6 - neurophysiology Flashcards
compare the effects of the sympathetic vs parasympathetic nervous systems on cardiac muscle
PARASYMPATHETIC
• in cardiac muscle, there are M2 receptors
• activated by ACh released from vagus nerve
• causes activation of G(l) protein —> inhibits adenyl cyclase —> inhibits production of cAMP —> activation of K+ channels —> K+ out of cell (hyperpolarisation) —> takes longer to reach threshold —> lower HR
SYMPATHETIC
• noradrenaline from sympathetic nerve activates beta-1 receptors
• activates G(s) protein
• different second messenger to increase HR
using a diagram, describe the effect of sympathetic and parasympathetic activation on the following organs: heart, brain, lungs, blood vessels, urinary bladder, liver.
redraw that diagram he used a billion times in the leccys
draw the structure of the ANS
CNS pre-ganglionic fibre autonomic ganglion (neurotransmitters + modulation of signal) post-ganglionic fibre varicosity (neurotransmitter) effector organ
using a diagram, describe how specific receptors control
heart rate
:P
what is the function of the autonomic ganglia
to either enhance or reduce a signal
list the different forms of motility in the GIT and with one sentence for each describe the functional importance.
1) gastric mixing
2) segmentation
– move chyme in both directions which allows greater mixing with the secretions of the intestines
3) peristalsis
– propulsion of bolus
4) migrating motor complex
– moves undigested remains to large intestine in between meals to empty stomach for next meal
– responsible for the rumbling experienced when hungry
describe the mechanism of defecation
parasympathetic nerve involved in contraction of smooth muscle (internal sphincter) which results in defection —> automatically controlled (early development)
later in development, gain control over external sphincter using skeletal muscle and motor neurons —> voluntary control
using a simple diagram explain how stress affects the sympathetic nervous system and the HPA axis
XD
using a diagram explain how olfaction affects different structures within the brain
B~D
justify this statement: the sympathetic nervous system and pituitary gland maintain homeostasis
hypothalamus and pituitary gland function to maintain homeostasis
they respond to changes in the body by releasing hormones and activating sympathetic/parasympathetic NS
how does negative feedback fail during chronic stress?
- more and more cortisol release
- neg. feedback begins to fail
- glucocorticoid receptors on hippocampus
• hippocampus logically controls stress response —>
suppresses cortisol
- over-excitation due to cortisol = suppression form hippocampus fails
- chronic stress leads to destruction of hippocampus —> memory loss + alzheimers + dementia
draw and described in order - the molecular events from motor neuron action potential generation through to the generation of a muscle action potential
1) AP arrives at motor nerve terminal
2) AP triggers the opening of VG Ca2+ channels = entry of Ca2+
3) Ca2+ dependant release of acetylcholine (ACh) from synaptic vesicles (exocytosis)
4) ACh traverses the synaptic cleft to bind to its receptor a ligand gated Ion channel (AChRs)
5) binding causes opening of this ion channel = large movement of Na+ in and a small movement of K+ out of the muscle cell = depolarisation
6) current flow between the depolarised post-synaptic membrane and adjacent membrane of muscle
7) local current flow opens voltage gated Na+ channels in the adjacent membrane
8) the resulting entry of Na+ causes the resting MP to rise from ~ -70 mV to -60mV = generation of a muscle action potential
9) ACh is subsequently destroyed by acetylcholine-esterase (enzyme in synaptic cleft)
what is the latent period?
muscle APs last for only 1 to 2 ms, whereas the muscle contraction that results can last about 50 ms
latent period = time delay between stimulation and contraction
what is myasthenia?
disease which causes the drop in the number of post-synaptic AChRs to such a level that causes muscle weakness
what is lambert-eaton syndrome?
auto immune self antibodies to the pre- synaptic voltage gated calcium channels
poor pre-synaptic release of neurotransmitter - leads to neuromuscular block
causes muscle weakness
what is spinal muscular atrophy ?
an autosomal recessive disease caused by a genetic defect in the SMN1 gene, which encodes SMN, a protein
widely expressed in all eukaryotic cells
SMN1 is apparently selectively necessary for survival of motor neurons
causes muscle weakness
what is the consequence of a mutation in the dystrophin gene
mutation in the dystrophin gene = no dystrophin (anchors muscle fibre to extracellular matrix)
dystrophin supports muscle fibre strength
absence of dystrophin reduces muscle stiffness, increases sarcolemmal deformability, and compromises mechanical stability
what is a motor unit?
briefly compare small and large motor units
motor unit = 1 motor neuron the number of muscle fibres it innervates
small motor units = fine control but weaker muscle contraction
large motor units = larger muscle contraction
state and explain henneman’s size principle
for a given synaptic input, motor neurons with the smallest cell bodies are activated 1st & large motor neurons are activated last
smaller neurons have higher membrane resistance and require lower depolarising current to reach spike threshold
small motor-neurons innervate small motor unit
large motor-neurons innervate large motor unit
compare the three types of motor fibres
TYPE I: – small MN – slow twitch – fatigue resistant – slow oxidative – low myosin ATPase activity
TYPE IIA: – medium MN – fast twitch – fatigue resistant – fast oxidative
TYPE IIX: – large MN – fast twitch – fatigable – fast glycolytic – high myosin ATPase activity
how does chronic denervation–reinnervation of muscle lead to fibre type grouping, type I in particular?
chronic denervation re-innervation events lead to type 1 fibre predominance
fast motor neurons die first
de-inervated tissue pumps out GFs
∴ local sprouting and expansion of surviving slow MNs
type I now dictates fast-twitch fibres
what do muscle spindles detect?
how are muscle spindles kept taut?
muscle spindles detect ∆length of muscle
spindle must always remain taut to maintain sensitivity to ∆length
gamma MN act on spindles to maintain their sensitivity during muscle contraction
what are golgi tendon organs and what do they detect?
golgi tendon organs are located in the tendinous insertions of muscle
detect changes in muscle tension
activated by increases in muscle tension and thus measure the degree of tension/load that the muscle is under
draw and briefly describe five types of interneuronal circuits
DIVERGENCE
black MN excite inhibitory MN —> no firing
white MN excite excitatory MN —> firing
withdrawal reflex
CONVERGENCE
many motorneurons excite the same MN
brain stem / cortex inputs
REVERBRATING
excited for longer by exciting self
FEED FORWARD INHIBITION
interneuron does not allow MN to fire
rhythmic activity
GATING
excitation and reciprocal inhibition
stretch reflex
