ELM 10 Nts

Question 1

What is the general function of a receptor in chemical transmission?

Answer 1

A receptor binds an information-transmitting molecule and, upon activation, passes on the information in a different form through a process called transduction. This leads to changes in cellular behavior.

Question 2

A receptor binds an information-transmitting molecule and, upon activation, passes on the information in a different form through a process called transduction. This leads to changes in cellular behavior.

Answer 2

The four main types of receptors are: Ligand-gated ion channels (LGIC)
G protein-coupled receptors (GPCRs), also known as metabotropic receptors
Tyrosine kinase receptors
Nuclear hormone receptors

Question 3

Describe ligand-gated ion channels (LGICs) and their function.

Answer 3

Ligand-gated ion channels are receptors that, upon binding of a ligand, undergo a conformational change that allows ions to flow through the channel. This change in ion flow alters the membrane potential of the cell, leading to changes in cellular function.

Question 4

What are G protein-coupled receptors (GPCRs), and how do they function?

Answer 4

GPCRs, or metabotropic receptors, are receptors that activate intracellular signaling pathways upon ligand binding. They do so by interacting with G proteins, which then initiate various downstream signaling cascades, ultimately leading to changes in cellular function.

Question 5

Explain the function of tyrosine kinase receptors.

Answer 5

Tyrosine kinase receptors are receptors that have intrinsic kinase activity. Upon ligand binding, they undergo dimerization and autophosphorylation, leading to the activation of downstream signaling pathways involving phosphorylation of target proteins. These pathways regulate various cellular processes.

Question 6

What is the role of nuclear hormone receptors?

Answer 6

Nuclear hormone receptors are transcription factors that, upon ligand binding, translocate to the nucleus and regulate gene expression. They control the transcription of specific genes, thereby influencing cellular processes and responses.

Question 7

What are the main families of neurotransmitter receptors?

Answer 7

The main families are ligand-gated ion channels (LGICs) and G protein-coupled receptors (GPCRs).

Question 8

: What is a characteristic feature of LGICs?

Answer 8

LGICs open in response to the binding of an agonist.

Question 9

What structural elements do all LGICs possess?

Answer 9

All LGICs have a pore, a ligand binding site, a coupling mechanism, and a desensitization mechanism.

Question 10

Can you describe the structure of nAChR?

Answer 10

nAChR is a pentamer of 5 similar subunits with a gate halfway through the membrane.

Question 11

How do LGICs like nAChR function in prey capture?

Answer 11

Ligands like Alpha bhangra toxin or substances produced by electric rays can target LGICs to paralyze prey, facilitating hunting.

Question 12

What is the structural characteristic of GPCRs?

Answer 12

GPCRs have a seven-transmembrane domain structure.

Question 13

What happens upon agonist binding to a GPCR?

Answer 13

Agonist binding induces conformational changes in GPCRs, leading to the activation of G proteins.

Question 14

: What is the main downstream consequence of GPCR activation?

Answer 14

GPCR activation triggers downstream signaling cascades through G protein-mediated pathways.

Question 15

What are some examples of receptors in Family A of GPCRs?

Answer 15

Receptors such as mAChR, dopamine receptors, and serotonin receptors belong to Family A of GPCRs.

Question 16

How do G proteins modulate cellular signaling?

Answer 16

G proteins can modulate cellular signaling by targeting effector proteins such as adenylate cyclase or phospholipase C, leading to the modulation of second messenger levels.

Question 17

What is the function of Gs proteins?

Answer 17

Gs proteins, containing As subunits, activate adenylate cyclase, leading to increased levels of cyclic AMP (cAMP) in the cell.

Question 18

What role do Gi proteins play in cellular signaling?

Answer 18

Gi proteins, with Ai subunits, inhibit adenylate cyclase, resulting in decreased levels of cyclic AMP (cAMP) in the cell.

Question 19

: What is the downstream effect of Gq protein activation?

Answer 19

Gq proteins, containing Aq subunits, activate phospholipase C, leading to increased production of inositol trisphosphate (IP3), diacylglycerol (DAG), and increased cytoplasmic calcium levels.

Question 20

How do receptors function in cellular signaling?

Answer 20

Receptors undergo conformational changes upon activation, transitioning into an active state. Prolonged agonist binding can lead to a desensitized state as a safety mechanism. These changes enable recognition of specific agonists through complementary protein structures.

Question 21

What are the main neurotransmitter categories and examples?

Answer 21

Neurotransmitter categories include monoamines (e.g., dopamine, serotonin), amines (e.g., acetylcholine), neuropeptides (e.g., substance P, endorphins), amino acids (e.g., glutamate, GABA, glycine), and others (e.g., nitric oxide, adenosine, ATP).

Question 22

What is Dale’s Principle, and does it hold true?

Answer 22

Dale’s Principle states that a neuron releases only one type of neurotransmitter. However, the original version isn’t entirely true, as neurons can release multiple neurotransmitters, adding flexibility to neural signaling.

Question 23

What are the criteria for a substance to be classified as a neurotransmitter?

Answer 23

o be classified as a neurotransmitter, a substance must be synthesized by neurons, present in synaptic terminals at sufficient concentrations, released upon presynaptic stimulation, evoke a response when applied to the postsynaptic cell, and have a mechanism for removal from the synaptic cleft.

Question 24

How is acetylcholine (Ach) removed from the synaptic cleft?

Answer 24

Acetylcholine is removed from the synaptic cleft by the enzyme acetylcholinesterase.

Question 25

What happens to glutamate released from glutamatergic terminals?

Answer 25

Glutamate is reuptaken by excitatory amino acid transporters or diffuses out of the synapse. Astrocytes can uptake glutamate via excitatory amino acid transporters (EAATs), metabolize it to glutamine, which can then be taken back into presynaptic terminals and converted back to glutamate.

Question 26

What are the main types of neurotransmitter receptors and examples?

Answer 26

Neurotransmitter receptors can be ionotropic (e.g., glycine receptors) or metabotropic (e.g., neuropeptides, dopamine, histamine). Some neurotransmitters, like glutamate, GABA, serotonin, acetylcholine, and ATP, can act on both ionotropic and metabotropic receptors.

Question 27

What are the two types of acetylcholine receptors (AChRs) and their characteristics?

Answer 27

cetylcholine receptors (AChRs) include nicotinic receptors (ionotropic) and muscarinic receptors (metabotropic). Nicotinic receptors are pentameric, have multiple subtypes, and are excitatory with a fast response. Muscarinic receptors are monomeric, have M1-5 subtypes, and can have excitatory or inhibitory effects with a slower response.

Question 28

How does cholinergic transmission demonstrate flexibility in the nervous system?

Answer 28

Cholinergic transmission demonstrates flexibility by utilizing both nicotinic and muscarinic acetylcholine receptors, allowing for both fast excitatory responses (via nicotinic receptors) and slower modulatory responses (via muscarinic receptors).

Question 29

What are the main types of glutamate receptors and their characteristics?

Answer 29

Glutamate receptors include ionotropic receptors (such as AMPA, kainate, and NMDA receptors) and metabotropic receptors (mGluRs). Ionotropic receptors mediate fast responses, while metabotropic receptors mediate slower responses via G protein signaling.

Question 30

What makes NMDA receptors special among glutamate receptors?

Answer 30

: NMDA receptors are highly permeable to calcium ions (Ca2+), are blocked by magnesium ions (Mg2+) at resting membrane potential, require glycine or D-serine as a coagonist, and require all four binding sites to be occupied for activation. They play a crucial role in synaptic plasticity and memory formation.

Question 31

Describe the sequence of events in a glutamatergic synapse involving AMPA, NMDA, and mGluR receptors.

Answer 31

Glutamate released from the presynaptic terminal activates AMPA receptors, causing local depolarization. This depolarization removes the Mg2+ block from NMDA receptors, allowing for increased depolarization and influx of Ca2+. Activation of mGluRs can lead to long-lasting depolarization, potentially strengthening the synapse through processes like long-term potentiation.

Question 32

What are the two types of GABA receptors and their functions?

Answer 32

GABA receptors include GABAA and GABAB receptors. GABAA receptors are ligand-gated chloride channels that mediate fast inhibitory responses by increasing chloride permeability. GABAB receptors are metabotropic receptors that mediate slower inhibitory effects by modulating intracellular signaling pathways.

Question 33

How do GABAB receptors function?

Answer 33

GABAB receptors consist of subunits B1 and B2 and function presynaptically to inhibit voltage-gated calcium channels, open potassium channels, and inhibit adenylyl cyclase, leading to hyperpolarization and inhibition of neurotransmitter release.

Question 34

What is the relationship between inhibitory glycine receptors and GABAA receptors?

Answer 34

Inhibitory glycine receptors are closely related to GABAA receptors and mediate inhibitory transmission, primarily in the spinal cord. They function as ligand-gated chloride channels and can have both excitatory (as a coagonist at NMDA receptors) and inhibitory actions.

Question 35

What are autoreceptors, and how do they regulate neurotransmitter release?

Answer 35

Autoreceptors are receptors for the neurotransmitter released by the nerve terminal in whose membrane they reside. When activated, they regulate the release of that neurotransmitter, typically through negative feedback inhibition, although positive feedback may occur in some instances. Autoreceptors often belong to the same receptor family as the neurotransmitter they bind.

Question 36

Describe the regulation of noradrenaline release from cardiac sympathetic neurons by autoreceptors.

Answer 36

Alpha 2 adrenoceptors on presynaptic nerve terminals act as autoreceptors, regulating noradrenaline release. These receptors are G protein-coupled receptors (GPCRs) that interact with Gi proteins. Activation of alpha 2 receptors inhibits adenylate cyclase, reducing cAMP levels in the nerve terminal. Decreased cAMP leads to reduced calcium influx, resulting in decreased noradrenaline release. In the central nervous system (CNS), alpha 2 receptors also play a role in neurotransmitter regulation.

Question 37

How does mirtazapine affect neurotransmitter release, and what is its therapeutic significance?

Answer 37

Mirtazapine, an antidepressant, acts as an antagonist of alpha 2 receptors. By blocking these receptors, mirtazapine increases noradrenaline and serotonin release in the synapse. The increased availability of these neurotransmitters is thought to contribute to the antidepressant effects of mirtazapine.

Question 38

What are heteroreceptors, and how do they function?

Answer 38

Heteroreceptors respond to a different neurotransmitter than the one present in the membrane where they are located. They have the potential to regulate presynaptic transmitter release by responding to neurotransmitters and regulatory molecules present in the extracellular fluid surrounding neurons.

Question 39

: Can you provide an example of heteroreceptor regulation in the brain?

Answer 39

In the striatum, nicotinic acetylcholine receptors act as heteroreceptors, regulating dopamine release. This regulation is crucial in conditions like Parkinson’s disease and schizophrenia, where dopamine transmission deficits or excesses contribute to symptoms.

Question 40

How do nicotinic acetylcholine receptors regulate dopamine release in the striatum?

Answer 40

Nicotinic acetylcholine receptors in the striatum increase dopamine release through two mechanisms: increased depolarization of the presynaptic nerve terminal, leading to greater calcium influx through voltage-gated channels, and direct calcium entry through the nicotinic receptor itself. This regulation plays a significant role in reward and mood pathways in the central nervous system.

Question 41

What is the significance of heteroreceptor regulation in the addictive nature of nicotine?

Answer 41

The widespread regulation of neurotransmitter release by nicotinic receptors, acting as heteroreceptors, contributes to the addictive nature of nicotine. This highlights the complex interplay between neurotransmitter systems and the potential for targeted interventions in addiction-related pathways.

Question 42

How are nicotinic acetylcholine receptors (nAChRs) regulated in the central nervous system (CNS)?

Answer 42

Peptides produced in the brain, such as Lynx1, can interact with nAChRs and modulate their activity, particularly during brain development. Lynx1, belonging to the Ly6 protein superfamily, regulates nAChRs and plays a role in synaptic remodeling, especially in the visual system.

Question 43

What is the role of Lynx1 in synaptic plasticity, and what is its evolutionary significance?

Answer 43

Lynx1 deletion in mice results in increased plasticity in visual pathways, suggesting its role in synaptic remodeling. Lynx1 belongs to the Ly6 protein superfamily, which is ubiquitous across organisms. This suggests an intriguing evolutionary hypothesis regarding the origin of α-neurotoxins in elapid snakes, such as cobras.

Question 44

What is the proposed evolutionary hypothesis regarding the origin of α-neurotoxins in elapid snakes?

Answer 44

The hypothesis suggests that a distant ancestor of elapid snakes may have possessed a Lynx1-like protein that regulated nAChRs. Over time, mutations in either the Lynx1-like protein or the nAChRs might have occurred, leading to the loss of regulatory function. Subsequent mutations could have transformed the Lynx1-like protein into potent α-neurotoxins.

Question 45

How do elapid snakes, like cobras, interact with their own neurotoxins?

Answer 45

Elapid snakes have likely developed resistance to their own neurotoxins, possibly through changes in the structure or function of their own nAChRs or other physiological adaptations. This resistance suggests a co-evolutionary arms race between elapid snakes and their prey or predators.

Question 46

What supports the evolutionary hypothesis regarding the origin of α-neurotoxins in elapid snakes?

Answer 46

Observations such as elapid snakes’ resistance to their own toxins provide some support for the evolutionary hypothesis. Further research into the molecular evolution of elapid toxins and their interactions with nAChRs could provide additional insights.