attaches to caudal vertebrae = hold cord in place
spinal nerve
root + ganglia
* covered CT to protect
internal anatomy spinal cord
grey matter divided horns
white matter divided funiculi (regions) w fasciculi w/in
grey matter horns
profiles of columns of cell bodies
1. sensory info from spinal nerve feeds into dorsal horn
2. motor info going to ventral root of spinal nerve originates ventral horn
3. lateral horn conts cell bods of symp NS + interneurons - only in thoracolumbar spinal segs
development spinal cord
- mantle seps -> alar + basal plates (symmetrical halves) -> dorsal + ventral horns (grey matter)
- marginal -> white matter
development PNS
- neuroblasts in basal plate -> lower motor neurones w axons growing out thru marginal layer -> vertebral canal
- neuroblasts in neural crest -> spinal ganglia -> sensory neurones as cytoplasmic process grows into alar plate
- neural crest cells AND preganglionic fibres from kateral horn -> autonomic ganglia
structure spinal cord segment
repeat going down cord
spinal cord segs arrangement down cord
at top nerves come out laterally, but as move down go caudal in column b4 leave laterally
named similarly to vertebrae
* but 8 cervical bc 1st 7 come out foramina cranial vertebra, then C8-> foramina caudal (7 C vertebra)
* segs + vertebrae start aligned but C3-T2 shorter = less, then after T3 longer = end of thoracic aligned again. lumbar = getting shorter bc less structures to supply + all rest segs w/in lumbar region vertebral column
how does cauda equina form
- late embryonic period = spinal cord + vert column same length all align + nerves emerge next to originating location
- vertebral column grows faster than spinal cord, pulling nerves w = cauda aquina
functional regions spinal cord
as opposed anatomical
grping based region supply not anatomical origin
* see where issue is in bod, match = see where lesion is
- cervical (neck) = C1-C5
- cervical intumescence: FL = C6-T2
- thoracolumbar (thorax + abdom) = T3-L3
- lumbosac intum (pelvic cavity, limb + perineum) = L4-S3
- caudal (tail) = Cd1-Cd5
dermatomes
skin zones in belts round bod (+ longitudinally in extremities) each sending sensory signals to 1 spinal cord seg
-> injury to spinal nerve associated characteristic pattern numbing of skin w/in zone - feeling stops then starts again as move caudal
useful to localise lesion
plexi
dorsal + ventral branches of spinal nerves connect w neighbours = form continuous dorsal + ventral networks
1. C6-T2 = brachial plexus
2. L4-S3 = lumbosacral plexus
what does larger ventral horns mean
more motor cell bods bc more neurones = more muscs needing innerv
ascending vs descending tracts
asc = sensory tracts from skin + musculoskeletal sys -> cerebral cortex
desc = motor tracts from cerebral cortex -> sk muscs
funiculi
funiculus = region cont diff bundles nerve fibres/axons
1. dorsal = sensory tracts
2. ventral = mixed sense + motor
3. lateral: lateral part sensory, rest mixed
fasciculi
fasciculus = bundle of same anatomical nerve fibres/axons
funiculus conts many fasciculi
fasciculi of dorsal funiculus
- fasciculus gracilis + fasciculus cuneatus involved awareness where bod parts are
- fasciculus proprius involved response to vibration
spinal reflex
local reflexes not requiring input or output from brain
components motor sys
- motor cortex - learn specific voluntary movements
- basal nuclei
- thalamus - decision making
- red nucleus (midbrain) - motor coord
- substantia nigra (midbrain) - maintain contact w rewarding stimuli = eye movement, planning movement
- nuclei in pons + med oblong
- spinal cord
- cranial + spinal nerves
- NMJ to integrate nerve + musc
- sk musc
integration motor sys
- cortex decides do movement
- -> brainstem -> bod to do it
- also -> pons -> cerebellum so knows what intended
- sensory from bod of what happened -> pons -> cerebellum
- cerebellum compares - need refine movement?
- sends that -> thalamus -> cortex
== feedback mech
structure somatic NS
upper motor neuron (UMN)
- exist wholly w/in CNS
- cell bods in brain + synapse on LMNs (directly or via interneurons
- initiate, reg, modify, terminate LMN activity (control them)
required voluntary movement sk musc
most go down spinal cord + synapse w LMN that leaves spinal cord
1. -> LMNs supplying flexor muscs travel in lateral funiculi
2. -> LMNs supplying extensor muscs travel in ventral funiculi
lower motor neurons (LMNs)
- cell bod in CNS + axon in PNS
- run via spinal or cranial nerves to innerv sk musc (from intumescences)
- a pot causes musc contraction
- can be influenced by >1 UMN
can fire w/o UMN input (reflexes)
normal sitch w LMNs
conscious = constant sub-threshold depol -> ACh -> musc tone + trophic support, e.g. help posture
what happens if damage LMN
muscs flaccid + atrophy w/in few days = lose reflexes, can’t contract
* same signs for damage anywhere on motor unit
what happens if damage UMN
extensor muscs dominant to maintain posture, tempered by inhibitory UMNs (most are inhib)
* they dampen signal so damage those to flexors = extensors take over = spasticity (legs stuck long etc) - voluntary control to flexors gone
reflexes + tone normal/incr bc no longer inhib, atrophy only mild due disuse, coordination/control decr but strength normal
damage spinal cord = signs UMN damage anything caudal to that pt
motor unit
LMN + NMJ + sk musc fibres
* small = few musc fibres per neuron = easier control, fine movement, e.g. muscs eyes, low force movements
* large = for more force bc more fibres contracting together
under what circumstance can musc not contract
as long as intact LMN can contract
* so intact sensory = can do reflex (damage UMN = reflex exaggerated bc inhib)
reflex defn
functional unit of NS
* innate reaction to stim present from birth
* sensory -> motor w/o influence higher centres (no UMN input)
would usually have sensory component -> brain so aware what’s happening
reflex vs response
innate vs learned behaviour
* no higher centre vs higher centre
e.g. of response = poke eye + blink - baby won’t do bc hasn’t learned it hurts
monosynaptic vs polysynaptic
mono = sensory neuron directly synapses w motor
poly = interneuron connects them
somatic reflexes one or other
ipsilateral vs contralateral
ipsi = sensory input + motor output same side
contra = opp sides
somatic reflexes one or other
intrasegmental vs intersegmental
intra = all sensory motor w/in same spinal seg
inter = crossing >1 seg
some somatic reflexes have components of both
flexor withdrawal reflex
== withdrawal reflex == nociceptive flexion reflex
noxious stimulus -> sensory neuron -> interneuron -> motor (polysynaptic) -> inhibit quads (extensor), stim hamstring (flexor)
* decussation -> other side so extensor muscs contract + can bearweight (no fall over)
nociception
pain b4 reaches forebrain + interped = neural signals
* caused noxious stimulus
musc spindle
stretch receptors - detect change in length of musc
* intrafusal musc fibres inside w sensory nerve fibres around to feedback
how make sure musc spindle still functions if musc shorter
shorter (e.g. musc contracted) = slackened = won’t detect stretch but need be active regardless to detect stretch
* **gamma motor nerve fibres **cause just intrafusal musc fibres still contract = keep spindle + nerves taut = can detect stretch
golgi tendon organ
at interface bet musc + tendon w extrafusal musc fibres running thru it
* detect contraction as tendon no move, musc does, golg shortens
* => dampens contr so musc no overcontract - no want pull musc off tendon
patella reflex
- strike patella tendon = stretches lil bit, picked up by musc spindles w/in quadriceps musc = sensory (1a afferent fibre) -> dorsal horn direct synapse (monosynaptic) -> motor (α motor neuron) in ventral horn -> musc contract (extrafusal fibres) + extend stifle joint
- 1a afferent also stims gamma motor neuron = contraction intrafusal fibres so spindle can still detect stretch
- musc contracts = stims golgi tendon organ, sends sensory (1b afferent) -> spinal cord dorsal horn -> inhibit α motor neuron to prevent overcontracting
- also causes motor neuron antagonistic musc inhibited so relaxes (hamstring) = intersegmental + via interneurons
path of neurons etc for voluntary movement + why
UMN -> γLMN -> intrafusal fibres contract -> activate musc spindle -> 1a afferent signal -> αLMN -> extrafusal fibres contract
==> amplification of signal
γ = gamma; == ‘γ-1a-α activation’
corticospinal tract
fine motor skills
== corticonuclear tract from cortex to cranial nerve nuclei
= cortex -> spinal cord, nerves nearly always decuss
UMN tract
rubrospinal tract
for skilled movements
* cortical input so can serve similar function to corticospinal tract in non-primates
red nucleus in midbrain -> spinal cord
UMN tract
tectospinal tract
orients head + eyes in response sight, sounds
tectum (root midbrain) -> spinal cord
UMN tract
vestibulospinal tract
for maintenance posture/balance
vestibular nuclei in med oblong -> spinal cord
UMN tract
reticulospinal tract
stabilises bod against gravity
reticular formation in med oblong -> spinal cord
UMN tract
pyramidal + extrapyramidal tracts
corticospinal runs caudally in ventral medulla + tracts form triangular shape (transverse section) = the pyramidal tract (fine voluntray movement)
all other UMN tracts extrapyramidal (all originate brainstem)
* mainly control posture + subconscious rhythmic movement
* but rubrospinal gens fine skilled movements in non-primates
species diffs in pyramidal vs extrapyramidal
horse = mostly big coarse movements, only fine in head, e.g. move lips
cat = fine mostly important FL + head + lil bit elsewhere
somatosensory
= things you’re aware of (as opposed autonomic)
* touch, pain (superficial + true), temp, proprioception, kinesthesia
special senses
- vision
- olfaction
- gustation
- audition (hearing)
- vestibulation (balance)
proprioception
understanding where part of bod is at any given time
* subconscious but can feel
kinesthesia
ability to tell if part bod moving
generalised organisation sensory sys
sensory receptor -> primary afferent -> spinal ganglion -> spinal cord -> synapse in thalamus -> interpreted as somatic sensory in cortex
1. touch decusses at midbrain (red)
2. pain decusses as enters spinal cord segment (purple)
general organisation motor sys
cortex -> (maybe synapse in brain stem if extrapyramidal tract) -> ventral root -> musc
* decusses at midbrain
modality of sense
what type of sense is it
also have modality of stimulus
types receptor
- mechanoreceptor - touch, proprioception, kinesthesia, pinprick/deep nociception
- chemical - pinprick/deep nociception
- heat - temp, pinprick/deep nociception
- cold - temp, pinprick/deep nociception
~mechanical, chem, temp
types mechanoreceptor
- Meissner
- Pacinian
- Merkel cell
- Ruffini endings
- free nerve ending (completely diff structure)
Meissner mechanoreceptor
- axon loops w non-neuronal support cells
- at superficial epidermal/dermal boundary (smooth skin)
- perceive flutter
- small receptive field
- rapidly adapting
neurone then structure
Pacinian corpuscle
typical mechanoreceptor (touch) of skin
* single neurone in w non-neuronal capsule (CT, layers prot)
* so bigger area that if touched will activate neurone = large receptive field
* rapidly adapting
* deep under all skin types (dermis + subcut)
* perceive vibration
merkel cell
- shallow in smooth + hairy skin
- slowly adapting
- small receptive field
- perceive press
ruffini ending
- lie deep in all skin types
- detect stretch - like golg tension organ not attached musc (means frequency continuous range)
- slowly adapting
- large receptive field
slowly vs rapidly adapting
slow = receptor registers steady state + then stims a pot, not whilst starting apply force
rapid = registers when stretching or relaxing (force is changing) - then rapid fires a pots
together bod always knows if force incr (stretching), decr (relaxing) or stable
receptive field sizes
size area 1 sensory receptor picks up from
* generally hairy skin + viscera big field, smooth (glabrous) skin small
* determines how well can distinguish bet diff pts on skin, pinpt exactly where feel
really basic how do receptors work
mechanical = ion channs open w movement + open stims a pot
chemical = ion channs open w chems, e.g. free nerve endings
free nerve endings
polymodal pain receptors = pick up range stimuli (pain, temp)
* can act as mechanoreceptors, chem receptors, etc
main somatosensory nerve fibres
Aα (I) = musc sensory, fastest, myelinated (72-120m/s)
Aβ (II) = mechanosensors (36-72m/s)
Aδ (III) = nociceptors/temp for ordinary pain, small, lightly myelinated (4-36m/s)
C-fibres (IV) = nociception (exclusively for pain, mainly inflammatory), small unmyelinated (0.4-2m/s)
ascending pathways
- dorsal column
- ventrolateral
- spinocerebellar
- spinocervical
dorsal column
== medial lemniscal pathway
for touch + proprioception
* esp touch discrimination
- synapses in gracile + cuneate nuclei in medulla
- then cross in medulla
- through medial lemniscus region in brainstem
- to thalamus
ventrolateral pathway
= anteriolateral
inc spinothalamic tract + spinoreticular tract for all modalities except proprioception, esp PAIN
spinothalamic = spine -> thalamus direct via medial lemniscus - pinprick + thermal stimuli
spinoreticular = spine -> reticular formation in medulla -> thalamus - true pain
cross in cord
spinothalamic is underdeveloped in non-primates
why is spinoreticular slower
synapses - okay bc pain supposed to be slow evolutionarily so can run away (+ also just no benefit to feeling it fast)
spinocerebellar
musc + joint proprioceptors -> synapse in dorsal horn -> cerebellum
for balance + movement, e.g. postural reflexes
* proprioception + kinesthesia
ipsolateral = no cross
occassionally cross twice
spinocervical
sep innerv sys for whiskers + fur where individual axon wraps round (= lanceolate ending) -> Aβ primary afferent -> through lateral funiculus -> lateral cervical nuclei in CR -> cross here -> medial lemniscus -> thalamus
for touch, pinprick, fleas
humans no have
sensotopic arrangement of sensory cortex
sensory to tail at top, head bottom bc structural arrangement w/in cortex
how is gait coordinated
pattern gened in spinal cord - each limb has central pattern generator (CPG)
* input from higher centres to refine but not necessary for basic function
faster gait = less overall contact time w floor
span defn
distance bod moves whilst foot stays on floor
stride defn
distance bet where same foot lands 2 consecutive times
pace gait
2 beat
LF + LH together, then RF + RH together
what do proprioceptors sense
- body position
- strength + speed of movement
all to ensure posture appropriate
diff proprioceptors
- musc spindles
- golgi tendon organs
- joint receptors for angle + press joints
- mechanoreceptors
- vestibular sys hair cells for orientation of head
difference bet having + demonstrating normal proprioception
may have it but w/o normal motor function can’t move legs = can’t correct it = can’t illustrate the awareness
types proprioception
conscious + subconscious
can be hard distinguish, most neurological tests testing both
subconscious proprioception
rhythmic movements - sitting, standing, breathing, chewing, scratching, basic locomotion, postural platform
proprioceptor -> neuron 1 -> synapse spinal cord grey matter -> spinocerebellar tract (neuron 2) -> ipsilateral cerebellum
input from head (CN V + VIII)
2 neurone sys, using input from somatic reflex arcs
what is postural platform
bod well balanced in correct position for x
deficit in subconscious proprioception
==> ataxia (loss of coordination)
alteration in rate, range, force movements
1. bod swaying - can’t find postural platform
2. base wide/narrow stance
3. non-intention tremor
bog obvious changes, but distinguish from weakness (test reflexes)
conscious proprioception
for complex voluntary movement, not needed basic locomotion
proprioceptor -> neuron 1 (dorsal column) -> cross in medulla -> neuron 2 -> thalamus -> neuron 3 (thalamocortical tract) -> contralateral somatosensory cortex (for perception what’s going on)
3 neurone sys
deficit conscious proprioception
- stumbling
- knuckling - turn their paw, they don’t turn it back
- intention tremor
more subtle than subconscious
spinal tracts of proprioception
conscious = dorsal column
subconscious = spinocerebellar
larger + on outside = more vulnerable damage
heavily myelinated
proprioception vs kinesthesia
sense vs awareness + ability perceive extent + refine
(of position + movement of bod)
same way that nociception is sense + pain is perception
functional regions cerebellum
- vestibulocerebellum coords balance + eye movements
- spinocerebellum coords musc tone + movement
- cerebrocerebellum for planning movements (in hemis)
anatomy mammalian ear label
overview how we hear
- sound = vibrating air steered in by pinna
- travels down auditory canal + vibrates tympanic mem
- oscillates malleus, incus + stapes
- sets up amplified vibration of littler oval window
- causes vibration in fluid-filled cochlea
anatomy of cochlea
what happens when cochlea vibrates
fluid (perilymph) in scala vestibuli vibrates as oval window vibrates, causing standard wave in basement mem as vibrations pass to round window for press release (allow more in at top)
endolymph + perilymph compositions
perilymph = normal extracellular fluid
endolymph = v high in potassium
what happens once basement mem in cochlea vibrates
- sensory hair cells fixed bet basement + tectorial mems bend as b mem vibrates
- ;sensory hairs’ cont ion channs opened by movement
- causes depol of hair cells = activation of current
how is frequency determined
- thinner parts b mem vib more easily at higher frequs (highest detected cells round thinnest part b mem in base cochlea)
- so each afferent nerve along cochlea has own characteristic frequ (CF) = frequ fire most readily at
- low frequ = neurones phase lock at same frequ as incoming souond wave + fire a pots at same frequ (bc can’t have b mem thick enough to have CF low)
- v high frequ = not poss so brain just detects which part basilar mem is vibrating + therefore pitch of sound = tonotopy
why can smaller animals hear higher frequs
smaller = faster vibrations = some neurones have higher characteristic frequs = can hear higher frequencies
frequency =?
equ + meaning of that
1/wavelength
incr frequ means decr wavelength
brainstem auditory evoked responses
make sound w electrodes over part brain that should do hearing then record electrical responses in brainstem
* used to test hearing, diagnose deafness etc
conductive deafness
sound cannot pass into ear due tumour, perforation ear drum, infec outer/middle ear, wax in ear canal, ear mites
may be reversible by treating root cause
nerve deafness
bc nerves associated w ear don’t function properly due:
* genetics, e.g. dalmations
* inner ear infec
* drug toxicity
* noise trauma
* age-related degeneration
means permanent deafness
innerv organ of Corti
most sensory sound info carried by type I afferents w axons making up auditory nerve from ‘hearing’ inner hair cells
outer hair cells = dampen + amplify frequs to filter sound (hence have afferents + efferents)
fewer inner hair cells but they have tonnes innerv
otoacoustic sounds
play pure tone into ear + slightly motile outer hair cells constr + relax, causing b mem wobble = nearly inaudible sound echoes back into middle ear
auditory pathway
cochlea -> medial geniculate nucleus in thalamus -> caudal colliculus in midbrain -> auditory cortex in cerebrum
all via auditory nerve (CN VIII)
how does animal determine location of sound
- time delay since arrive at 1 ear before other
- volume difference due shielding by head so sound louder on closer side
vestibular sys does what
- senses equilibrium (dynamic + static) = conscious perception of balance
- informs other syss abt changes in bod orientation relative to gravity + acceleration/deceleration of head
- used maintain balance thru reflexes
path of vestibular sys
sensory receptors w/in labyrinth of inner ear then sensory afferent info via vestibular portion of vestibulocochlear n (CN VIII)
labyrinth of inner ear structures
- crista ampullaris
- otolith organs (= maculae)
crista ampullaris
in ampulla of semicircular canals
cupula (attached roof ampulla) = gel capsule w hair cells attached mem at base
move head = endolymph in inner ear moves = cupula moves = hairs bend, movement sensed by hair cells = signal down CN VIII
detect rotary movement for input for dynamic balance
* only input during acceleration or deceleration, not if rotation continuous
DETECT HEAD MOVEMENT
otolith organ
gelatinous mass w calcium carbonate crystals (== otolith stones) in over hair cells on mem semicircular canals
1. hair cells oriented horizontal = utricle
2. hair cells oriented vertical = saccule
move head = gravity drags heavy stones = hairs bend, movement sensed by hair cells = signal down CN VIII
detect linear accel/decel + tilt of head for input for static balance
DETECT HEAD POSITION
how are hair cells sensory
hair cells have longer cilium at one end - hairs can move towards or away from it
1. towards = depol mem = incr frequency a pots of neuron
2. away = hyperpol mem = decr frequ a pots of neuron
allows work out orientation of head
pathway nerves in vestibular pathway
vestibular sys input down CN VIII -> synapse in medulla oblongata + pons (vestibular nuclei) -> decuss then:
1. up via thalamus to vestibular area in cerebral cortex for perception of balance
2. to occulomotor, trochlear + abducent nerves for occular muscs, => eyes to correct position when moving head in reflexes
3. -> accessory nerve nucleus for orientating head + neck in reflexes
4. down UMN vestibulospinal tract for orienting bod + limbs correct position
5. tracts to cerebellum to refine movement then back to nuclei in feedback loop
several diff pathways
reflex defn
automatic, unconscious, unlearned response to stim
postural reflexes
- vestibular reflex
- tonic neck reflex
- righting reflex
- vestibulo-ocular reflex to maintain stable image (keep eyes still so no blurry)
vestibular reflex
vestibular organs detect change in head angle relative to gravity => limb movements to reduce angle of tilt + keep head stable
uses vestibulospinal tract
tonic neck reflex
musc spindles in neck detect change in head:neck angle => limb movements to maintain horizontal head angle
neck muscs have higher density musc spindles than any other muscs
how can animal stand still + move its head
lift head whilst stood still = vestibular reflex sys + tonic neck reflex sys counteract => can move head around + stand still
righting reflex
uses vestibular + tonic neck reflex pathways + skin press sensors
1. vestibular organs correct head position relative to gravity (= facing down)
2. rest body adjusted to align w head
3. otolith organs detect acceleration towards ground => limbs extend
mostly in cats
vestibulo-ocular reflex
fixes image on retina during head rotations
vestibular sensory input + motor out via CN III, IV + VI
* slow drift eyes in opp direction to rotation as head moves then quick flick in same direction
prolonged rotation => post-rotatory nystagmus in opp direction due movement endolymph
physiological nystagmus
flickering of eye
pathological nystagmus seen in vestibular disease
what causes motion sickness
visual info used w vestibular input to determine head position + conflict bet 2 causes motion sickness as vestibular neurones synapse on vomiting centre in medulla oblongata
vestibular disease
- peripheral resulting from disease or damage to sensory organs (utricle, saccule, semicircular canal, CNVIII)
- central resulting disease or damage to vestibular nuclei/central connections (brainstem, cerebellum)
clinical signs vestibular disease
- ataxia
- head tilt
- circling
- nystagmus
- vestibular strabismus - eye in wrong position
- wide-based stance (bc unsteady)
- vomming + salivation
general concept of olfaction
odour mols = gases or dissolved in vapour droplets, then sensed by chemoreceptors
* odour detected at lower conc than taste
olfactory organ adaptations
- 2 pairs nares - external nostrils + internal nasopharynx
- extensive network turbs => massive SA for sensory epithelium olfactory cells
- mucosa v vascularised
species variation in olfactory centre
rhinecephalon huge in most mammals except whales, primates, birds (birds from middle earth acc still big)
how is dog sense smell useful to humans
- rescue, e.g. find ppl in snow
- watch dogs, even in silent dark
- sniff out drugs + explosives
- medical detection dogs, e.g. falls in blood sugar for diabetics
- truffle pigs
- pest control
odour receptors
- in olfactory cell in nasal epithelium
- receptors G-prot coupled
- individual smells have diff receptors w diff G-prots w diff 2nd messenger enzs
noseblind
become desesitised to specific smell whilst all others work fine
* no happen for taste or vision bc 1 taste affects others
how do olfactory receptors transduce signal
chem -> electrical (-> a pot) by 1 of 2 2nd messenger syss:
1. G prot activates adenylyl cyclase, then via cAMP opens ion chann => depol => a pot
2. G prot activates phospholipase C pathway to open Ca2+ chann => depol => a pot
structure + arrangement olfactory cells
they are the primary afferent sensory neurones
* dendrite ends enlarged w cilia
* cilia cont receptor prots + are embedded in mucous on mem
* axons of cells come together form CN I
surrounded basal stem cells to gen new olfactory cells when damage = can grow back fairly high degree + have short lifetime as replaced by mitosis
olfactory pathway
olfactory neurons unmyelinated axons -> CN I -> thru foramen in cribriform plate -> into olfactory bulb -> synapse w mitral/tufted cells -> olfactory pathway -> olfactory tubercle then:
1. -> olfactory cortex in temporal lobe -> organise olfactory reflexes + -> limbic centre hence emotional response w/o having noticed smell
2. -> frontal cortex (bypassing thalamus) -> conscious perception of smell
each mitral cell receives input from cells containing 1 receptor type
Schwann cells
2 types surrounding neurons
1. around Aα neurons, laying down myelin
2. around other neurons holding together + making sure continue right direction, no prod myelin
found only PNS, not CNS
olfactory ensheathing cells
cells same structure as Schwann cells type 2 surrounding olfactory cells - it’s these that give ability to regen
* experiments to see if can use this property to repair spinal cord damage
anosmia
loss of sense of smell
olfactory eversion test
something v strong under nose + look for visible response to see if CN I working
vomeronasal organ
VNO
sep structure associated w olfactory bulb ventrally in nose to detect pheromones
* important in sexual behaviour
in dogs the anal glands prod pheromones
role of pheromones
important for repro
1. mating calls + signals (Flehmen to promote stim of VNO by lip up + wrinkling nose to aspirate fluid into it)
2. maternal bonding w offspring so bitches known own young
also alongside normal odour detection + visual behaviour for social interactions bet animals
potential human uses pheromones
- separation anxiety
- noise phobias - dog appeasing pheromone (DAP) (or use proper training, CDs to cancel out sound)
- performance - equine appeasing pheromone
not proven, esp since subjective but no objective improvements reported
why did animals develop taste
- eat food + use taste determine if safe to ingest or spit out
- find nutrients required (e.g. fruit, salt) yummy so meet corporeal needs
taste cell structure
taste cells clustered into taste buds, sat in pits (taste pores) in papillae on surface tongue
* have microvilli cont receptors
* taste cells synapse onto axon (no have own)
* surrounded basal cells to regen + replace damaged/killed cells
taste buds of catfish
has loads bc muddy water + can’t see so everything in, taste what nutritious + should swallow
* carnis less bc eating less variety (more visually selective)
flavours of taste cell receptor
- salt = ENac for any inorganic salt (via Na+ chann)
- sweet = T1R2 + T1R3 7 domain for non-ionised organics
- sour = H+ for acids
- bitter = T2R - often plant toxins
- others asw
each has specific transduction pathway
species diffs in taste cell receptors
- rumis like sweet, not artificial
- cats have mutant sweet receptor gene = indifferent to sweet, like aas
taste cell transduction
- 2nd messenger sys via adenylyl cyclase using cAMP/via phospholipase C to cause depol
- direct ion chann coupling to cause depol
either way depol => a pot -> Ca influx -> NT local release -> excite primary sensory neurones
taste pathway
- primary afferent -> Nucleus tractus solitaris (NTS) thalamus -> cortex -> integration
- primary afferent -> NTS -> brainstem -> reflexes -> dribble
- primary afferent -> NTS -> limbic sys -> emotional response
CN VII, IX + X involved
how is sensory smell + taste different/same
- odour detected at lower conc than taste
- 1 taste affects others as overall constructed varying components but individual smells diff receptors = no affect each other
- can become desensitised specific smell whilst all others work fine, not for taste
- taste cells synapse onto axon (olfactory cells have own)
- both have stem cells alongside to replace damaged/killed cells
- taste cells have microvilli as opposed cilia olfactory
- taste cell transduction via 2nd messenger sys or direct ion chann coupling, olfcatory only by 2nd messenger sys
- taste pathway = CN VII, XI, X involved; smell = just CN I
classifications of memory
- declarative - knowing, e.g. spatial memory in animals (maps - migrating birds)
- non-declarative - knowing how (esp prevalent early life)
types of memory
- development - esp bc memory can involve formation synapses (cats)
- conditioned so something becomes reflex response (Pavlov’s dogs)
- habitualisation = no longer does instinctive reaction bc thing happened enough w no neg effect that desensitised
- long term potentiation
what is memory
changing a neuronal process in brain
stages of memory
- short term = change in a pot firing
- intermediate = changes to prot synth
- long term = growing new synapses + connections (actual structural changes)
a process from 1 to next
why not all short term mems become long term
filtering bc if remembered everything would have no capacity remember useful stuff
* vast majority stuff immediately forgotten
types amnesia
retrograde = forget memories from past
anterograde = can’t remember anything new
what is long term potentiation + where
process by which synaptic connections bet neurons become stronger by more frequent activation
* allows brain change in response experience
* same size stim gives bigger post syn pot every time (if stim same part brain)
1st discovered in hippocampus
how does long term potentiation work
- low level glutamate release activates AMPA receptor on post syn mem
- NMDA glutamate receptor not activated at low levels bc Mg2+ blocking it
- frequent a pots + AMPA activation causes pos ions move in => mem depol => Mg2+ moves out NMDA = unblocked
- => Ca2+ can move in through NMDA ion channs
- => prot synth more AMPA receptors (CREBs involved in this)
- => post syn neuron more sensitive glutamate so bigger depol at each subsequent activation
pos feedback loop = Hebbian learning
what are CREBs
family of prot transcription factors involved memory consolidation
how can you see LTP has occurred
spines on dendrites = neurite growth due LTP w excitatory receptors
* during repetitive activity see new spines
> 1 synapse on 1 neuron
stronger impact on post syn mem
* primary reinforcer = stimulus biologically important to organism, e.g. food, water => involuntary response, e.g. drooling
* conditioned (2nd) reinforcer, e.g. clicker, hence why this makes training work better
easier learn + remember response so eventually only need primary cue
where do neurone structural changes for memory take place
hippocampus in medial temporal lobe
* used to form new memories
* spatial learning tasks but not ‘skills’ tasks
where do memories then go for storage
- factual = -> cortex for long term storage (v long term = temporal lobes)
- skills -> basal ganglia, cerebellum + cortex
cognitive dysfunction
alzheimer’s in animals - canine or feline
-> start pooping in house
-> get stuck in corners
BACE enz causes incr β-amyloid prot = incr phosphorylation of Tau prot = decr memory:
1. neurofibrillary tangles w/in neurons
2. amyloid plaques
comparison alzheimer’s humans + dogs
- β-amyloid placques in both
- neurofibrillary tangles not always in dogs
- acetylcholine dysfunction in both
- tau may not be part of it in dogs
where are nuclei of CNs generally
all in brainstem, except I + II
CN I
olfactory - sensory only (smell)
* originates olfactory bulbs of forebrain
then:
-> contralateral olf bulb
->contralat piriform lobe
-> piriform lobe
-> limbic sys, hypothalamus + reticular formation
CN II
optic - sensory only
* from optic chiasm region
-> visual cortices
-> pretectal nuclei for reflex eye movement => CN III + contralat CN III
CN III
occulomotor - motor only
* somatic to extraocular muscs + levator palpebrae superioris
* autonomic (parasymp) to constrictor musc of iris
optic n. + vestibular nuclei -> midbrain nuclei -> periaqueductal grey matter
* also contralat motor cortex input to grey matt for conscious control
CN IV
trochlear - somatic motor only
* to dorsal oblique extraocular
motor cortex + vestibular nuclei => trochlear nucleus
* = conscious control + reflexes for balance
CN V
trigem
* facial sensation
* motor -> mastication muscs + extensor tympani of ear
contralateral motor cortex -> motor nucleus -> mandib branch (conscious control)
sensory nuclear complex -> motor nucleus of VII (for facial expression) + -> contralat somatosensory cortex (for awareness)
CN VI
abducens - motor only
* somatic motor -> lateral rectus + retractor bulbi
contralat motor cortex + vestibular nuclei -> rostral medulla oblong (nuclei)
CN VII
facial
* taste rostral 2/3 tongue
* touch of medial pinna
* autonom visceral motor -> salivary glands
* somatic motor ro muscs facial expression + buccinator + caudal 1/2 digastricus
pathways of CN VII
trigem sensory nuclei + nucleus of solitary tract (for taste) ->
1. contralateral somatosensory cortex for conscious perception
2. reticular formation w autonomic nuclei, cause salivation (also has input from CN V)
contralateral motor cortex + CN V + CN VIII -> rostral med oblong for motor output
CN VIII
vestibulocochlear = sensory only
2 sets nuclei:
1. spiral ganglion -> cochlear nuclei in med oblong -> pons (olivary complex) + midbrain (caudal colliculus) -> auditory cortex for awareness (L = sequential pattern, e.g. speech; R = tonality)
2. vestibular ganglion -> vestibular nuclei ventral to cerebellum ->
* spinal tracts
* CN nuclei for reflexes, e.g. air movement
* cerebellum to refine motor movement
* contralateral somatosensory cortex for perception of balance
* vomiting centre
CN IX
glossopharyngeal
* taste caudal 1/3 tongue
* pharyngeal + middle ear sensation
* bp info from baroreceptors at carotid sinus
* visceral efferent to salivary glands
* somatic motor to pharyngeal + laryngeal muscs - swallowing
pathways CN IX
nucleus of solitary tract (taste component)
-> contralat somatosensory cortex for perception
-> nucleus ambiguus (w contralat mmotor cortex input) for motor reflexes
-> motor + autonomic nuclei of other CNs for reflexes
-> lateral brainstem w autonomic nuclei for salivation in response taste
CN X
vagus
* taste from root tongue
* sensation from viscera, external ear canal, pharynx, larynx
* motor autonom (parasymp) -> viscera
* somatic motor -> pharyngeal, laryngeal + oesophageal muscs
pathways CN X
nucleus of solitary tract
-> contrtalat somatosensory cortex
-> motor + autonom nuclei other CNs for reflexes
-> nucleus ambiguus (w input contralat motor cortex bc conscious movement) for motor
-> lateral to 4th ventr where autonomic nuclei sit
CN XI
accessory - motor only
* to larynx + muscs of thoracic girdle
nucleus ambiguus -> CN X AND -> C7 for neck/shoulder muscs
CN XII
hypoglossal - motor only to tongue muscs
contralat motor cortex AND other CNs for reflexes (e.g. withdrawal) –> caudal medulla oblongata
generally where do diff nuclei types sit
motor nuclei = ventral
autonomic efferent = lateral
sensory = dorsal
when do we not do CSF tap
if risk of high press in brain, e.g. oedema w lesion
* stick needle in = release press = risk herniation into brainstem
stages of neurological exam
- mentation (general being, behaviour)
- posture
- gait
- postural reactions
- spinal reflexes
- cranial nerve assessment
- palpation
- nociception - pain responses
1st 3 hands off bc once start pain etc general stuff will change
how do we test conscious proprioception
paw replacement test for paw righting reflex
* = lift paw, place on dorsal surface, should move it back
* don’t lift too far or lose balance + testing subconscious proprioception
testing subconscious proprioception
- paper under paw + drag it outwards - dog should bring foot back to retain postural frame
- hopping test = 1 leg held up + pull bod to other side - even hopping both ways? (also lil bit conscious bc moving -> 1 side = paw slightly rolling -> 1 side
- wheelbarrow test (subtle deficits) - testing strength asw (don’t if spinal injury poss bc damage)
jumping on + off box test
needs coordination + balance + strength etc - looking for subtle deficits
testing withdrawal reflex
pinch paw + should withdraw leg - testing sensory + motor
cutaneous trunci reflex
using dermatomes - gentle pinching caudal -> cranial - shld cause cut trunc musc under skin contract lil bit
perineal reflex
gently irritate perineal region -> musc contraction + twitching tail
* no = damage S1 - S3
perineum = region bet genitals + anus
menace reflex
poke in eye/waft air towards eye -> close eyelids
* cortical nerve from telencephalon
testing vestibular function
move head side to side + look for normal physiological nystagmus (vestibulocochlear input)
once localised lesion, next steps?
- bloods: haemotology (testing bcs), endocrine testing (hormones), serology (for antibodies), toxicology (for toxins)
- urine
- ultrasound of abdom if non-CNS or eye for retina, rostral optic nerve + retrobulbar area
- radiography - plain, e.g. look for osteoarthritis as cld affect results/contrast die in subarach space + highlight lesions
- fluoroscopy = lots radiographs for moving image - see dye moving thru = see blockage
- computed tomography = lots radiographs together from diff angles
- MRI - more detail of lesion, but more spenny
- CSF sampling
- pharmacological testing, e.g. myesthenia gravis w acetylcholinesterase - if temp fixes then diagnosed
- electrical testing
to identify disease process
why CSF tap b4 contrast study radiography
otherwise just get sample of dye
types electrical testing
- electroretinogram - check if eye visual behind cataract b4 surgery to fix
- electromyography - direct stim musc to see if motor working (if get response)
- test hearing
what structures make up limbic sys
hippocampus, amygdala, hypothalamus, cingulate gyrus
amygdala does?
involved in fear responses
label
neurons
receipt, generation, conduction + transmission of stimuli as electric signals (waves of depol)
* large nucleus w prominent nucleolus
* soma/perikarion w prominent RER
* multiple dendrites receiving info from adjacent or distant neurons
* single axon projecting signal from soma -> effector cell
astrocytes
- create + maintain BBB
- uptake + recycle NTs
- maintain extracellular pH + osmotic press (by uptake K+)
- support metabolic demands of neurons
- support neuron migration during neurogenesis
protoplasmic in grey matter + fibrillar in white matter
oligodendrocytes
small cells w round picnotic nucleus responsible production myelin in CNS
* long + complex mem projections compose myelin sheaths + isolate axons
in H&E appear surrounded by clear halo (lipids)
microglia
macrophage-like cells in CNS for active immune surveillance
* resting = ramified morphology then -> ameboid after activation (rod cells)
neuropil
space bet neuronal + glial cell bods made dendrites, axons, synapses, glial cell processes + microvasculature
label
label
middle of gyrus = darker pink = white matter full myelin
label
lateral ventricle lining?
ependymal cells
spinal cord histology
