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Flashcards in 6 - neurophysiology Deck (43)
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compare the effects of the sympathetic vs parasympathetic nervous systems on cardiac muscle

• 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

• 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

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



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



using a diagram explain how olfaction affects different structures within the brain



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

– small MN
– slow twitch
– fatigue resistant
– slow oxidative
– low myosin ATPase activity

– medium MN
– fast twitch
– fatigue resistant
– fast oxidative

– 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

black MN excite inhibitory MN —> no firing
white MN excite excitatory MN —> firing
withdrawal reflex

many motorneurons excite the same MN
brain stem / cortex inputs

excited for longer by exciting self

interneuron does not allow MN to fire
rhythmic activity

excitation and reciprocal inhibition
stretch reflex


draw a diagram of the patella reflex



draw a diagram of how the crossed extensor and withdrawal reflex work together during locomotion



why is a patient with a spinal cord injury and supported by a harness able to walk on a tread mill ?

i don't actually know the answer to this can any1 help :(


name and briefly describe two mechanisms used for postural adjestments

feed forward:
– anticipatory
– preprogrammed from experience
– unlike reflexes

– compensatory
– stereotyped
– show a space time organisation
– like reflexes


describe the reflex(es) controlled by the vestibular nuclei

vestibular nuclei receive afferents which signal head postion WRT gravity

signals via vestibulospinal tract to control multiple relfexes

lateral nuclei = controls proximal limbs to maintain stance

medial + superior = coordination of eye with head movements

inferior = integrates afferents + cerebellum to higher areas


describe the reflex(es) controlled by the reticular formations

maintaining posture via feed-forward mechanisms

medullary (lateral) reticular formation = inhibitory to extensor muscle tone

pontine (medial) reticular formation = facilitates extensor muscle tone