Concepts/Pathways Flashcards
What is the difference between ischemia and infarction.
Ischemia is the reduction of blood flow to an organ. Below what is needed for normal metabolism.
Infarction is what results from prolonged ischemia. It is the end point where the cells die.
What is an acoustic neuroma?
An acoustic neuroma is a noncancerous growth that develops on the eighth cranial nerve. Also known as the vestibulocochlear nerve, it connects the inner ear with the brain and has two different parts. One part is involved in transmitting sound; the other helps send balance information from the inner ear to the brain.
What is the difference of a focal lesion and diffuse lesion + examples of signs and lesions
A focal lesion is an infection, tumor, or injury that develops at a restricted or circumscribed area of neural tissue. These produce focal neurological signs.
- example of focal lesion signs
1. Loss of pain and temperature on half the face
2. Loss of the ability to repeat a spoken word
3. Loss of vision in one eye
Diffuse or general lesions: Neurodegenerative diseases (advanced Parkinsons disease), psychiatric disorders, inflammatory disorders, infections, malnutrition, genetic disorders, compression of the brain.
examples of non focal:
headache, tiredness, confusion, disorientation.
What are the 6 kinds of time courses and examples?
- Episodic - migraines, seizures
- recent onset and episodic - expanding brain tumor
- Relapsing, remitting - multiple sclerosis
- Sudden onset, lasting deficits - stroke
- Slow, progressive - neurodegenerative diseases
- Progressive over short time period - expanding tumor
Describe the series of events in an action potential
- Enough graded potentials activate voltage gated sodium channels (-50mV)
- Sodium influxes, the neuron depolarizes significantly.
- Then the sodium channels close and potassium channels open, hyperpolarizing until the voltage gated potassium channels close.
- inactivated sodium channels are no longer inactive.
With all the exocytosis at the nerve terminal, wouldn’t the membrane be huge?
There is a process of endocytosis to remove membrane from the nerve terminal.
Adaptor proteins connect clathrin to vesicular membrane forming clathrin coated pits.
Clathrin assemble into coat, curving membrane.
Dynamin ring comes and pinches off membrane.
Coated vesicle is then moved away from terminal along the actin filament
Hsc70/Auxillin - remove the clathrin. Can start storing NT again
How are neurotransmitter regulated?
Can increase (facilitate) or decrease (inhibit) neurotransmitter release
Autoreceptor - feedback regulation – binding of transmitter inhibits its
own further release
Excess released neurotransmitter can be inactivated by:
- Reuptake by specific transporters.
-Degradation by specific enzymes
• Acetylcholine (acetylcholinesterase) • Catecholamines (MAO; COMT) • Neuropeptides
-astrocytes at a tripartate synapse: Metabolize neurotransmitters (GABA, glutamate, serotonin, etc.)
Glutamate
The major excitatory neurotransmitter in the CNS • Contained in approximately 50% of all neurons, and virtually all
excitatory neurons.
• Post-synaptic receptor type:
Metabotropic: May be excitatory or inhibitory, depending on the state of
the neuron.
• Ionotropic: NMDA (N-methyl-D-aspartate), kainate and AMPA. **All
excitatory
NMDA is both a voltage-gated and ligand-gated Ca2+ ion channel • The receptor is blocked by Mg2+ at resting membrane potential
• Uses the AMPA receptor and influx of Na+ to depolarize the membrane
to remove the Mg2+ block
It is both a voltage-gated and ligand-gated Ca2+ ion channel • The receptor is blocked by Mg2+ at resting membrane potential
• Uses the AMPA receptor and influx of Na+ to depolarize the membrane
to remove the Mg2+ block
NMDA activation in the presence of depolarization, enables
Ca2+ to enter cell.
• Increased intracellular [Ca2+ ] can activate calcium-dependent
signaling cascades.
• Intracellular signals can produce long-term synaptic changes
that are important for
• development of synapses • regulating neural circuits • learning and memory (Long-term potentiation; LTP)
• Long-term changes include changes in dendritic spines and
insertion of AMPA receptors: Increased responsiveness of post-synaptic neurons after repeated stimulation of neurons (e.g., in hippocampus).
.
•
Glutamate excitotoxicity:
Trauma and disease that impair ATP-generation can cause
increased glutamate release or decreased glutamate reuptake.
• Glutamate NMDA channels allow Ca2+ to leak into cells.
• Increased Ca2+ causes increased water uptake and stimulation of
intracellular enzymes that degrade proteins, lipids, and nucleic acids
• Examples of conditions thought to be associated with
glutamate toxicity: ALS, Alzheimer’s, tumors, oxygen
deficiency, ischemia, trauma, repeated seizures.
GABA
Major inhibitory neurotransmitter of the CNS • Contained in about 30% of CNS neurons
- Post-synaptic receptor type:
- Ionotropic: GABAa receptor, GABA gated Cl-channel
- Metabotropic: GABAb functionally linked to potassium or calcium ion channels
Dopamine
3 pathways
Mesolimbic pathway: -Reward pathway (addiction)
- Schizophrenia
- Depression
Nigrostriatal Pathway: Control of movement
-Parkinson’s disease
Mesocortical pathway:
Working memory
Schizophrenia
ADHD
Involved in reward-motivated
behavior and motor pathways
CNS- Neurons originate in
brainstem regions (ventral
tegmental area and substanstia
nigra) 46
Drugs that influence dopamine transmission: • Anti-psychotics (-) • Nicotine, cocaine,
methamphetamine (+) • Amphetamines (Adderall) (+) • Methylphenidate (Ritalin) (+)
Acetylcholine
Main neurotransmitter in the PNS and ANS, but also has
neuromodulator functions in CNS
• PNS- Neuromuscular junctions
• ANS- sympathetic (pre-) & parasympathetic (pre- & post-
ganglionic) neurons
• CNS- Neurons originate in the basal forebrain (nucleus basalis)
and the brainstem (dorsolateral midbrain-pons) and have
widespread connections to the cortex
- Involved in arousal, attention, memory and motivation • Nucleus basalis degenerates in Alzheimer’s disease
- Associated with memory loss, personality change and dementia
Drugs that influence ACh transmission in the CNS: • Nicotine (on nictotinic
receptors) (+) • Atropine (-) • Scopolamine (-)
Describe the general rules for herniated discs and the nerves they impinge
So in the cervical vertebrae, because the corresponding nerve exits above the vertebrae, a C5-C6 herniated disc impinges on C6 nerve.
In the lumbar its the same but for a different region. The interventricular foramen is large so the corresponding spinal nerve exits above the disc.
So an L4-L5 herniation will not impinge onf the L4 nerve but rather the L5 as it is traveling in the cauda equina. Impinging the L5 nerve.
Terms for weakness, the 4 P’s
Paralysis: weakness so severe that a
muscle cannot be contracted.
• Paresis: weakness, or partial paralysis.
• Plegia: severe weakness or paralysis.
– e.g., Diplegia refers to bilateral lower limb
weakness. Quadriplegia to all 4 limbs. – Hemiplegia refers to one side of the body
weakness (arm and leg)
• Palsy: imprecise term for either weakness
or no movement.
Explain the scoring for muscle strength.
Interpret the scoring for spinal cord stretch reflexes
.0/5 No contraction
1/5 Muscle flicker, no movement
2/5 Movement, but not against gravity 3/5 Movement against gravity, but not against resistance
4/5 Movement against some resistance 5/5 Normal
0+ absent 1+ trace 2+ normal 3+ brisk 4+ non-sustained clonus 5+ sustained clonus 1-3 can look normal so always refer to opposite side for asymmetry or even with upper and lower
Describe the receptor, circuit and functions of the stretch reflex, golgi-tendon
reflex and flexor withdrawal reflexes.
.Stretch reflex - 1. Muscle stretch receptor excited (connected to Ia afferent) 2. Ia afferent makes an excitatory synapse onto quadriceps motor neurons,
causing muscle contraction
3. Ia afferent also makes an excitatory synapse onto an inhibitory interneuron,
which inhibits hamstring (flexor) motor neurons
(L3,L4)
Golgi tendon reflex
Stimulus: Muscle tension Circuit: GTO > lb > lb inhibitory interneuron > motor neuron to homonymous muscle
(also excites antagonist muscles)
Flexor withdrawal - stimulated leg flexes to withdraw after cutaneous receptor activated > cutaneous afferent fiber from nociceptor alpha, < activates interneurons which inhibit the extensors and activate flexor in pained foot > for opposite foot the opposite happens, extensor activated, flexor inhibited to stand
Describe the function of a central pattern generator.
Central pattern generators (CPGs) are biological neural networks that produce rhythmic patterned outputs without sensory feedback. … CPGs have been shown to produce rhythmic outputs resembling normal “rhythmic motor pattern production” even in isolation from motor and sensory feedback from limbs and other muscle targets.
Central pattern generators are neuronal circuits that when activated can produce rhythmic motor patterns such as walking, breathing, flying, and swimming in the absence of sensory or descending inputs that carry specific timing information.
