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