Tutor profile: Sakshi C.
Subject: Health and Medicine
What are some sites of cholinergic transmission, receptors involved, and drugs acting on them?
1. Site of action: CNS Type of receptor: Muscarinic and Nicotinic Drug as selective agonist: Oxotremorine(Muscarinic), Carbachol(Nicotinic) Drug as selective antagonist: Atropine(Muscarinic), Curare(Nicotinic) 2.Site of action : Sympathetic and parasympathetic ganglia Type of receptor: Nicotinic Drug as selective agonist: Dimethyl Phenyl Piperazinium Drug as selective antagonist: Hexamethonium 3.Site of action : Adrenal medulla Type of receptor: Nicotinic Drug as selective agonist: Dimethyl Phenyl Piperazinium Drug as selective antagonist: Hexamethonium 4. Site of action: All of the postganglionic parasympathetic system and some of the postganglionic sympathetic system Type of receptor: Muscarinic Drug as selective agonist: Muscarine Drug as selective antagonist: Atropine 5.Site of action: Skeletal msucular system Drug as selective agonist: Phenyl trimethyl ammonium Drug as selective antagonist: Curare
How does light activate the rod cells in our eyes and help us "see"?
The rods and cones in the eyes are called photoreceptor cells because of their function as receptors of visual stimuli. Rod cells are stimulated by weak light, such as a single light bulb in a big room. These photoreceptor cells are known to synapse with layers of interneurons innervated by many photoreceptor cells, where they are transported to the visual cortex of the brain to be interpreted. Rod cells have G-protein coupled receptors or GPCRs that are sensitive to light and are known as rhodopsin. These receptors found on cellular surfaces act as signal receivers for the cells, in this case, light and are covalently linked to retinal, a light-absorbing pigment. The activating signal for rhodopsin is a photon of light that binds to retinal. On binding, retinal undergoes a conformational change to its 'trans' form, causing a corresponding change in rhodopsin. This change enables it to bind to the G alpha subunit of rhodopsin, GTP is exchanged for GDP. In the absence of light, the membrane of the rod cell is transformed into a depolarized state, and this causes continuous neuronal stimulation. They are depolarized as both Na and Ca ions are allowed into the cell through non-selective ion channels, which open in response to cyclic guanosine monophosphate (cGMP). Light absorption closes these non-selective ions channels, and the membrane potential within becomes more negative due a decrease in cGMP (light causes activation of cGMP phosphodiesterase, an enzyme that converts cGMP to 5'-GMP, reducing cellular cGMP levels). The membrane becomes hyperpolarized, fewer neurotransmitters are released. A reduction in neurotransmitter release transferred to brain as a series of neurons is interpreted in the brain as "light", enabling us to see.
Minor mutations in the nucleotide sequence are seen in every cycle of cellular DNA replication. What mechanisms does the cell have that prevent these mutations from being passed on to the next generation of cells, during every round of replication?
Cells have certain "proofreading" mechanisms that scan for errors in the nucleotide sequence. One of these is the methyl directed mismatch repair system that removes any errors in replication. In prokaryotes, certain dimers of the mismatch repair system perform several functions to correct these errors. The MutS recognises errors due to the strains they cause in the DNA structure, causes a conformational change in itself and unstacks base pairs on the DNA at the site. It recruits MutL, which activates MutH, making an incision on the DNA strand. Later, a protein called helicase unwinds the double-stranded DNA from the site of the incision all the way to where the mismatch has occurred, digests this portion creating a gap which is filled by an enzyme called DNA Polymerase. They are later sealed together with the help of an enzyme called DNA ligase.
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