Nervous System, Neurons, and Neurotransmitters Flashcards
Nervous system breakdown
Nervous system:
1. Central nervous system (CNS)
2. Peripheral nervous system (PNS)
PNS:
1. Somatic nervous system (SNS)
2. Autonomic nervous system (ANS)
ANS:
1. Sympathetic nervous system
2. Parasympathetic nervous system
Central nervous system (CNS)
Brain and spinal cord
Peripheral nervous system (PNS)
Signals between the CNS and rest of the body
Somatic nervous system (SNS)
- Signals between CNS and skeletal muscles
- Voluntary actions
Autonomic nervous system (ANS)
- Signals between CNS and smooth muscles, organs
- Involuntary actions (unless learned to control through biofeedback)
Sympathetic nervous system
- Prepares body for action (fight-or-flight)
- Can cause rapid physiological changes
Fight-or-flight physiological changes
- Pupil dilation
- Sweating
- Increased heart rate
- Increased respiration rate
- Inhibited digestion
- Inhibited sexual activity
Parasympathetic nervous system
- Returns body to resting state (after fight-or-flight)
Two types of cells in nervous system
- Neurons
- Glia
Neurons function
Communicates information within nervous system
Glia function
Provides neurons with structural support, insulation, and nutrients
Neuron structural components
- Dendrites - receives information
- Soma (cell body) - contains classic cell parts (nucleus, mitochondria, etc.)
- Axon - transmits information
Myelin
- Produced by glia
- Insulates some neuron axons
- Speeds up conduction between neurons
Two processes driving communication in CNS
- Conduction
- Transmission
Conduction in the CNS
Electrochemical process:
Cell rests (negatively charged)
>
Dendrites stimulated
>
Cell membrane channels open
>
Sodium ions enter
>
Cell depolarized (less negative)
>
Action potential triggered
Action potential
- Electrical impulse
- All-or-none responses (intensity of a stimulus not based on action potential intensity but number of action potentials)
Transmission in the CNS
Typically chemical process (AKA synaptic transmission):
Action potential reaches axon terminal >
Neurotransmitter released to synaptic cleft
>
Neurotransmitter produces effect on postsynaptic neuron
>
Neurotransmitter inactivated
Neurotransmitter inactivation
- Can be reabsorbed into presynaptic neuron
- Can be broken down by enzymes
Neuroplasticity
The brain’s ability to change in structure and function throughout development and in response to life experiences
Four types of neuroplasticity
- Homologous area adaptation
- Cross-modal reassignment
- Map expansion
- Compensatory masquerade
Homologous area adaptation
If brain area damaged early, functions shift to corresponding area in opposite hemisphere, can lead to less function in corresponding area
e.g., left parietal lobe takes over for damaged right parietal lobe
Cross-modal reassignment
If sensory brain area deprived of stimuli, function in that area changes
e.g., blindness leads to “somatosensory input” (visualizing mentally) in that area
Map expansion
Temporary or permanent enlargement of a cortical area, usually when learning a new skill
e.g., practicing an instrument
Compensatory masquerade
If brain area damaged, person will use another brain area with function that compensates for lost function
e.g., using memory of landmarks to compensate for loss of visuospatial ability
Two types of neurotransmitters
- Small-molecule neurotransmitters
- Neuropeptides
Based on size and synthesis
Small-molecule neurotransmitters
- Smaller
- Synthesized and stored in axon terminal
Neuropeptides
- Larger
- Synthesized in cell body and transmitted to axon terminal
Two types of neuropeptides
- Enkephalin
- Endorphin
Both endogenous opioids with analgesic and euphoric effects
Dopamine
- Excitatory or inhibitory
- Movement, personality, mood, sleep
Parkinson’s and dopamine
Low dopamine in substantia nigra
Tourette’s and dopamine
High dopamine in caudate nucleus
Schizophrenia and dopamine
High dopamine activity (according to dopamine hypothesis)
Four types of dopaminergic pathways
- Mesolimbic
- Mesocortical
- Tuberoinfundibular
- Nigrostriatal
Mesolimbic dopaminergic pathway
- Begins in ventral tegmental area (evidence that dorsolateral prefrontal cortex signals motivation for reward)
- Ends in ventral striatum (nucleus accumbent)
- Reward circuit (e.g., substance use)
Mesocortical dopaminergic pathway
- Begins in ventral tegmental area
- Ends in prefrontal cortex
- Emotion, motivation, executive function
Tuberoinfundibular dopaminergic pathway
- Begins in hypothalamus
- Ends in pituitary gland
- Hormone regulation, inhibits prolactin
Nigrostriatal dopaminergic pathway
- Begins in substantia nigra
- Ends in dorsal striatum (caudate nucleus and putamen)
- Purposeful movement
Acetylcholine
- Excitatory or inhibitory
- Movement (muscle contraction), arousal, attention, memory
Myasthenia gravis
Autoimmune disorder
Muscle weakness due to destruction of acetylcholine receptors at neuromuscular junctions
Acetylcholine and Alzheimer’s
Low acetylcholine in entorhinal cortex and hippocampus related to early memory loss
Glutamate
- Excitatory
- Movement, emotions, learning, memory
Glutamate-induced excitotoxicity
Excessive glutamate
Can cause cell damage and death
Linked to stroke, seizures, neurogenerative disorders (Huntington’s, Alzheimer’s)
Norepinephrine
- Excitatory
- Arousal, attention, learning, memory, stress, mood
Norepinephrine and mood
- Low norepinephrine = depression (based on catecholamine hypothesis)
- High norepinephrine = mania
Serotonin
- AKA 5-HT
- Inhibitory
- Arousal, sleep, sexual activity, mood, appetite, pain
Serotonin and related disorders
Low serotonin:
1. Depression
2. Suicide
3. Bulimia
4. OCD
5. Migraines
High serotonin:
1. Anorexia
2. ASD
3. Chronic schizophrenia w/ large ventricles and/or cerebral atrophy
Gamma-aminobutyric acid (GABA)
- Inhibitory
- Memory, mood, arousal, sleep, motor control
GABA and related disorders
Low GABA:
1. Insomnia
2. Seizures
3. Anxiety
4. Huntington’s
GABA and Huntington’s disease
Degeneration of GABA and acetylcholine cells in basal ganglia contribute to motor symptoms
Psychoactive drug classes
- Agonists
- Partial agonists
- Inverse agonists
- Antagonists
Agonists
Mimic or increase effects of neurotransmitter
Direct = increase neurotransmitter by binding to receptor site and acting as the neurotransmitter
Indirect = increase neurotransmitter without binding to receptor site
Partial agonists
Produce similar but weaker effects than neurotransmitter/agonist
Inverse agonists
Produce opposite effects to neurotransmitter/agonist
Antagonists
Block or reduce effects of neurotransmitter/agonist
Direct = A
