Human Brain Week 1- Neuroanatomy, Neuronal Excitability, Signal Propagation, Synaptic Transmission

neurons vs glial cels

neurons- function unit that receive and process info

glial- supporting cells

axoplasmic transport

substances produced in soma, transported to presynaptic terminals, travel up and down axons

bipolar vs multipolar cells

bipolar- 2 primary projections from cell body

multipolar- multiple dendrites, one axon

gray matter

primarily neuron cell bodies

types of gray matter

ganglia (in PNS), nucleus (in CNS), and cortex (on surface of brain)

white matter

bundles of axons in CNS (ex- tracts, leminscus, fasiculus, column, peduncle, capsule)

where is white and gray matter in the brain vs in the SC

in brain white matter on inside and gray on outside

in SC white matter on outside and gray on insdie

PNS

NS outside vertebral column and skull

includes peripheral nerves, CN

CNS

nervous encased by bone

SC, brainstem and cerebellum, cerebrum

brainstem

medulla, pons, midbrain

primarily white matter tracts, nuclei for some CN

cerebellum

2 hemispheres with midline vermis

coordination of movement

connected to brainstem via cerebellar peduncles

parts of the diencephalon

thalamus, hypothalamus, epithalamus, subthalamus

thalamus function

relay and process information, regulate consciousness

hypothalamus

below thalamus, regulates homeostasis, growth, and behaviors

epithalamus

around thalamus, pineal gland, regulates endocrine sys

subthalamus

inferior and lateral to the thalamus, regulates movement

cerebral hemisphere lobes

frontal, parietal, temporal, occipital, limbic, insular

what is the surface of the cerebrum

gray matter

what is beneath the surface of the cerebrum

white matter (corpus callusom and internal capsule)

more gray matter (basal ganglia, amygdala, hippocampus)

CNS- spinal cord

sensory info to brain and motor commands from brain to periphery

how does the spinal cord process information

reflexive movements and central program generators

what makes up the cerebral spinal fluid system

ventricles and meninges

ventricles

2 lateral, 3rd, and 4th

meninges

pia, arachnoid, dura

parts of the dura in the meninges

falx cerebri- infold of dura at midline

tentorium cerebelli- horiz infold bw occipital lobe and cerebellum

brainstem and cerebellum blood supply

vertebral and basilar arteries

cerebral hemisphere blood supply

branches off of the circle of willis

what artery is the most common for strokes

MCA

characteristics of cell membrane as a capcitor

concentration and electrical gradients

semipermeable membrane

membrane channels

types of membrane channels

leak, modality gated, ligand gated, voltage gated

neurons

receive, process, and generate output due to electrical potential

what is the resting membrane potential

-70 mV

why is the resting membrane potential negative

negative charged molecules can't diffuse out

passive ion diffusion through channels

NA+/K+ pump -> 2K+ in and 3 Na+ out

receptor potential

generated at peripheral receptor of sensory nerve

uses modality gated channel

modality gated channel characteristics

ions through, receptor potential is graded, excitatory

synaptic potential

generated at post synaptic membrane

uses ligand gated channel

ligand gated channel characteristics

ions through, graded, can be excitatory or inhibitory

how do local potentials spread

passively spread across cell with decreasing amplitude

spatial and temporal summation

changes membrane potential and generates or prevents generation of AP at axon hillock

local potentials are ______

passive! gradual, don't last long or travel far

action potentials

large depolarizing signal conducted along axon

not graded (all or none)

depends on voltage gated Na or K channels

where are Na+ channels distribuated

throughout axon at trigger zones and axon hillocks

what happens if summation of AP meets the threshold

AP generated at one segment of axon and triggers down the line

threshold stimulus intensity

15 mV

-70 -> -55

order of events of AP

resting potential, threshold potential, depolarization, repolarization, hyperpolarization

resting potential

Na/K channels closed

threshold potential

Na+ channels open and Na+ in=depolarizes ion

depolarization

subsequent Na+ channels open depolarizing the membrane, then close quickly after opening

repolarization

K+ channels open and K+ out= decrease + charge in axon

hyperpolarization

K+channels open and K+ continues out=return to rest

absolute vs relative refractory pd

abs- cannot generate AP bc Na channels closed

relative- during repolarization and hyperpolarization AP can be generated but requires greater local potential

propagation

AP causes large change in membrane potential and spreads passively to adjacent areas=opening of adjacent Na channels and generate AP all down axon

what is propagation dependent on

passive properties of the axon and opening of voltage gated channels

how to determines speed of propagation

diameter of axon, myelination

nodes of ranvier

spaces between myelin sheath

high density of voltage dependent channels

passive current flow through myelin sheath

where are AP generated

at nodes of ranvier

length constant

decreased in current flow over distance

how to maximize length constant

maximize resistance of axonal plasma membrane, intracellular axoplasma, and extracellular medium

membrane potentials

number of ions to flow to generate resting membrane potential is low, concentrations of ions are constant, separation of charges restricted to vicinity of membrane

glial cells

support network for neurons

involved in myelination, signaling/cleaning/nourishment, and defense

myelination cells

oligodendrocytes- in CNS

schwann cells- for peripheral nerves (myelinated and unmyelinated)

how do glial cells help with signaling/cleaning/nourishing

astrocytes (CNS)

signaling- Ca, gap junction, relase NT

cleaning- absorbs K, NT, cellular debris

nourshiment- est blood/brain barrier

defense of glial cells

microglial cells (CNS) -> phagocytes

important for dev, stroke, head trauma, etc

if overactive can damage healthy structures

how does communication between neurons and target cells occurs

through neuromessengers

info transmission at synapses or extra synaptic sites

where are synapses located

axodendritic, axosomatic, or axoaxonal

what are the first three steps that happen at the synpase

1- AP arrives at presynaptic terminal

2- membrane depolarizes and opens voltage gated Ca++ channels

3- Ca++ in=synaptic vesicles move to release site

what are the last four steps that happen at the synapse

4- synaptic vesicles fuse with presynaptic terminal and release NT in the clef

5- NT diffuse across

6- NT binds to receptors

7- receptor gets activated

once a NT binds to a receptor and gets activated, what happens?

opens channels or triggers intracellular messengers

excitatory vs inhibitory post synaptic potential

excitatory- depolarization because migrates into cell

inhibitory- if NT binds with Cl- hyperpolarizes cell

what determines amount of NT released

activity at the axoaxonic synpase

presynaptic facilitation vs inhibition

facilitation- causes by depolarization, greater release of NT from following neurons (opens Na+ or Ca+)

inhibition- causes hyperpolarization (opens Cl-)

neurotransmitters

chemicals released from presynaptic neuron and act on post synaptic receptors

neuromessengers

chemicals released into extracellular fluid and bind with extrasynaptic receptors

what do both neurotransmitters and neuromessengers do

activate ion channels or proteins inside post synaptic neuron

site of action for NT vs NM

NT- synapse

NM- extrasynaptic sites

mode of action for NT vs NM

NT- EPSP or IPSP

NM- open ion channels, stim 2nd messenger sys

time span of NT vs NM

NT- ms to min

NM- min to days

what determines if a receptor is excitatory or inhibitory

the type of receptor, not the NT

mechanisms to elicit effect in post synaptic target

ligand gated ion channels or g-protein activation of ion channels

how does g-protein activation of ion channels work

NT binds receptor->protein changes shape->activates g protein->breaks free and binds with membrane ion channel->channels changes shape and opens

g protein 2nd messenger sys

diverse and long lasting changes

regulates mood, pain perception, mvmt, motivation, cognition

how do postsynaptic neurons regulate the number of receptors

by either inactivation or internalization

disorders of synaptic function

neuromuscular junction (dec NT release or post synaptic receptors)

channelopathy (dysfunction of ion channels)