Exam 1 material Flashcards
What are the three main divisions of the brain? Excluding the spinal cord.
Prosencephalon (forebrain)
Mesencephalon (midbrain)
Rhombencephalon (hindbrain)
What makes up the prosencephalon (forebrain)?
Telencephalon
Diencephalon
What falls under the telencephalon?
cerebral hemispheres cerebral cortex subcoritical white matter basal ganglia basal forebrain nuclei
What falls under the Diencephalon?
hypothalamus
thalamus
epithalamus
What makes up the mesencephalon (midbrain)?
Cerebral peduncles
midbrain tectum
midbrain tegmentum
What are the 2 branches of the Rhombencephalon (hindbrain) and what falls under each?
Metencephalon (pons and cerebellum)
Myelencephalon (medulla)
Directions in brain. Flip at midbrain. what are they above and below the midbrain?
Below: for ease going in order of North East South West …Rostral (nose), Dorsal (back), Caudal (tail), Ventral (front)
Above: rotate the below 90 degrees counterclockwise.
directions of planes
Horzontal plane (axial) sagittal plane coronal plane (frontal)
Classical neuron anatomy arrangement
Dendrites -> cell body -> axon -> synapse to other dendrites
multiple orientations and configurations
Main functions of Glia cells (4)
- supportive of neurons
- maintain nutrition
- manage waste
- balance ions
*they interact on different levels to form synaptic connections.
Types of Glia cells
Astrocytes
oligodendrocytes / schwann cells
Ependymal cells
microglia
Astrocytes (functions)
encase synapse, regulate chemical environment
Oligodendrocytes vs Schwann cells (functions)
Oligo: CNS myelin. have multiple arms
Schwann: PNS myelin
Ependymal cells (functions)
Cerebral spinal fluid, lines central canal and spinal cord
Microglia (functions)
just like macrophages, but in the brain.
immune stuff.
Glutamate (excite or inhibit?)
Excitatory neurotransmitter
GABA (excite or inhibit?)
Inhibitory neurotransmitter
Acetylcholine
Muscles / Autonomic
receptor types: Nicotinic and Muscarinic
Norepinephrine
Sympathetic
Neuromodulation: What 2 neurotransmitters?
Dopamine (motor system…)
Seratonin (mood)
Cord segmentation
- segmented from development
- four groups
- Cord ends around L1, then caudal equina
Ventral vs dorsal roots
Ventral (front) roots - motor
Dorsal (back) roots - sensory
White and gray matter in regards to brain and spinal cord.
in brain, white is on the inside.
flips in spinal cord (white on outside)
White vs gray matter
White = mostly fat , myelin gray = mostly cell bodies
Frontal lobe (functions)
- primary motor cortex
- “expressive” language (left-side)
- “executive function”
Parietal lobe (functions)
- primary sensory cortex
- spatial processing
- multimodal (all the senses?) integration
Circle of Willis
Allows the blood supply of the brain to “communicate with each other”
- connects various areas. front to back. side to side.
CT scans (goods, bads, etc.)
- Fast.
- no big contraindications
- LOT of radiation
Good: blood, bone (bright white!), general outlines
Bad: soft tissue resolution
MRI scans (good, bad, etc.)
-No radiation
-very high resolution
several contraindications, and slow
Good at: soft tissue, weird things
Bad at: bone (invisible), blood (confusing)
contrast in imaging
used to detect leaks/tears/highlighting
Membrane potentials: Electrical currents
current has to be caused by a flow of ions.
no flow = no current.
Need: ion gradient, permeable membrane.
I = V/R
Nernst equation conceptual
E = …
it calculates the resting membrane potential required to maintain ion gradient
- only considers one ion!
Goldman-Hodgkin-Katz equation (conceptual)
similar to nernst but includes multiple ions!
adds a term in the equation for every ion in the system.
Mammalian neuron. Is the concentration higher on the inside or outside?
Potassium
Sodium
Calcium
Potassium - inside conc higher
Sodium - outside conc higher
Calcium - outside conc higher
Action potential (what order of channels)
initially due to sodium channels opening (3 NA). then they close. potassium channels open (2 K) and it under shoots (hyperpolarization)
Passive conduction vs active
passive - decays over distance
active - is constant over distance
What channel has a “trap door”
sodium. causes a refractory period.
Why is it important to have different receptor types?
to eliminate cross-talk. make it more specific
Myasthenia Gravis
autoimmune disease
-destroys ACh receptors
Ionotropic vs metabotropic receptors
ionotropic: paired to an ion channel
metabotropic: paired to a G-protein
Acteylcholin: Nicotinic receptor
inotropic excitatory (non-selective) -found in brain, autonomic ganglia (sympathetic/parasympathetic) and motor endplate
Acetylcholin: Muscarinic receptor
- Metabotropic excitatory
- found in brain, parasympathetic end-organs
ACh: clinical apps
- Succinylcholine
- Nicotine
- Muscarin:
- Succinylcholine: Director nicotinic ACh activator (paralytic drug. contract until no ACh to contract)
- Nicotine: Mild nicotinic ACh activator (jitters)
- Muscarin: Mild muscarinic ACh activator (massive parasympathetic response)
Glutamate
Excitatory found in brain. (physical trauma can cause release -> lead to seizures)
- ionotropic receptors: NMDA (main..big bro)**,AMPA (lil bro), Kainate
- metabotropic receptors: mGluRs
GABA
Inhibitory found in brain. Alcohol in low dose GABAa agonist. High dose also glutamate antagonist.
- ionotropic receptors: GABAa,GABAc, chloride channels.
- metabotropic receptors: GABAb
Glycine
GABA’s lil bro
- similar as GABAa receptors
- inhibitory, inotropic, chloride channels
- found in spinal cord
Dopamine
Metabotropic…found in brain: 2 paths.
Mesolimbic pathway: linked to mood.
Nigrostraital pathway: initiation of movement. (motor control)
*also active peripherally as a vasoconstrictor.
Dopamine applications. one for each pathway
Nigrostriatal path: loss of output leads to Parkinson’s
Mesolimbic path: observed in Schizophrenics. drugs can fix but can cause hallucinations.
Norepinephrine (central and peripheral functions)
Excitatory metabotropic receptors: alpha and beta adrenergic
Centrally: wakefulness (wake cycles)
Peripherally: sympathetic response (maintains vascular tone)
Where is norepinephrine produced?
Locus coeruleus
Epinephrine
norepinephrine lil bro (same receptors)
- found less in CNS
Histamine (central and peripheral function)
-Metabotropic receptor
Centrally: arousal, nausea (vestibular funct?)
peripherally: immune reactions, gastric acid secretion
Serotonin
found in brain.
mood regulator
*SSRI antidepressants increase serotonin
electrical synapses
direct flow of ions through gap junctions
chemical synapses
electrical signal transduced through a chemical diffusing across a gap
Axonal transport
nucleus - DNA - RNA - ER - RER - Golgi apparatus -> microtubules transport down
Lambert Eaton
similar to myasthenia gravis, but antibodies are to calcium channels
Early development main steps (6)
1) zygote
2) Morula
3) Blastocyst
4) Bilaminar embryo
5) Gastrulation
6) Neurulation
zygote
initial fertilized cell
Morula
zygote dives several times (16-32 cells total)
- same overall volume
- happens over several days
Blastocyst
- Morula cavitates, forming Yolk sac
- clump of cells inside blastocyst: Inner cell mass
- forms around time of implantation, about a week old
Bilaminar embryo
A second cavity forms (the Amnion) on the other side of the inner cell mass
-composed of two layers (hypoblast and epiblast)
Hypoblast layer
next to yolk sac. does NOT contribute to final embryo
Epiblast layer
next to amnion. ALL cells from the final embryo derive from these cells
Gstrulation
- formation of 3-layer embryo by folding into itslf
- hypoblast cells (next to yolk sac) are obliterated
-converts the epiblast cells (next to amnion) to: Ectoderm, Mesoderm, and Endoderm
Ectoderm
during gastrulation epiblast cells converted to this.
***source of skin/nervous system
Mesoderm
during gastrulation epiblast cells converted to this.
***source of muscle/bone/connective tissue
Endoderm
during gastrulation epiblast cells converted to this.
***Source of GI and GU system
Neurulation
Folding of Ectoderm in onto itself to form the neural tube
-Mediated/signaled by the notocord (which turns into intervertebral discs)
- Floorplate
- Roofplate
- Neural crest
Floorplate (formed during Neurulation)
- Anterior-most part of neural tube
- Forms motor neurons
Roofplate (formed during Neurulation)
- Posterior-most part of neural tube
- forms sensory neurons
Neural crest (formed during Neurulation)
- forms from edge of neural tube before it seals
- migrate away from neural tube and forms 4 things
4 things: peripheral ganglion, facial bones, melanocytes (skin pigment), parts of heart (valves/septums)
What are the four parts formed when the neural crest moves away from the neural tube?
1) peripheral ganglion
2) facial bones
3) melanocytes (skin pigment)
4) parts of heart (valves/septums)
Nerve anatomy (3 layers/parts)
Epineurium
Fascicle
Perineurium
Epineurium
connective tissue covering of nerve
Fascicle
collections of axons within nerves
Perineurium
connective tissue covering of fascicles
3 main types of injury
Neurapraxia
Axonotmesis
Neurotmesis
Neurapraxia
- loss of conduction, without any physical disruption
- frequently compression-type injury
- leads to disruption of myelin, microtubules, edema, or some other easily repairable block to action potential conduction
- usually returns to function in several days
Axonotmesis
- disruption of axons, with intact connect tissue
- can repair through Wallerian degeneration and regrowth
- Wallerian degeneration takes 2-3 weeks
- nerve regrows at 1mm/day or about 1 inch/month
Neurotmesis
- Disruption of entire nerve
- will NOT regrow properly unless epineurium is surgically repaired
- if repaired, injury repairs as in axonotmesis
Location/mechanism of injury
-most common nerves injured are in extremeties
mech:
compression (mechanical/ischemic; usually neurapraxic)
laceration (usually neurotmesis)
traction (usually axonotmesis)
uncommon causes (chemical, heat, radiation)
Wallerian degeneration
- takes 2-3 weeks
- nerve distal to injury site degenerates and is phagocytized.
- proximal axon regresses, forms growth cone
- process coordinated by Schwann cells
Axon regrowth requires what 4 things?
1) clearing of old neuron (Wallerian degeneration)
2) a conducive environment (from the Schwann cells)
3) a physical conduit (intact epineurium)
4) no physical obstruction (ABSENCE of glial scar)
Is the final repaired axon/synapse pattern exactly the same as pre-injury?
No. is similar to the original but never reconstitutes the original complexity
Nerve repair in CNS
1) wallerian degeneration similar to in PNS
2) No Schwann cells, debri cleared by microglia and astrocytes
3) instead of creating conducive envir., glia overproliferates and forms glial scar that are a physical barrier to axon regrowth ***
Neurogenesis in CNS
1) very little if any
2) neurogenesis observed in olfactory bulb (smell) and hippocampus (memory) in lower animals
3) neurogenesis only observed in hippocampus in humans
Hebb’s postulate
Basically if input and output correlate it stays and strengthens.
if different it weakens and changes.
Long-term potentiation
synapses with synchronous or high-frequency firing are strengthened.
*can be modulated by chemical channels
Long-term depression
synapses associated with excessive stimulation are down-regulated.
*can be modulated by chemical channels
General principles of plastiity (based on what, limited resources, limited to what?)
- develops based on feedback from experience
- limited resources so all specialization comes at a cost to other cortex
- plasticity is limited to “nearby” cortex (horizontal connections)
Neuromuscular junction
- nerves synapsing directly on muscles
- affected by diseases to muscles, proteins, neurotransmitters
Peripheral nerves
- relatively consistent in their location and innervation
- innervate specific areas of body
- little overlap
Peripheral plexuses
- “reorients” nerves
- because it mixes multiple nerves together, can caused deficits
Spinal roots
- collect all sensory/motor input from a level
- sensitive to pathology around bony spine
Lower vs upper motor neuron
Lower motor neuron synapses on the muscle
upper motor neuron from descending pathways
*injury to each produces classic syndromes
Motor unit organization
- each motor neuron innervates multiple muscle fibers
- usually all contained within one muscle
- each muscle fiber only innervated by one motor neuron
- motor units vary in size and number of contacts
- depolarizing neuron generally activates all connected fibers
Fiber types
Type 1: slow twitch
-low force, non-fatiguable, oxidative metabolism
Type IIa: fast fatigue-resistant
-intermediate
Type IIb: fast twitch (fast fatiguable)
- strong force, high fatiguable, energy from ATPase
Size principle
- slow twitch activated first
- increasing force requires larger unit recruitment
motor unit response to stimulation
after injury: motor unit organization degenerates
after chronic stim: fiber types can adapt
spinal cord organization: White matter
- descending tracts
- inter-level connections
spinal cord organization: Grey matter
- alph-motor neurons
a) medial: axial
b) lateral: appendicular
c) span across multiple spinal levels - interneurons
spinal cord organization: Ventral roots
- exiting motor nerve fibers
- combine with posterior sensory fibers to form spinal root
- exit through bony foramina
Lower motor neuron syndromes
- flaccid paralysis
- hyporeflexia
- atrophy (use it or lose it)
- fibrillations
- fasciculations
fibrillations vs fasciculations
Fibrillations: spontaneous electrical activity in muscles (seen on EMG)
Fasciculations: Spontaneous gross muscle contraction (occur in unorganized pattern)
Muscle spindle (what are the parts sensitive to?)
Group 1a: sensitive to dynamic stretch
Group II: sensitive to static stretch
Gamma-motor neurons - spindle gain
** responsible to stretch reflex
Golgi tendon organ GTO (sensitive to what? and prevents what?)
Group Ib sensory fibers - sensitive to muscle contraction
***prevents overexertion of muscles
Flexion/Crossed-extension reflex (what happens?)
1) input from nociceptive pathway (pain)
2) ipsilateral flexion (withdrawal)
3) contralateral extension (support)
