1. General Neurophysiology
Axonal transport
Degeneration and regeneration in the nervous system
Transduction of signals at the cellular level
Reflex arch
Central pattern generator

2. Axonal transport (axoplasmatic transport) Anterograde
Proteosynthesis in the cell body only (ER, Golgi apparatus)
Retrograde
Moving the chemical signals from periphery

3. Anterograde axonal transport
Anterograde axonal transport fast ( mm/day) MAP kinesin/mikrotubules moves neurotransmitters in vesicles and mitochondria   slow (0,5 – 10 mm/day) unknown mechanism structural components (cytoskeleton - aktin, myosin, tubulin), metabolic components   Retrograde axonal transport fast ( mm/day) MAP dynein/ mikrotubules old mitochondria, vesicles (pinocytosis, receptor-mediated endocytosis in axon terminals, transport of e.g. growths factors),

4. Axonal transport in the pathogenesis of diseases
Rabies virus
Replicates in muscle cell
Axon terminal (endocytosis)
Retrograde transport to the cell body
Neurons produce copies of the virus
CNS – behavioral changes
Neurons innervating the salivary glands (anterograde transport)
Tetanus toxin (produced by Clostridium tetani)
Toxin is transported retrogradely in nerve cells
Tetanus toxin is released from the nerve cell body
Taken up by the terminals of neighboring neurons

5. Axonal transport as a research tool
Tracer studies
Anterograde axonal transport
Radioactively labeled amino acids (incorporated into proteins, transported in an anterograde direction, detected by autoradiography)
Injection into a group of neuronal cell bodies can identify axonal distribution
Retrograde axonal transport
Horseradish peroxidase is injected into regions containing axon terminals. Is taken up and transported retrogradely to the cell body. After histology preparation can be visualized.
Injection to axon terminals can identify cell body

6. Neuroneogenesis Neurons do not proliferate Exceptions
Exceptions
- olfactory epithelium
- dentatum gyrus (stem cells)
- olfactory bulb
Generaly
Lost neurons are not replaced (proliferation of glia, astrocytic scar)

7. Myelin sheath of axons in PNS (a membranous wrapping around the axon)
Degeneration and regeneration in the nervous system
Myelin sheath of axons in PNS (a membranous wrapping around the axon)

8. Myelin sheath of axons in PNS (a basal lamina)

9. Injury of the axon in PNS
Compression, crushing, cutting – degeneration of the distal axon - but the cell body remains intact (Wallerian degeneration, axon is removed by macrophages)
Schwann cells remain and their basal lamina (band of Büngner)
Proximal axon sprouts (axonal sprouting)
Prognosis quo ad functionem
Compression, crushing – good, Schwann cells remain in their original orientation, axons can find their original targets
Cutting – worse, regeneration is less likely to occure

10. Injury of the axon in PNS
Amputation of the limb
Proximal stump fail to enter the Schwann cell tube, instead ending blindly in connective tissue
Blind ends rolle themselves into a ball and form a neuroma – phantom pain

11. Myelin sheath formation in CNS

12. Injury of the axon in CNS
Oligodendrocytes do not create a basal lamina and a band of Büngner
Regeneration to a functional state is impossible
Trauma of the CNS
proliferation and hypertrophy of astrocytes, astrocytic scar

13. Transduction of signals at the cellular level
Somatodendritic part –
passive conduction
of the signal, with decrement
Axonal part –action potential, spreading without decrement, all-or-nothing law

14. Axon – the signal is carried without decrement

15. Dendrite and cell body – signal is propagated with decrement

16. Signal propagation from dendrite to initial segment

17. Origin of the AP electrical stimulus neurotransmitter on synapses

18. Axonal part of the neuron AP – voltage-gated Ca2+ channels –neurotransmitter release
Arrival of an AP in the terminal opens voltage-gated Ca2+ channels,
causing Ca2+ influx,
which in turn triggers transmitter release.

19. Somatodendritic part of neuron
Receptors on the postsynaptic membrane
Excitatory receptors open Na+, Ca2+ channels membrane depolarization
Inhibitory receptors open K+, Cl- channels
membrane hyperpolarization
EPSP – excitatory postsynaptic potential
IPSP – inhibitory postsynaptic potential

20. Excitatory and inhibitory postsynaptic potential

21. Interaction of synapses

22. Summation of signals
spatial and temporal

23. Transduction of signals at the cellular level
EPSP
IPSP
Initial segment AP
Ca2+ influx
Neurotransmitter
Neurotransmitter releasing

24. Neuronal activity in transmission of signals Discharge configurations of various cells
EPSP
IPSP

25. Influence of one cell on the signal transmission
1.AP, activation of the voltage-dependent Na+ channels (soma, area of the initial segment)
2. ADP, after-depolarization, acctivation of a high threshold Ca2+ channels, localized in the dendrites
3.AHP, after-hyperpolarization, Ca2+ sensitive K+ channels
4.Rebound depolarization, low threshold Ca2+ channels, de-inactivated during the AHP, activated when the depolarization decreases (probably localized at the level of the soma
Threshold
RMP

26. Reflex arch
Knee-jerk reflex

27. Sir Charles Scott Sherrington
Research on reflexes
Ivan Petrovich Pavlov
Russia
nobelist 1904
Sir Charles Scott Sherrington
Great Britain
nobelist 1932
                  

29. Behavior as a chain of reflexes?
LOCUST
Two pairs of wings
Each pair beat in synchrony but the rear wings lead the front wings in the beat cycle by about 10%
Proper delay between contractions of the front and rear wing muscles

30. Donald Wilson’s Experiment in 1961

31. To confirm the hypothesis
Identify the reflexes that are responsible for the flight pattern
Deafferentaion = the elimination of sensory input into the CNS
Remove sense organs at the bases of the wings
Cut of the wings
Removed other parts of locust s body that contained sense organs
Unexpected result
Motor signals to the flight muscles still came at the proper time to keep the wings beat correctly synchronized

32. Extreme experiment
Reduced the animal to a head and the floor of the thorax and the thoracic nerve cord
Elecrodes on the stumps of the nerves that had innervated the removed flight muscles
Motor pattern recorded in the absence of any movement of part of animal – fictive pattern
Locust flight systém did not require sensory feedback to provide timing cues for rhythm generation
Network of neurons
Oscillator, pacemaker, central pattern generator

33. Central pattern generator
Model of the CPG for control of muscles during swimming in lamprey

34. Central pattern generators
A network of neurons capable of producing a properly timed pattern of motor impulses in the absence of any sensory feedback.
Swimming
Wing beating
Walking
Gallop, trot
Licking
Scratching
Breathing

35. Summary

36. Axonal transport (axoplasmatic transport) Anterograde
Proteosynthesis in the cell body only (ER, Golgi apparatus)
Retrograde
Moving the chemical signals from periphery

37. Degeneration and regeneration in the nervous system
Damaged (differenciated) neurons are not replaced
Trauma of the CNS – glial scarf
Axons in CNS
Axons in PNS

38. Transduction of signals at the cellular level
EPSP
IPSP
Initial segment AP
Ca2+ influx
Neurotransmitter
Neurotransmitter releasing

39. Reflex arch
Central pattern generators Pacemakers