University:
Western Sydney University
Course:
MEDI 2003 | Clinical Sciences 2
Academic year:

2024
Views:

223

Pages:

2
Author:

Mariam A. A.

ENDOCYT OSIS AND EXCOCYT OSIS • • Exocytosis Constitutive secretory pathways e.g. secretion of proteins and elements of the extracellular matrix Regulated secretory pathways e.g. neurotransmitter release Secretory pathways • Proteins are ‘tagged’ to enter specific secretory pathways • E.g. mast cells (histamine), alpha-cells of the pancreas (insulin), goblet cells (mucus) Membrane adds to the plasma membrane, contents are released Chem machinery: PSP-syntaxin binding to cell membrane → release of PSP → SNARE complex → exocytosis Membrane fusion: Secretory cell structure – active zones • Vesicles are targeted to specific areas: o Basal vs. apical membranes o Contain different membrane proteins are microdomains • Vesicle pools form at pre-synaptic zones Pathologies/drugs • Botulism and tetanus toxins inhibit exocytosis • Levetiracetam (used to treat epileosy) o Binds to a synaptic vesicle glycoprotein o Reduces neurotransmitter release Endocytosis Pinocytosis – “cell drinking” • Induced by changes in extracellular environ (amino acids, proteins, ions) • • Non-specific in terms of vesicle content Maintains plasma membrane size Phagocytosis • Ingestion of bacteria or other material by phagocytes e.g. macrophages Receptor-mediated endocytosis Endocytic pathway 1. Endocytosed vesicle first encounters an ‘early endosome’ with which it fuses 2. Early endosomes have a low pH due to proton pumps in the membrane surface – low pH promotes dissociation of the substrate from receptor 3. Cargo is then returned to membrane or transferred to a ‘late endosome’ (will fuse with lysosome) 4. Lysosome contains enzymes to break the cargo into its constituent parts e.g. a low density lipoprotein particle is broken down in cholesterol, amino acids and fatty acids • Specialised endocytic pathway e.g. neurons and NMJ Endocytosis related disease – Atherosclerosis low density lipoprotein (LDL) particles are taken up by endocytosis → genetic disorders can stop this uptake meaning LFL particles accumulate in the blood causing atherosclerotic plaques