Answer:
Antibiotic resistance can evolved in bacterial population in the following ways:
Explanation:
- In response to constant exposure to antibiotics some members of a bacterial population develop some beneficial mutations in some essential genes that gives them survival advantage in terms of food and space over the sensitive bacterial strains and hence they are capable of out-competing the sensitive bacteria.
- This happens due to the process of Natural Selection.
- These genes are called antibiotic resistance genes and bacteria usually carry them on plasmids in form of cassettes where genes resistant to multiple drugs are incorporated. These plasmids are called the MDR or Multi-Drug Resistance Plasmids.
- These resistant plasmids can be easily transferred among bacterial populations by conjugation, transformation or transduction or direct plasmid transfer.
- The resistant genes encode for proteins that render the drug ineffective by promoting their efflux from the cells, preventing their entry into the cell, chemically modifying them such that they become non-functional or altering the target site of the drug.
Long-term potentiation (LTP) is considered a cellular correlate of learning and memory. The presence of G protein-activated inwardly rectifying K(+) (GIRK) channels near excitatory synapses on dendritic spines suggests their possible involvement in synaptic plasticity. However, whether activity-dependent regulation of channels affects excitatory synaptic plasticity is unknown. In a companion article we have reported activity-dependent regulation of GIRK channel density in cultured hippocampal neurons that requires activity oF receptors (NMDAR) and protein phosphatase-1 (PP1) and takes place within 15 min. In this study, we performed whole-cell recordings of cultured hippocampal neurons and found that NMDAR activation increases basal GIRK current and GIRK channel activation mediated by adenosine A(1) receptors, but not GABA(B) receptors. Given the similar involvement of NMDARs, adenosine receptors, and PP1 in depotentiation of LTP caused by low-frequency stimulation that immediately follows LTP-inducing high-frequency stimulation, we wondered whether NMDAR-induced increase in GIRK channel surface density and current may contribute to the molecular mechanisms underlying this specific depotentiation. Remarkably, GIRK2 null mutation or GIRK channel blockade abolishes depotentiation of LTP, demonstrating that GIRK channels are critical for depotentiation, one form of excitatory synaptic plasticity.
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