lecture_10_10_19 - IV.D.1.c.ii. Metabotropic receptors can...

Info iconThis preview shows pages 1–3. Sign up to view the full content.

View Full Document Right Arrow Icon

Info iconThis preview has intentionally blurred sections. Sign up to view the full version.

View Full DocumentRight Arrow Icon
This is the end of the preview. Sign up to access the rest of the document.

Unformatted text preview: IV.D.1.c.ii. Metabotropic receptors can have complex far-reaching effects In lecture, we told you that when neurotransmitter is released at a presynaptic bouton, it diffuses in the synaptic cleft and subsequently binds to receptors on a postsynaptic cell. In many situations, these postsynaptic receptors undergo conformational changes (upon binding of neurotransmitter) which enable them to become ion channels. For example, when the neurotransmitter g-aminobutyric acid (GABA) is released from presynaptic neurons, it diffuses across the synaptic cleft and binds to postsynaptic "chloride receptors" (which have a high affinity for GABA). Finally, the "GABA-bound chloride receptors" undergo a conformational change that opens them and allows chloride to flow across the postsynaptic membrane according to its net driving force. In contrast to the relatively rapid form of "ion-gated" chemical transmission (where neurotransmitter binds to receptors that are ion channels), a slower form of chemical transmission exists. Under slow synaptic transmission, the postsynaptic receptors are not ion channels. Rather, when neurotransmitter binds to these so-called "metabotropic receptors", an intracellular second messenger cascade is initiated ultimately leading to changes in the electrical (and/or long term physiological) properties of the postsynaptic neuron. For example, when glutamate is released from presynaptic cells in the hippocampus (a brain region thought to be important for the early stages of memory formation), "metabotropic glutamate receptors" bind this neurotransmitter and an intracellular second messenger cascade is initiated. One possible outcome of this second messenger cascade is to activate cAMP-dependent protein kinases which phosphorylate potassium channels. Phosphorylation of these potassium channels leads to their closure and the membrane potential being driven to a more positive (depolarized) voltage. For practice, we want you to think about the multitude of other possible outcomes that can result when neurotransmitter binds to either "ion- gated" or "metabotropic" receptors. What postsynaptic channels might be phosphorylated following presynaptic neurotransmitter release? Will phosphorylation lead to an opening or closure of these channels? How many ions is a ligand gated channel conductive to (one/many)? Might there be "ion gated" or "metabotrophic" receptors on a presynaptic neuron? Can binding of a neurotransmitter to a metabotropic receptor lead to changes in gene expression or neurotransmitter synthesis? time Postsynaptic voltage Presynaptic stimulus time-65-60-40 IV.D.2.c. change concentrations of ions and measure psp. IV.D.2.b. The psp is depolarizing, so is the synapse excitatory?...
View Full Document

This note was uploaded on 11/16/2011 for the course NPB NPB 100 taught by Professor Campbell during the Spring '10 term at UC Davis.

Page1 / 11

lecture_10_10_19 - IV.D.1.c.ii. Metabotropic receptors can...

This preview shows document pages 1 - 3. Sign up to view the full document.

View Full Document Right Arrow Icon
Ask a homework question - tutors are online