a+p exam 4 notes summary / study guide

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i'm fucking drunkenedified rn ngl let's see where this shit goes

i figure i might as well put this shit on gemini b/c there is presently no content on gemini other than gemini focused content and konpeito.media so half-assed bio content from halfway through a semester that only tells the parts of the story i feel like i want to review and was created while fucking wasted is somehow still beneficial to gemini imhqtbho

but like predominantly this is here for me so go fuck yourself

leftovers from previous unit

400 um for diffusion
40 um is a cell

glu --nmda-> ca[2+] --cam, nNOS-> no --gs-> cGMP --> pkg --> ion channels and stuff

i literally have no idea what any of this means and i probably won't study it and i'm hoping it's not really on the exam; he didn't seem too keen on it iirc. tbf i haven't been to the review session yet so we'll see what the other ta guy thinks?

the review session

no funcs

- dilates sm musc
- immune response
- long term potentiation

V I S I O N

rudiments

anatomical type stuff

light goes as follows:
- cornea
- anterior chamber
- pupil
- lens
- focused by zonule fibers / ciliary muscle
- vitreous humor
- retina
- center (fovea) has highest acuity
- optic disc is blind spot b/c that's where optic nerve innervates so no detectors beneath

a random thing

melanopsin does circadian clock and melatonin acts there to induce sleep

idk if i need to know this

resolution

as frequency of light v, resolution v

"more waves --> more info"

convergent systems amplify (a la rods [pure photon detectors; no color])
separate paths resolve (a la cones [see color])

so in a convergent system you can perceive a signal with less stimulus, but you have a lower resolution in interpreting that signal

whereas in a parallel system you need more stimulus to produce the signal because it is unamplified but you get greater detail in that image

this is because convergent systems are summative and parallel systems (i literally made up the term parallel; he didn't give a name for these, but they're the not convergent ones but they aren't strictly speaking convergent b/c they start split???) are what they are. the issue with convergent systems is that this summation comes from adding the total stimulus at n different receptors and as a consequence you lose the acuity you would gain from looking at each of those independently

dark current et al

rhodopsin is the visual pigment of rods; cone-opsin of cones (the latter may have been tongue in cheek but i don't know for certain)

in absence of light (in the dark) photoreceptors have what is called a dark current, which comes from a depolarizing inward current that can be disabled by light.

basically, if you hit the rhodopsin/retinal complex with light, it isomerizes cis-retinal to trans-retinal, activates α subunit and dissociates it from the β/γ complex ("just like they always do"), which activates phosphodiesterase, breaking down cGMP, which was holding the na/ca channel that created the 40 mv dark current open

however, a counterbalancing outward k channel which was holding the cell at that 40 mv resting membrane potential is still open, thus hyperpolarizing across the membrane, moving the potential from -40 to -65 mv???

more to come soon; i need to go get another fifth of jack but like idk what will happen when i go back to my room so maybe this will be it for the night but like it better not

ok hello im back but my roommate being a shit and won't stop talking dude i'm trying to study you fuck

that's absolutely why i got a bottle of fucking jack

remember how ca comes in the na channel too? as ca content gets too high (too high dark current), it inhibits guanylate cyclase, the enzyme that converts gtp to cgmp, thereby inhibiting ability to conduct through the cgmp-gated channel that brough the ca in to begin with

this also inhibits the cgmp's binding to the channel

meanwhile rhodopsin kinase inhibits pde and ca inhibits rhodopsin kinase, so ca activates pde

pde converts cgmp to gmp (hurting dark channel)

so ca hurts dark current in 3 ways:

- activates pde, breaking cgmp into gmp
- inhibits gc, preventing gtp conversion into cgmp
- prevents cgmp from binding to dark current channel even when it exists

the overall pathway:

ca --cgmp-> in -| cgmp ---> gmp
             \       ^ pde
              +-| gc | ---
              |     gtp |
              |         |
              \--| rhodopsin
                     kinase

however if you push too high, you'll bleach out from the light (think getting flashbanged, right?) and this is because you have to convert that trans-retinal back into cis-retinal

- na/ca channel only open in presence of cgmp
- depol happens
- cgmp can be impacted by ca primarily or by retinal stuff

how is recovery from bleaching conducted?

for rods:

- abc moves trans retinal into rpe; converted by rpe65 to cis retinal which goes back to rod

for cones:

- cis ret in cones is converted by light to trans form, then brought to muller cell then converted to cis ret, then back to cone
- (or it can go by rpe like in rods)

___because they can also use muller cells, cones recover more quickly than rods___

color shit

there are three cone pigments:
- s
- short
- blue
- m
- medium
- green
- l
- long
- red

mix them to get other stuff (as per rgb type rules, basically, like yellow is produced by mixing red and green rods, if ya feel me)

ganglion cell types and stuff

- p ganglion cells
- project to parvocellular neurons in lat geniculate
- 70% of ganglia
- visual acuity

- m ganglion cells
- magnocellular neurons (larger than parvocellular) in lat geniculate
- from all cones and rods
- best with moderately-sized objects
- motion
- luminance

- k ganglion cells
- apparently just for the color blue?
- also lateral geniculate but didn't say what type of cell?

retina and visual fields stuff

- nasal retina
- sees temporal space
- crosses before optic chiasm
- temporal retina
- sees nasal space
- does not cross

meyer's loop in the temporal lobe processes top field
dorsal optic radiation in the parietal lobe processes lower field

proceeds from retina to chiasm to tracts to lgn to radiations

as you go further back, damaging an area does different stuff

damage to fovea loses middle of image
optic nerve kills whole eye's vision
chiasm loses mirrored sides of vision [the lateral sides, i believe idk tho]
tract loses same side (either left or right) [left tract loses right side of image]
meyer's loop loses either both top l or both top r
dorsal optic radiation is same but bottom l or bottom r instead
any further back does weird shit where center of image is spared (macular sparing) but like it's pretty unpredictable and stuff b/c more and more has been processed by that point the further back you go

visual pathways

dorsal is the "where" pathway; ventral pathway is "what" pathway

        where in space                identification
       parietal cortex                temporal cortex
      vis. guided mvmts             recognition/interp
   e.g., navigating a crowd       e.g., identifying a rose
     m cells --> magno                p cells --> parvo

color vision misc stuff

- dichromatic vision
- one type of cone is fucked
- protanopia: loss of red
- deuteranopia: loss of green
- tritanopia: loss of blue
- anomalous trichromacy
- absorbance wavelengths shifted in some way
- protanomaly: weirdness w/ red perception
- deuteranomaly: weirdness w/ green perception
- tritanomaly: weirdness w/ blue perception
- monochromatic vision
- very rare

those color blindness test plates you've seen before are named ishihara plates

taste???

sensory systems encode:
- modality
- location
- intensity
- timing

modalities are activated by particular receptors

receptors

- umami
- t1r1 + t1r3
- sweet
- t1r2 + t1r3
- bitter
- t2r
- sour
- type iii
- protonated sour tastant enters and protonates proton-sensitive channel, deactivating it
- salty
- complete fucking mystery

ok hello next day has arrived, last night i only drank a wee bit of the new bottle of jack before things went off the rails; maybe 4 or 5 shots only. i was honetsly sober by the endd;;;

i just drank the remainder wtwenty minutes ago? it is time

exam is tomorrow

oprepare your study



!!!




let us comtinue

in a trimeric g-protein, α leaves βγ complex and does some signalling

lots of differnt types of α

also different variants of βγ (5 & 14 types respectively)

ok im worse now thatn i was last night like at least last night idont think i made any typos but now i've made like a lot looking back and a lot of this is incomprehensible? like today i had the remainder of the jack (what like 13-4 shots?), 2 beers, 1 lil baby pint bottle of vodka

oh,., there's something to talk about in a legit gemini blog post, although i should probably be sober to write it: my pushing of the boundaries of """functional""" alcoholism. as a case-study, there's the time i was hospitalized because adam sandler isn't funny. i'll probably put a link here to it when i've written and published it. it's a fabulous story and you should all read it. i mean nobody is reading this tho so who cares ayy

for now, i have a fucking exam to study for which is what this si supposed to be about fuck


for t1r and t2r receptors (so sweet, bitter, umami):

the ligand binds gpcr; α dissoc. from βγ

then proceeds as follows:

βγ --> plc --dag-> ip3 -------\
 α --> pde --| camp --> pka -| ip3r --> ca[2+] --> trpm5 --> na+ --> more na+ by nav --> depol --> calhm1 --> atp + neurotransmission of sensation

this neurotransmission occurs by the loss of atp through pannexins (or the hemichannel calhm1)

calhm1 = calcium homeostatic modulator 1 btw

p2x and hemichannel transfer atp; p2y transfers adp

p2x does afferent projections; p2y interacts between cell types @ the sensor

afferent can also use 5-ht

2 releases atp; has 5ht/gaba receptors; 3 has p2y and can be modulated by that

tissues shit

lmao my notes begin wtih my realization that my lab partner wasnt there that day and as a consequence iw as going to have to take the group quiz on my fucking own

and guess what, i was done literally 20 minutes before any of the other groups and i got a fucking 95 which is better than any of the grades we got on those quizzes together before now so fuck yeahhhh~

but she knows the content better than me negl i think we just take a while b/c indecisionand i did well only b/c due to her absence i studied like a FUCK ton in lecture

the point of all of this is to say that this tissues lecture didn't get a whole lotta notes from me, so ayy

there's a review session @ 7 tonight that i gotta go to (it is presently 4:20 btw mlaoo)

wow this is really bad; this whole modification is really bad.

continuing:

tissue types

- nervous
- epithelial
- muscle
- connective

nervous

senses deviations, signals for homeostatic response

ok im relistening to the lecture
my typing is really loud in the recording lol

what is important about the biochemistry

- maintaining polarization status
- neurotransmitters exist

cell features

- large cell body
- long cell processes
- dendrites have lots of branching

cell types

- glia
- more supportive in function
- neurons
- main ones
- long bodies
- long processes

functions

- send and receive electrical signals very quickly
- process sensory info
- encode via pattern / frequency

location

- in cns/pns
- this was a pretty silly slide
- why the fuck did you put this here [redacted prof name]

embryonic stem cell layer

arises from ectoderm

regenerative capacity

- glia do a pretty good job
- neurons do a pretty bad job

arrangement

- connected in series usually
- cell bodies usually in groups
- motor cell bodies in vent horn
- sens cell bodies in dors root gang
- lots and lots of glia per neuron
- very cellular tissue

vascularity

- very metabolic --> very vascular

innervation

- not in any way

identification

- large cell bodies
- something else

muscle

biochem

- ca causes ctrxn
- ctrctile proteins: actin/myosin

cell features

               striated     nuclei          gap junctions   fibers
    cardiac    +            1 central       y               branch
    skeletal   +            multi periph    n               parallel
    smooth     -            1 central       y               layers

function

- contraction

germ cell layer

from mesoderm

regenerative capacity

only smooth regens

innervation

yes

vascularity

yes

organization

- skel: all fibers parallel
- card: branching
- sm: in layers

epithelial tiss.

features

- desmosomes
- tight junctions
- basement membrane
- allows there to be an apical surface
- three types
- squamous --> passive maintenance of boundary
- cuboidal --> active secretion/absorption
- columnar --> lots of active absorption, + moving cilia, doing other things; secreting mucus; etc, etc...

function

- absorption/secretion
- filtration
- protection
- differentiation
- sensation

location

- anywhere anything lines anything
- any gland or organ that needs to secrete or do any bullshit

germ cell layer

- skin from ecto
- gi from endo
- pericardium/peritineum/other shit from meso

so all three!

regenerative capacity

fast

organization

either simple, stratified, pseudostratified

vascularity

no

innervation

hell yeah

misc notes

simple cuboidal for secretion/abs in kidney y'know

connective tissue

misc notes first

cells make & secrete ecm but cell bodies themselves aren't the focus

biochem

idk she didn't really say much whatever

types

- fibroblasts (make matrix); fibrocytes (live in it)
- chondroblasts (make cartillage); chondrocytes (live in it)
- osteoblasts (make bone); osteocytes (live in it)
- adipocytes (live in fat and other conn tissues)
- leukocytes (white bc)
- erythrocytes (red bc)

where

between any other

function

produce that matrix

embryonic germ cell origin

mesoderm

regenerative capacity

pretty good