09. L8-14 Brain and NS Flashcards
Long-term potentiation
long-lasting strengthening of synaptic connections due to high frequency stimulation / activation
Long-term depression
long-lasting weakening of synaptic connections due to low frequency stimulation / activation
Glutamate
Main excitatory neurotransmitter in the nervous system. Involved in learning and memory.
GABA
Gamma-amino butyric acid, main inhibitory neurotransmitter in the nervous system. involved in calming the stress response/slowing physiological arousal
Excitatory neurotransmitter
makes post-synaptic neuron more likely to fire an action potential
Inhibitory neurotransmitter
makes post-synaptic neuron less likely to fire an action potential
Lock and Key process
process of neural communication in the synapse (between neurons)- “key” is neurotransmitter, “lock” is receptor site
synapse
includes 3 key components- synaptic gap, pre-synaptic terminal button, and post-synaptic dendrite
Classical conditioning
Learning model. Unconscious in nature/ involuntary process of creating an association between two previously unrelated stimuli
Neutral stimulus (NS)
elicits no relevant response before conditioning
Unconditioned stimulus (UCS)
elicits reflexive/involuntary response before conditioning
Unconditioned response (UCR)
reflexive/unconscious response to UCS before conditioning
Conditioned stimulus (CS)
previously the neutral stimulus, produces learned response AFTER conditioning
Conditioned Response (CR)
learned response to CS after conditioning
Operant conditioning
voluntary/conscious behaviour learned by associating antecedent with behaviour and resulting consequence
Antecedent
discriminative stimulus - precedes or prompts the learner’s behaviour
Behaviour
voluntary action of learner, comes after antecedent
Consequence
applied after behaviour- can be reinforcement or punishment to increase or decrease the likelihood of behaviour being repeated.
reinforcement
increases likelihood of behaviour being repeated in future
punishment
decreases likelihood behaviour being repeated in future
Positive reinforcement
ADDITION of POSITIVE stimulus
negative reinforcement
REMOVAL of negative/aversive stimulus (positive outcome for learner)
Plasticity
Neural plasticity refers to the manner in which the brain changes in response to stimulation from the environment.
positive punishment
ADDITION of NEGATIVE stimulus
negative punishment (response cost)
REMOVAL of positive/desirable stimulus (bad outcome for learner)
5 stages of developmental plasticity
Proliferation
Migration
Synaptogenesis
Synaptic Pruning
Myelination
adaptive plasticity
Neural changes due to one or more of the following:
* A change in the environmental conditions (i.e., adapting to environmental changes)
* Learning new concepts
* Re-learning something after brain injury.
2 types of adaptive plasticity
sprouting
New dendrites grow to enable new connections between neurons after damage
rerouting
Neurons near damaged area seek new active connections with healthy neurons
Proliferation
unborn baby’s neurons divide and multiply at a rapid rate
Migration
new neurons in the foetus and newborn move to their location in Nervous System
Myelination
development of thick myelin sheaths which speeds up neural transmission (i.e., makes messages more efficient). This process continues through to very late adolescence.
Synaptogenesis
creation of multiple connections between neurons.
Synaptic Pruning
the removal of connections that have not formed strong pathways and are no longer needed
Traumatic Brain Injury (TBI)
- type of ABI that occurs when an *external force causes damage to the brain. *
- brain slams against the inside of the skull- brain tissue may bleed, bruise, stretch, tear, twist or become swollen.
Non-traumatic brain injury
damage to the brain caused by internal factors, e.g. lack of oxygen (stroke), tumor, or degenerative disease
Parkinson’s Disease
neurodegenerative disease classified by death of dopamine-producing neurons in the substantia nigra, leading to motor and non-motor symptoms
Dopamine
neurotransmitter involved in motivation and voluntary movement
Biological underpinnings of Parkinson’s disease
- Dopamine-producing neurons in the substantia nigra die/degenerate,
- leading to less Dopamine production and less available for Basal Ganglia-
- therefore slowed and less coordinated motor movements (motor symptoms)
Epilepsy
Gut-brain axis
Bi-directional relationship between the brain (CNS) and gut (digestive tract/enteric NS). Gut microbiota impacts brain functioning, mental health, stress etc (and vice versa)
Concussion
type of traumatic brain injury caused by a blow to the head or by a hit to the body that causes the head and brain to move rapidly back and forth.
This sudden movement can cause the brain to bounce around or twist in the skull, disrupting neuronal activity and sometimes stretching and damaging brain tissue and cells.
Chronic traumatic encephalopathy (CTE)
neurodegenerative disease caused by repeated blows to the head/ repeated concussions. Leads to significant memory deficits, cognition problems, and mental health disorders including depression and suicide ideation.
Neurofibrillary tangles
Build up of Tao proteins INSIDE neurons (within axon) which cause a tangle/clump to form that blocks transmission and leads to neuron death
Motor symptoms of parkinson’s disease
Tremor, rigidity, poor balance, poor posture, slowed motor movement (Bradykinesia)
Non-motor symptoms of Parkinson’s disease
sleep issues, fatigue, cognitive decline, depression and anxiety
Sensitive period
the period of time when an organism is more responsive to certain stimulation
Critical period
the narrow period of time where development is preprogramed for learning to occur. If learning does not occur in this window, it will never occur.
