Long-term potentiation enhances the release of which neurotransmitter into the synaptic cleft. True or False

It is true and Transmitter is Amino acid glutamate

Explanation:

Long time potration can be generated through several signal transduction pathways, activated by the activation of ionotropic and metabotropic receptors. Glutamate receptors have been of great interest since their ligand, the amino acid glutamate, is the predominant excitatory neurotransmitter in the mammalian nervous system. The most commonly studied form of LTP is that which depends on the activation of the N-methyl-D-aspartate (NMDA) subtype of the glutamate receptor. This receptor is of particular interest since it forms an ionic channel, the opening of which depends on the degree of depolarization of the postsynaptic cell at the precise moment when the glutamate neurotransmitter binds to it. This makes the receiver / channel a "coincidence detector" that explains the LTP properties of the input specificity and associativity. The input specificity arises because LTP is induced only in those synapses in which glutamate has bound to the receptor NMDA, while associativity arises from the need for multiple excitatory synapses to be coercive (that is, associated in time and space) so that there is sufficient postsynaptic depolarization to unlock the channel. NMDA receptors / channels are also permeable to calcium ions, well understood as critical initiators of signaling cascades that lead to induction of LTP. Surprisingly, activation of the NMDA receptor and elevated intracellular calcium can also trigger LTD. It is the space-time nature of the calcium signal, along with its general amplitude as backed by other sources of calcium, that determines the direction of synaptic change.

the answer to your question is:

c. complementary base-pairing

b tumor cells have a cell wall instead of a membrane

explanation:

tumor cells different from normal cells because tumor cells have a cell wall instead of a membrane.