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![Blebbing
In cell biology, a bleb is a protrusion, or bulge, of the plasma
membrane of a cell, caused by localized decoupling of
the cytoskeleton from the plasma membrane. Blebbing or zeiosis is
the formation of blebs.
During apoptosis (programmed cell death), the cell's cytoskeleton
breaks up and causes the membrane to bulge outward.[5] These bulges
may separate from the cell, taking a portion of cytoplasm with them,
to become known as apoptotic bodies. Phagocytic cells eventually
consume these fragments and the components are recycled.
Blebbing also has important functions in other cellular processes,
including cell locomotion, cell division, and physical or chemical
stresses.
55](https://image.slidesharecdn.com/contraction-160624093314/75/Contraction-55-2048.jpg)
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Contraction
- 1. EXCITATION CONTRACTION & SECREATION PREPARED BY:SYEDKASHIF I st YEAR M PHARM SUBMITTED TO:DR M A AZEEM SIR AL-AMEN COLLEGE OF PHARMACY 1
- 2.
- 3. CONTENTS EXCITATION I. Introduction II.Synapse & its components III. Neurotransmitters & their release IV. Neurohumoral transmission 3
- 4. DEFINITION The activityproduced in an organ, tissue, or part, such as a nerve cell, as a result of stimulation. The cells get excitated through signals sent by the nervous system The signals may be chemical or electrical Electrical signals are seen mostly in lower group of organisms where as chemical signals are seen in the higher group of organisms The signals transmitted by the nervous system are transmitted through the nerve cells called NEURONS 4
- 5. A neuron A neuron: Nerve cell Trasmits signals in the form of action potential. Parts: The cell body (soma or); The dendrites, Receive information from other neurons Axon, which conducts electrical impulses away from the cell body. Terminal buttons ( terminal knobs, boutons, end-feet, or synaptic knobs) 5
- 6.
- 7. Synapse The junctionbetween the axon terminals of a neuron and the receiving cell is called a synapse. 7
- 8. Synapse Components ofsynapse: Pre-synaptic neuron : the neuron that secretes the transmitter substance. Postsynaptic neuron: the neuron on which the transmitter acts. Synaptic cleft: The space that seperates the pre-synaptic terminal from the postsynaptic neuron. Neuromuscular Junction ( NMJ): Pre-synaptic neuron: Motor neuron Post synaptic: Muscle cell. 8
- 9.
- 10. Synapse The pre-synaptic neuron contains: The transmitter vesicles The transmitter vesicles contain the transmitter substance that, when released into the synaptic cleft called neurotransmitters. 10
- 11. Neurotransmitters. A chemicalsubstance secreted by a nerve ending into the synapse. Acts on receptor proteins in the membrane of the next neuron to excite the neuron, inhibit it, or modify its function. E.g. Acetylcholine, Norepinephrine, Epinephrine,Gamma-aminobutyric acid (GABA), Glycine 11
- 12.
- 13. NEUROHUMORAL TRANSMISSION Itis the process in which an impulse is transmitted between the presynaptic & postsynaptic neuron by means of neurohumoral mediator signals resulting in enhancement or inhibition of the response The nerve cells transmit their messages across the synapse by releasing chemical mediators from nerve ending into the synaptic cleft Influx of Ca ions during nerve impulse releases the neurotransmitter from synaptic vesicles of the presynaptic nerve into the synaptic cleft that reach the postsynaptic receptor site & exert their action 13
- 14. STEPS INVOLVED INNEUROHUMORAL TRANSMISSION 14
- 15. 1) Conduction ofimpulse or action potential 15 axon • inside • outside K+ ions • high • low Na & Cl ions • low • high
- 16. The membranepotential of the axon is -70mV The conc. Of these ions is maintained by Na-K pump Once the action potential reaches the presynaptic nerve fibres Na permeability is increased hence Na moves in causing depolarization The membrane potential is +20mV Depolarization also opens K channels causing its efflux This concentration of ions is brought to normal by Na-K pump which pumps 3 Na ions out & 2 K ions in bringing the potential back to normal During this process the ionic currents are generated that activate the channels present on the adjacent neurons 16
- 17. 2) Release ofneurotransmitter The neurotransmitters are formed in the nerve terminals & stored in synaptic vesicles of the synaptic bulb Once the action potential reaches the presynaptic nerve fibres it activates the Ca channels present in the nerve terminals The intraterminal Ca level increases causing the snaptic vesicles to fuse with the axon which causes the neurotransmitters to release into the synaptic cleft by a process called as exocytosis 17
- 18. 3) Interaction ofthe neurotransmitter The neurotransmitters released into the synapse join the post junctional receptors present on the postsynaptic nerve & exert their action either EXCITATORY or INHIBITORY RESPONSES ARE OF TWO TYPES EXCITATORY POSTSYNAPTIC POTENTIAL(EPSP) INHIBITORY POSTSYNAPTIC POTENTIAL(IPSP) 18
- 19. EXCITATORY POSTSYNAPTIC POTENTIAL(EPSP) In EPSP the permeability of axonal membrane to all cations (Na K Ca) is enhanced Na & Ca move inside the membrane causing depolarization K ions move out EPSP occurs only when the neurotransmitter is ASPARTATE or GLUTAMATE 19
- 20. INHIBITORY POSTSYNAPTIC POTENTIAL(IPSP) In IPSP the axonal permeability to K & Cl ions is enhance IPSP involves influx of Cl ions & efflux of K ions IPSP occurs only when the neurotransmiters are either glycine or GABA 20
- 21. 4)TERMINATION of neurotransmitter It can occur by either combining with certain receptors on the postsynaptic membrane as in the case with adrenoreceptor binding drugs ex; noradrenaline Or it may get inactivaetd by certain enzymes present at the receptor site as in the case with Ach 21
- 22.
- 23. CONTENTS CONTRACTION 1. CONTRCTIONIN SKELETAL MUSCLES Introduction Types of contraction Basic Physiology of contraction Excitation-contraction coupling Sliding filament theory 2. CONTRACTION IN CARDIAC MUSCLES Excitation-Contraction coupling in cardiac muscles 23
- 24. DEFINITION Muscle contractionis the activation of tension-generating sites within muscle fibers 24
- 25. TYPES OF CONTRACTION CONTRACTIONS ISOTONIC CONCENTRICECCENTRIC ECCENTRIC(IN MOVEMENT) ISOMETRIC 25
- 26. TYPES An isometriccontraction of a muscle generates tension without changing length In isotonic contraction, the tension in the muscle remains constant despite a change in muscle length. This can occur only when a muscle's maximal force of contraction exceeds the total load on the muscle. In concentric contraction, muscle tension is sufficient to overcome the load, and the muscle shortens as it contracts. This occurs when the force generated by the muscle exceeds the load opposing its contraction. In eccentric contraction, the tension generated is insufficient to overcome the external load on the muscle and the muscle fibers lengthen as they contract Eccentric contractions normally occur as a braking force in opposition to a concentric contraction to protect joints from damage. 26
- 27. PHYSIOLOGY For voluntarymuscles, all contraction (excluding reflexes) occurs as a result of conscious effort originating in the brain. The brain sends signals, in the form of action potentials, through the nervous system to the motor neuron that innervates several muscle fibers Involuntary muscles such as the heart or smooth muscles in the gut and vascular system contract as a result of non-conscious brain activity or stimuli endogenous to the muscle itself There are three general types of muscle tissues Skeletal muscle responsible for movement Cardiac muscle responsible for pumping blood Smooth muscle responsible for sustained contractions in the vascular system, gastrointestinal tract, and other areas in the body. 27
- 28.
- 29. EXCITATION-CONTRACTION COUPLING Themembrane potential of a skeletal muscle cell is depolarized by an action potential This depolarisation activates non-gated voltage sensors, DHPRs(dihydropyridine receptors The Ca release channels) This activates RyR(the ryanodine receptor i.e voltage-gated L-type calcium channels ) type 1 via foot processes (involving conformational changes that allosterically activates the RyRs) As the RyRs open, calcium is released from the SR into the local junctional space, which then diffuses into the bulk cytoplasm to cause a calcium spark The near synchronous activation of thousands of calcium sparks by the action potential causes a cell wide increase in calcium giving rise to the upstroke of the calcium transient. 29
- 30. The calciumreleased into the cytosol binds to Troponin C by the actin filaments, to allow cross-bridge cycling, producing force and, in some situations, motion The sarco/endoplasmic reticulum calcium-ATPase (SERCA) actively pumps calcium back into the SR As calcium declines back to resting levels, the force declines and relaxation occurs 30
- 31. SLIDING FILAMENT THEORY The sliding filament theory describes a process used by muscles to contract. It is a cycle of repetitive events that cause a thin filament to slide over a thick filament and generate tension in the muscle. It was independently developed by Andrew F. Huxley and Rolf Niedergerke and by Hugh Huxley and Jean Hanson in 1954. When a muscle cell contracts, the thin filaments slide past the thick filaments, and the sarcomere shortens. This process comprised of several steps is called the Sliding Filament Theory. It is also called the Walk Along Theory or the Ratchet Theory 31
- 32.
- 33. STEPS INVOLVED Beforecontraction begins, An ATP molecule binds to the myosin head of the cross-bridges. The ATPase activity of the myosin head immediately cleaves the ATP molecule but the products (ADP+P) remains bound to the head. Now the myosin head is in a high energy state and ready to bind to the actin molecule. When the troponin-tropomyosin complex binds with calcium ions that come from the sarcoplasmic reticulum, it pulls the tropomyosin so that the active sites on the actin filaments for the attachment of the myosin molecule are uncovered. Myosin head binds to the active site on the actin molecule. 33
- 34. The bondb/w the head of the cross bridges(myosin) & the actin filaments causes a the bridge to change shape bending 45° inwards as if it was on a hinge, stroking towards the centre of the sarcomere, like the stroking of a boat oar. This is called a POWER STROKE. This power stroke pulls the thin filament inward only a small distance. Once the head tilts, this allows release of ADP & phosphate ions. At the site of release of ADP, a new ATP binds. This binding causes the detachment of the myosin head from the actin. 34
- 35. A newcycle of attachment-detachment-attachment begins. Repeated cycles of cross-bridge binding, bending and detachment complete the shortening and contraction of the muscle. 35
- 36. After the ATPhas bound to the myosin head, the binding of Myosin to Actin molecule takes place: 36
- 37. Once the actinactive sites are uncovered, the myosin binds to it: 37
- 38.
- 39.
- 40. Shortening of theMuscle: • The thick and thin filaments DO NOT shorten. • Contraction is accomplished by the thin filaments from opposite sides of each sarcomere sliding closer together or overlapping the thick filaments further. • The H-zone becomes smaller as the thin filaments approach each other. • The I band becomes smaller as the thin filaments further overlap the thick filaments. • The width of the A band remains unchanged as it depends on the thick filaments and the thick filaments do not change length. 40
- 41. CONTRACTION IN CARDIACMUSCLES Cardiac muscle fibers contract via excitation-contraction coupling, using a mechanism unique to cardiac muscle called calcium-induced calcium release. Excitation-contraction coupling describes the process of converting an electrical stimulus into a mechanical response. Calcium-induced calcium release involves the conduction of calcium ions into the cardiomyocyte, triggering further release of ions into the cytoplasm. Contraction in cardiac muscle follows the sliding filament model of contraction. 41
- 42. 1)excitation contraction coupling(ECC) The physiological process of converting an electrical stimulus to a mechanical response. 2)calcium-induced calcium release (CICR) A process whereby calcium can trigger release of further calcium from the muscle sarcoplasmic reticulum. 3)T-tubule Deep invagination of the sarcolemma, which is the plasma membrane, only found in skeletal and cardiac muscle cells. 42
- 43. Cardiomyocytes arecapable of coordinated contraction, controlled through intercalated discs. The IDs spread action potentials to support the synchronized contraction of the myocardium. In cardiac, skeletal, and some smooth muscle tissue, contraction occurs through a phenomenon known as excitation contraction coupling (ECC). ECC describes the process of converting an electrical stimulus from the neurons into a mechanical response. In muscle tissue, the electrical stimulus is an action potential and the desired mechanical response is contraction. 43
- 44. In cardiacmuscle, ECC is dependent on a phenomenon called calcium-induced calcium release (CICR), which involves the conduction of calcium ions into the cell triggering further release of ions into the cytoplasm. Like skeletal muscle, the initiation and upshoot of the action potential in ventricular muscle cells is derived from the entry of sodium ions across the sarcolemma in a regenerative process. However, in cardiac muscle, an inward flux of extracellular calcium ions through calcium channels on theT-tubules sustains the depolarization of cardiac muscle cells for a longer duration. Contraction in cardiac muscle occurs via the sliding filament model of contraction . In the sliding filament model, myosin filaments slide along actin filaments to shorten or lengthen the muscle fiber for contraction and relaxation. 44
- 45. The pathway ofcontraction can be described in five steps: An action potential, induced by pacemaker cells, is conducted to contractile cardiomyocytes through IDs, specifically gap junctions. As the action potential travels between sarcomeres, it activates the calcium channels in the T-tubules, resulting in an influx of calcium ions into the cell. Calcium in the cytoplasm then binds to cardiac troponin-C, which moves the troponin complex away from the actin binding site. This removal of the troponin complex frees the actin to be bound by myosin and initiates contraction. The myosin head pulls the actin filament toward the center of the sarcomere, contracting the muscle. Intracellular calcium is then removed by the sarcoplasmic reticulum, dropping intracellular calcium concentration, returning the troponin complex to its inhibiting position on the active site of actin, and effectively ending contraction 45
- 46. This animation showsmyosin filaments (red) sliding along the actin filaments (pink) to contract a muscle cell. 46
- 47.
- 48. CONTENTS Introduction Mechanisms I.Classical II. Non classical Blebbing 48
- 49. DEFINITION Secretion isthe process of elaborating, releasing, and oozing chemicals, or a secreted chemical substance from a cell or gland. In contrast to excretion, the substance may have a certain function, rather than being a waste product. The classical mechanism of cell secretion is via secretory portals at the cell plasma membrane called porosomes. Porosomes are permanent cup-shaped lipoprotein structure at the cell plasma membrane, where secretory vesicles transiently dock and fuse to release intra-vesicular contents from the cell. 49
- 50.
- 51. MECHANISM The proteinsto be secreated are synthesised in the ribosomes & translocated into the rough ER lumen where they get glycosylated & the molecular chaperones aid protein folding Misfolded proteins are usually identified here and retrotranslocated by ER-associated degradation to the cytosol, where they are degraded by a proteasome. The vesicles containing the properly folded proteins then enter the Golgi apparatus. 51
- 52. In theGolgi apparatus, the glycosylation of the proteins is modified and further posttranslational modifications, including cleavage and functionalization, may occur. The proteins are then moved into secretory vesicles which travel along the cytoskeleton to the edge of the cell. More modification can occur in the secretory vesicles (for example insulin is cleaved from proinsulin in the secretory vesicles). Eventually, there is vesicle fusion with the cell membrane at a structure called the porosome, in a process called exocytosis, dumping its contents out of the cell's environment 52
- 53.
- 54. NON CLASSICAL MECHANISMS There are many proteins like FGF1 (aFGF), FGF2 (bFGF), interleukin-1 (IL1) etc. which do not have a signal sequence. They do not use the classical ER-golgi pathway. These are secreted through various nonclassical pathways. At least four nonclassical (unconventional) protein secretion pathways have been described. They include 1) direct translocation of proteins across the plasma membrane likely through membrane transporters, 2) blebbing, 3) lysosomal secretion, and 4) release via exosomes derived from multivesicular bodies 54
- 55. Blebbing In cellbiology, a bleb is a protrusion, or bulge, of the plasma membrane of a cell, caused by localized decoupling of the cytoskeleton from the plasma membrane. Blebbing or zeiosis is the formation of blebs. During apoptosis (programmed cell death), the cell's cytoskeleton breaks up and causes the membrane to bulge outward.[5] These bulges may separate from the cell, taking a portion of cytoplasm with them, to become known as apoptotic bodies. Phagocytic cells eventually consume these fragments and the components are recycled. Blebbing also has important functions in other cellular processes, including cell locomotion, cell division, and physical or chemical stresses. 55
- 56.
- 57. REFERENCE https://en.wikipedia.org/wiki/Muscle_contraction https://en.wikipedia.org/wiki/Secretion https://www.boundless.com/physiology/textbooks/boundless-anatomy-and- physiology-textbook/the-cardiovascular-system-18/cardiac-muscle-tissue- 174/mechanism-and-contraction-events-of-cardiac-muscle-fibers-874-8546/ K D TRIPATHI page no. 80-82 57
- 58.