Neuro (Part 2) Flashcards
Motor control
Cortex
Basal nuclei
Cerebellum
Dorsal root
Sensory
Ventral root
Motor
Antagonistic muscle
Extensor vs. flexor
Motor unit
Single alpha motor neuron and all muscle fibers it ennervates
Motor pool
Group of alpha motor that innervate muslce
Muscle spindle
Stretch detectors
Innervated by 1a afferent sensory neurons
Extrafusal fibers
Generate force and movement
Innervated by alpha motor neuron
Intrafusal fibers
Respond to muscle movement
Innervated by gamma motor neurons
Golgi tendon
Monitor tension to prevent muscle
Innervated by type 1b afferent
Divergence
I signal to multiple areas
ex. leg withdrawal
Convergence
Multiples neurons meet
Involved interneurons
Reverberating circuit
Maintain input through excitatory, positive feedback
ex. working memory
Rhythmic circuit
Switch between activating and inhibiting
ex. Walking, stance vs. swing
Primary primary cortex
Somatopically organized
Project to spine
Cross over laterally
Control small groups of muscle
Supplementary motor cortex
Programming and coordinating
Planning and executing
ex. rehearsing
Premotor cortex
Set related neurons fire before and until action completed
Planning and execution
Posterior parietal cortex
Integrates visual info for movement i.e. depth perception
Cerebellum
Initiation, coordination and modulation based on sensory input
Made up of parking cells with dense dendrites
Climbing fibers
Strong pathways in cerebellum
Parallel fibers
Weaker pathways in cerebellum
Basal nucleus
Planning and execution
D1 neurons
Promote action
D2 neurons
Indirect, inhibit action
Basal nuclei VS Cerebellum
Basal nuclei is higher order aspect of movement
Cerebellum is execution of movement
Parkinson’s Disease
Symptoms: reduced and slowed movement, 3 Hz tremor
Cause: loss of dopaminergic neurons in substantial nigra
Treatment: L-Dopa, DBS
MPTP
Kills dopamine neurons - Parkinson’s like symptoms
Huntington’s disease
Symptoms: involuntary movements, cognitive impairment, mood disorders
Cause: CAG repeats, polyglutamine disease, autosomal dominant
Treatment: gene therapy, stem cells
Tardive dyskinesia
Symptoms: involuntary movement, cognitive impairment, mood disorders
Cause: long term use of antipsychotics leads to dopamine hypersensitivity
Treatment: discontinue antipsychotics
Somatic VS. Autonomic
Somatic: voluntary, peripheral, monosynaptic
Autonomic: involuntary, central, disynaptic, direct inhibition
Sympathetic VS Parasympathetic
Sympathetic = fight or flight, more organ innervation, ACh then NE
Parasympathetic = rest and digest, less organ innervation, ACh then ACh
Dually innervated
Adrenal gland
Cortex = endocrine glan
Medulla = chromatffin, excitable neuroendocrine
Enteric nervous system
Myenteric plexus - outer, gut motility
Submucosal - inner, gut secretions
Heart experiment
Heart submerged in ACh bath without electricity still functioned - chemical signals, discovery of ACh
Hormone pathway
Hypothalamus release hypophysiotropic hormone to pituitary
Pituitary release anterior pituitary hormone to gland
Gland release third hormone to target
Anterior pituitary
Gland
Growth, metabolism, reproduction
Posterior pituitary
Neural tissue
Water balance, birth + lactation
Pineal gland
Secretes melatonin, internal clock
Explicit/declarative memory
Semantic - facts
Episodic - autobiographical
Implicit/Non-declarative memory
Skills
Conditioning
Ranges of memory
STM (5-7 units)
ITM
LTM
vLTM
Anterograde amnesia
Cannot form new memories
Retrograde amnesia
Can’t remember past
Hippocampus
Trisynaptic pathway with pyramidal neurons
Perforant pathway
Entorhinal cortex to granule cells in dentate gyrus
Mossy fiber
Granule cells to CA3
Schaffer collaterals
CA3 to CA1
HM
Removal of bilateral hippocampus led to anterograde amnesia and retrograde amnesia
Able to learn
EP
Encephalitis damaged medial temporal lobe
Anterograde amnesia
Semantic and episodic memories from earlier in life in tact
Morris Water Maze
animals learn to find platform, even without platform
can’t learn with hippocampal lesions
Age & LTM
Age disrupts LTM
Pavlovian conditioning
Contextual - learn to fear environment
Cued - learn to fear sound
New environment - no fear until sound cue
Hippocampal lesion, slow to learn but able to learn fear over time
Long term potentiation
Encoding of memories
Hebb’s postulate
Cells that fire together, wire together
Synaptic strength increases
Rapidly induced, cooperatively, associativity
Cooperativity
Must reach threshold
Associativity
Activation of strong pathway can boost weak pathway
Tetanus
High frequency stimulation which can strengthen EPSP
AMPA receptors
Faster, depolarized by influx of Na+
NMDA receptors
Slower, depends on AMPA, blocked by Mg2+
Removal of Mg2+ block
Na+ influx causes depolarization, repulsion of positive charges removes Mg2+
Elevation of Ca2+
Necessary for LTP
Ca2+ and Calmodulin
CAMKII depends on Ca2+ and calmodulin, open active site, persistently open
CAMKII
Activates AMPA receptors through phosphorylation
Recruits AMPA receptors
Memory consolidation
Encoded over time with lability which decreases over time
Labile stage
Memory is sensitive to post-experience at first but overtimes, less disruptablee
Range of LTP
E-LTP to L-LTP, depends on amount of high frequency
LTM
Requires new proteins
CREB
Promotes new proteins
Autism
Lack of specific proteins
Fragile X
Excess methylation, spindly neurons
mGluR
Target for synaptic plasticity
Plays roles in LTD