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BAB - Coggle Diagram

- - - - brain only, fibrous
    - - membranous, dural reflections
        
        tentrorium cerebelli
        
        falx cerebelli
        
        falx cerebri
        
        diaphragma sella
    - - avascular anervous
        
        upward arachnoid granulations
    - - tight, adhering layer
      - denticulate ligament and filum terminale
      - highly vascularised by underlying vessels
    - - internal jugular veins
    - - CSF and middle meningeal artery
      - lens haematoma in trauma
    - - crescent haematoma with free bleeding in the elderly
  - - - ependymal cell lining forming choroid plexus
      - filters plasma with connective tissue
      - 2 in each hemisphere with horns
      - volume increases with age
    - - between left and right thalamus
      - supraoptic recess above optic chiasm
      - infundibular recess above optic stalk
    - - between pons and medulla
      - drains into spinal canal bathing spinal cord and subarchnoid cisterns
      - reabsorbed into circulation in arachnoid granulations
    - - low glucose and K, high wbc fluid for buoyancy to remove pressure and chemical environment maintenace
  - - - in AP03
- - - - light enters via transparent cornea through aqueous humour through pupil then lens then vitreous humour then hits the retina
      - fovea focusses image
      - lens attaches via zonule fibres for focussing image
      - aqueous humour nourishes avascular cornea- then is reabsorbed by the anterior chamber after secretion into the posterior chamber then travelling through the iris
    - - open angle- sclerosis of the veins slowinf reabsorption- less severe and asymptomatic for years
      - iris may adhere to cornea blocking aqueous humour reabsorption
      - treated by surgery (esp open-angle) or beta blockers to reduce aqueous humour production or prostaglandin analogues to increase blood flow and drainage
    - - photochemical cells
        
        types
        
        rods
        
        rhodopsin in membranes of many dense intracellular discs for high sensitivity white vision
        
        rhodopsin= retinal chromophore and opsin (GPCR) with cyclic GMP gated cation channels
        
        high sensitivity via many rods connecting to 1 ganglion cell so tiny light levels produce a response
        
        low acuity as many rods produce the same response level from one ganglion
        
        cones
        
        3 photopigment opsins (red, green, blue) where each cone has 1, found in infoldings of cell membanes with low surface area and density for low sensitivity colour vision
        
        1 cone goes to 1 ganglion so low sensitivty but high acuity of vision
        
        outer photopigment section, inner organelle segment, and synaptic terminal segment
      - bipolar cells
        
        direct connection between photochemical cells and ganglion cells
        
        on bipolar cells
        
        in dark with high glutamate they hyperpolarise i.e. are inhibitory
        
        in light with low glutamate they depolarise i.e. are excitatory
        
        off bipolar cells
        
        depolarise in dark with more glutamate i.e. excitatory
        
        hyperpoalrise in light with less glutamate i.e. inhibitory
      - ganglion cells
        
        generate APs travelling into optic nerve, can also be on or off
      - horizontal amacrine cells
        
        modulate transmissions between photochemical cells and ganglion cells
    - - blind spot
        
        optic disc where axons of optic nerve neurones collect
      - peripheral retina
        
        rods so high sensitivity for light yet low acuity
      - macula
        
        central retina, more cones
      - fovea
        
        all cones so less photopigment and less sensitivity but higher acuity
    - - dark
        
        rhodopsin is inactive so cGMP is high
        
        cGMP gated cation channels are open causing na influx dark current giving -30mV membrane potential
        
        depolarised state causes glutamate release signalling bipolar cell
      - light
        
        rhodopsin absorbs light flipping 11th C hydrogen from cis-11 making molecule all trans
        
        activates opsin causing GTP to bind to GPCR G protein
        
        G protein activates PDE breaking down cGMP into GMP
        
        this closes cGMP gated cation channels causing low Na influx so hyperpolarisation
        
        this reduces glutamate release to bipolar cells
        
        transmission through retina
        
        indirect pathway
        
        surround with less influence
        
        uses amacrine cells for contrast at image borders via opposite electrical responses in basal and ganglion cells compared to direct pathway
        
        direct pathway
        
        photoreceptor cell hyperpolarises in light- bipolar cell- ganglion cell
        
        central with greater influence so it predominates surround
        
        transmission to brain
        
        into optic nerve to optic chiasm where nasal nerves swap to the ipsilateral optic tract
        
        binocular field is where left and right fields overlap
        
        nasal hemiretinas see temporal hemifields and vice versa
  - - - olfactory nerve
      - cribriform plate
      - basal cells, supporting cells, and olfactory cells
        
        olfactory cell
        
        sensory afferent itself unlike in taste
        
        replaced every 4-8 weeks
        
        generated in lateral ventricles then migrate and wire themselves
        
        can be used for ND disease research
        
        hundreds of cell types each for a different response levels to different chemicals, generated similar to antibody generation
      - olfactory cell cilia and mucous
    - - binds to olfactory cells damaging them causing anosmia
      - if person has sufficient basal cells (stem cells) can regenerate
      - returned smell is miswired similar to after cribriform plate damage
    - - binding- GPCR events- intracellular cascade- depoalrisation- AP
      - adaptation may occur for familiar scents
      - process
        
        1st order neurone
        
        from olfactory epithelium synapsing in the glomeruli of olfactory bulb
        
        2nd order neurone
        
        from olfactory cell through olfactory tract and cribriform plate into the olfactory cortex
        
        no 3rd order neurone due to being oldest sense
        
        information travels to other parts of cortex as well
        
        via the MD thalamus to the orbitofrontal cortex (i.e. thalamus after cortex which is unique) behind eyes where recognition of smell occurs
        
        to the limbic system
    - - common with age and chemo due to high replacement (lower compliance) impacting qol and nutritional quality
      - epileptics can percieve smell before fits due to adjacent brain region being affected
      - Parkinson's early symptom is loss of smell and depression also causes anosmia
  - - - salty
        
        na influx via non-gated na channels causing depolarisation
      - sweet, umami, bitter
        
        different GPCR subunits, usually T1R and T2R
        
        sweet= T1R2 and T1R3
        
        umami= T1R1 and T1R3
        
        bitter= T2R x 2
      - sour
        
        h influx inhibits k channels preventing K efflux causing depolarisation
        
        also enters via TRP channels causing depolarisation
    - - tongue, palate, pharynx, and GIT
      - large surface areas with papilla ridges and furrow taste buds
      - taste buds
        
        taste cells
        
        each taste cell detects one sub-modality
        
        basal cells- form new taste cells
        
        slows down with age
        
        sensory afferents
        
        replaced every 2 weeks
      - transduction
        
        chemical binds- receptor potential- v. gated ca channels cause ca influx- Nt release- sensory afferent excited to produce AP
        
        1st order neurone
        
        from tongue to CN7/9/10 for front, bac, and non-tongue receptors to synapse at gustatory nucleus of medulla
        
        2nd order neurone
        
        second order neurones from gustatory nucleus to VLM medulla
        
        3rd order neurone
        
        third order neurones from VPM medulla to primary gustatory cortex, with parts entering the lateral fissure
        
        collaterals
        
        side branches from 1st order neurone for swallowing and salivation for satiety and palatability
    - - common in over 80s with nutritional and QoL consequences, as is anosmia
      - side-effect for mental health drugs and chemo (anosmia also) due to high rate of replacement
        
        these have lower ompliance due to this
- - - - types
        
        fasciculus cuneatus
        
        lateral column for above T6 upper limb to nucelus cuneatus
        
        fasciculus gracilis
        
        medial column for below T6 lower limb to nucleus gracilis
        
        trigeminothalamic
        
        trigeminal, facial, glossopharyngeal, and vagus nerves
      - neurones
        
        1st order
        
        from skin to ipsilateral medulla oblongata synapsing at nucleus gracilis, cuneatus, or trigeminal
        
        2nd order
        
        from medulla oblongata, decussating at medial lemniscus of white matter to travel contralaterally to thalamus as internal arcuate fibres, synapsing here
        
        3rd order
        
        from contralateral thalamus, ascending through ventral posterolateral cortex and internal capsule of white matter, synapsing at the sensory cortex of the post-central gyrus
      - touch, proprioception, vibration- a beta axons
    - - types
        
        lateral
        
        pain and temperature
        
        anterior
        
        crude-touch and pressure
      - crude touch, pain, and temperature- a delta and c axons
      - neurones
        
        1st order
        
        from skin, ascending 1-2 vertrebral levels synapsing at the dorsal horn's substantia gelatinosa
        
        2nd order
        
        from substantia gelatinosa to decussate becoming contralateral forming anterior and lateral tracts through the spinal leminiscis of the brainstem synapsing in the thalamus' ventral posterolateral nucleus (VPN)
        
        3rd order
        
        from thalamus' VPN, ascending through internal capsule white matter synapsing at the primary sensory cortex of the post central gyrus
        
        burning pain terminates at reticular formation of brainstem activating nervous and limbic systems
    - - unconscious proprioception
      - neurones
        
        1st order
        
        from skin to synapse at Clarke's nucleus of spinal cord
        
        2nd order
        
        dependent on type
      - types
        
        anterior spinocerebellar
        
        proprioception in the lower limb- fibres decussate once at spinal level then again at the cerebellar peduncle so end up in ipsilateral cerebellum via the superior peduncle
        
        posterior spinocerebellar
        
        proprioception in the lower limb- travels ipsilaterally to cerebellum via inferior peduncle
        
        rostral spinocerebellar
        
        proprioception in the upper limbs- travels ipsilaterally
        
        cuneocerebellar
        
        proprioception in the upper limbs- travels ipsilaterally
- - - - adapted receptors activate at threshold then stops firing- detect stimulus changes
      - proprioception of an object
      - vs tonic receptors that detect strengths of stimuli
  - - - muscle proprioception- thickest and fasted
    - - skin mechanoreception- thick and fast
    - - pain and temperature
    - - temperature and pain- unmyelinated
  - - - superficial
        
        meissner's corpuscle
        
        papillary epidermis, rapidly adapting, light touch, and vibration, grip adjustment
        
        merkel's receptor
        
        digits and mouth more than glabrous skin
        
        slowly adapting, sustained light touch, form and texture of objects
      - deep
        
        ruffini's corpuscle
        
        bulbous collagen apparatus responding to stretch, grasping and slippage prevention (decrease with age)
        
        pacinian corpuscle
        
        rapidly adapting fro deep touching, poking, and high frequency vibration
        
        fully encapsulated nerve ending with lamellae layers
      - hair follicle receptor
        
        rapidly activating light touh receptor for constant hair deflection- nerve is wrapped around hair
    - - bare nerve ending with specialised ion channels to be cooling or warming sensing
      - cooling- TRPM8
        
        cooling channel from 10-38 alsoa ctivated by menthol, a delta and c axons
        
        also excited by hot temperatures as paradoxical cold firing
      - warming- TRPV3/4
        
        warming channel from 29-45, c axons
      - slow adapting causing numbness, poor indicators of actual temperature- this is done by the brain coupling all signals
    - - free nerve endings with non-adapting/tonic receptor with high threshold whereby adequate stimulus will damage tissues
        
        high theshold mechanoreceptors
        
        a delta axons for well-localised prickling pain
        
        polymodal nociceptors
        
        c axons for mechanical stimuli, noxious chemicals, inflammation chemicals, and heat over 46
        
        poorly localised burning sensation or dull pain
        
        poor localisation for viscera due to axonal divergence to multuple cell bodies
        
        e.g. TRPV1 which is also sensitive to capsaicin (chili)
      - pain
        
        subjective limbic combo with nociception from injury, extreme pH, extreme temp, inflammation, and noxious chemicals
        
        pathway/gate theory
        
        nociceptive stimuli enter substantia gelatinosa aka lamina 2 of dorsal root horn- non-noxious info goes deeper
        
        interneurons inhibit or stimulate signals- pain must overcome the former as they both supply the same spinal cord cell body
        
        associate with limbic system, pain matrix, and cortex
        
        inhibitory interneurones can be inhibited by nociceptors, but activated by a beta mechanoreceptor fibres
        
        rubbing activates these causing inhibition of pain signals but no other neurones as these have higher thresholds
        
        TENS gives controllable current to activate the a beta mechanoreceptors but not the c nociceptors meaning acupuncture, lower back pain, and parturition are less painful
        
        intrinsic analgesia
        
        gate is closed to stop pain via 5-HT, noradrenaline, and enkephalin (endogenous opioid) release in dorsal horn
        
        nociplasticity
        
        facilitated pain
        
        chronic pain causes peripheral and central sensitisation
        
        peripheral sensitisation- allodynia
        
        allodynia
        
        1 more item...
        
        antidromic reflex- pain AP propagates up and down axon branches causing CGRP and substance P release- the axon reflex
        
        these diffuse to BVs, binding with receptors causing acute phase effects releasing prostaglandins, bradykinin, H, cytokines, and NGF aka the inflammatory soup
        
        high levels cause sensitisation of free nerve endings reducing threshold for AP generation- esp polymodal recceptors
        
        antridromic nature means overlapping territories may also experience allodynia aka secondary allodynia
        
        central sensitisation- hyperalgesia and secondary allodynia
        
        chronic pain
        
        hyperalgesia
        
        1 more item...
        
        more acute signals means high AP frequency which releases substance P that binds to NK-1 receptor plus normal glutamate-AMPA binding causing hyperpolarisation pushing out the Mg block of the NMDA receptor
        
        now glutamate can also bind to NMDA opening it for Ca/Na influx causing protein phosphorylation via a cascade causing hyperalgesia in this 2nd order neurone
        
        acute pain
        
        low frequency AP firing propagation releases excitatory glutamate binding to AMPA transmitting AP. NMDA receptor is blocked by Mg so second order neurone transmits signal with high fidelity
    - - joint position, muscle length/movement, acceleration, tension
      - a alpha axons- as these are the quickest
      - muscle spindles
        
        fibrous capsule of muscle aka intrafusal fibres wrapped around 1a axons in parallel so stretch stretches them causing APs
      - golgi tendon organs
        
        muscle/tendon junctions as 1b afferents in series with muscle so tension causes APs
- - - - neurulation
        
        anencephaly
        
        spina bifida
    - - 3D mapping
        
        dickkopf and noggin vs retinoic acid (AP)
        
        sonic hedgehog (DV)
        
        (ML)
      - cortical migration
        
        migration
        
        inside-out layering
        
        radial glia
        
        cortical dysgenesis
        
        lissencephaly
        
        differentiation
        
        differential genes
        
        axon growth
        
        growth cones and chemoattractants
        
        fasciculation
        
        proliferation
        
        ventricular zone
        
        zika virus
  - - - NGF (neurotrophic factors)
      - refinement
        
        neurodegenerative diseases