Lecture 8 Flashcards
Gray matter
Cortex and deep nuclei
White matter
Tracts (axons + myelin)
Precentral gyrus
Frontal lobe responsible for motor control
Postcentral gyrus
Parietal lobe, for somatic sensory input from receptors in skin and muscles, somatosensory cortex
Tempura lobe
Auditory centers
Occipital lobe
Primary area responsible for vision and coordinating eye movement
Insula
Encoding of memory and integration of sensory information with visceral responses, receives refectory, gustatory, auditory, and pain info
Histamine
Promotes wakefulness
Adenosine and GABA
Promote sleep
Serotonin
Reduces REM sleep, stimulates non-REM sleep
ACh
Promotes wakefulness
Norepinephrine
Wakefulness and alertness (fight or flight)
REM sleep
Dreams occur, lambic system active, respiratory and heart rate irregular, consolidation of nondeclaritave memories
Non-rem sleep
Allows for metabolic repair and synaptic plasticity, respiratory and heart rate regular, consolidation of spatial and declarative memories
Parkinson’s disease cause
Degeneration of dopaminergic neurons from the substantia nigra to the corpus striatum
Motor circuit mechanism
Globus pallidus sends inhibitory GABA releasing neurons to thalamus which sends excitatory axons to the motor cortex of the cerebrum
This process allows for the stimulation of the appropriate movements and inhibits unwanted movements
Brocha’s area
Controls motor aspects of speech
Brocha’s aphasia
Slow, poorly articulated speech but no impairment in understanding
Wernicke’s area
Controls understanding of words
Wernicke’S aphasia
Production of rapid speech with no meaning “word salad”
Language comprehension is destroyed
Lambic system
Along w hypothalamus plays important role in emotion
CASH
Cingulate gyrus, amygayla, septal nuclei, hippocampus
Cingulate gurus
Lambic system, unpleasant stimuli/pain
Amygdala
Lambic system, memory/fear/anger
Hippocampus
Memory, lambic system
Septal nuclei
Addiction, reward, lambic system
Working memory
Very short-term, pre frontal cortex
Alzheimer’s disease
Most common type of dementia
Alzheimer’s cause
Loss of cholinergic fibers in the hippocampus and cerebral cortex, accumulation of plaque, accumulation of intracellular proteins forming neurofibrillary tangles
LTP
High frequency stimulus required, glutamate is released presynaptically and binds to the NDMA receptor, mg2+ is blocking NDMA pore, mg2+ removed by glutamate or d-serine activating AMPA receptors depolarizing the postsynaptic cell, with the mg2+ removed Na+ and Ca2+ enter the cell, Ca2+ inserts more AMPA receptors into the membrane, Ca2+ binds to transcription factor CREB and causes expression of genes necessary for adding dendritic spines and additional receptors
Lip change to synapse
Long term structural change
Regulating LTP
NO released into the synapse allows presynaptic axon to change so more glutamate is released increasing LTP
Endocannabinoids lift inhibition from GABA releasing neurons on the synapse strengthening it
Epithalamus
Choroid plexus → CSF
Pineal gland → melatonin
Reticular activating system
Pons + reticular formation, ascending arousal system
Arousal hormones
Polypeptide hormones, orexin, hypocretin-1
RAS inhibition
During sleep Neurons from hypothalamus release GABA to inhibit arousal pathways
Corticospinal tracts
Located in motor cortex, most fibers decussate, involved in voluntary motor control
Extrapyramidal tract
Originate in brain stem, important for initiating body movements
Components of a reflex arc
Sensory receptor, sensory neuron, synapse/ integrating center, motor neuron, effector (muscle or gland that responds)
