NAS W5 Flashcards
INHIBITORY NEURONE
when active, produces neurotransmitters which inhibit neurones it makes synaptic contact with
INHIBITED NEURONE
one which is firing less because inhibitory neurotransmitter has been released from neurones it synapses with
REFLEX
- stereotyped (always same response) involuntary reactions of CNS to specific sensory input
- brings about rapid response
CLINICAL RELEVANCE OF REFLEX
- stereotyped so we can test for a known reflex to see issue
- e.g. autonomic (involuntary) pupillary reflex - shine light in eye & expect pupil to constrict
FUNCTIONS OF REFLEX
protective, postural control, homeostasis
INTEGRATION CENTRE
contains interneurons (between sensory & motor & are in CNS & take info from reflex arc & relay it to other interneurons)
HYPERFLEXIA
when communication between brain (CNS) & integration centre is damage so there is unregulated reflex arc
TYPES OF PROPRIOCEPTORS
muscle spindles & golgi tendon organs
MUSCLE SPINDLE8
- stretch exceeds threshold = AP firing = depolarisation = sensory neurone releases neurotransmitter (excitatory) to increase motor activity (AcH released leads to contraction to prevent damage to skeletal muscle)
- monosynaptic (no interneurones)
CROSS-EXTENSOR REFLEX
we can simultaneously extend one muscle (extensor) & relax another (flexor) to get reflex (excitatory neurotransmitter leads to contraction but also releases inhibitory neurotransmitter which stops firing of excitatory so muscle relaxes)
GOLGI TENDON ORGANS
- prevent damage due to overwork
- polysynaptic (have interneuron (it is inhibitory)
- we lift something heavy = activates muscle spindles= muscle contracts & applies compression to nerve endings = golgi tendon organ activated so AP form in sensory afferent = AP depolarise synaptic terminal & release neurotransmitter (excitatory so causes interneuron to fire more AP) but interneuron releases inhibitory neurotransmitter so no AP in motor neurone & no AcH in muscle so no contraction (called reverse myotatic reflex)
SKELETAL MUSCLE NEURONE SUPPLY
somatic nervous system (voluntary)
SMOOTH MUSCLE NEURONE SUPPLY
autonomic nervous system (modifies muscle by increasing or decreasing myogenic activity not generating it)
GLANDS
autonomic nervous system (NS modifies secretions of glands to get effect)
TYPES OF DAMAGE TO NERVE (ENDO, PERI, EPINEURIUM)
- NEUROPRAXIA (least severe) - nerve loses ability to function normally due to myelination damage BUT only temporary
- AXONOTMESIS (mid-severe) - axons & myelin sheaths damaged but endo, peri & epi neurium stay intact (in renervation, Schwann cells provide adjacent segment with protection as guide endo, peri, epi on where to attach nerve sprouts)
- NEUROTMESIS (most severe) - entire nerve completely severed so there is no complete recovery
HOW NEURONES REACT TO INJURY
MINUTES - neurone stops conducting AP beyond site of injury & 2 cut ends of axon pull apart, seal themselves & swell at same time
HOURS - degeneration of synaptic terminal (leads to accumulation of vesicles) & astroglia pull terminals away from postsynaptic cell
DAYS/WEEKS - proximal segment to cell body undergoes chromatolysis & in distal segment, distal stump of axon degenerates
FATE OF PROXIMAL SEGMENT OF SEVERED NERVE (CHROMATOLYSIS)
- cell body becomes active & produces lots of proteins for repairing cell so cell body volume increases & gets bloated so nucleus displaced from centre to periphery.
- injured nerve seals wounded stump (form neuroma) so this segment of nerve doesn’t die & could regenerate to innervate peripheral structures
FATE OF DISTAL SEGMENT OF SEVERED NERVE
axon dies due to loss of nutritional support from cell body (Wallerian digestion) & is digested by phagocytes but they save myelin, epi, peri, endo to form hollow tubes that guide new growth of axon in proximal end
FATE OF DENERVATED MUSCLE (ACUTE (now) & CHRONIC (later))
ACUTE - muscle paralysed & can’t do reflex & immediately starts fasciculation but this ends if no re-innervation
CHRONIC- as fasciculations die down, muscle loses bulk due to denervation (denervation atrophy) or lack of use (disuse atrophy) so dies & goes muscle tissue replaced with connective
TREATMENTS TO NERVE INJURY
nerve repair (remove damaged section & reconnect healthy ends), nerve graft, pain relief meds, electrical stimulation
SUMMARY OF HOW NEURONS IN PNS REGENERATE AXONS
- after degeneration of distal axon & myelin, macrophages clean up debris & induce schwann cells to divide
- myelin-forming schwann cells repopulate nerve sheaths
- macrophages induce Schwann cells to make nerve growth factor & axons sprout & some enter new Schwann cell tubes
- Axonal growth cones successfully grow
