random things that seem importand

Question 1

receptor-mediated signaling

Answer 1

• neurotranmitters bind to specific receptors on the postsynaptic neuron
• binding causses either the opening of ion channels or the activation of second messsenger system, altering the postsynaptic activity.

Question 2

explain the transmitter-gated ion channels

Answer 2

1. Neurotransmitters released by the presynaptic neuron bind to specific binding sites on the transmitter-gated ion-channel
2. This causes a conformational change in the receptor protein, which opens a channel in the plasma membrane
3. Ions (e.g., Na+ or K+) flow into or out of the postsynaptic neuron through the open channel
4. Changes in ion concentrations affect the resting potential of the postsynaptic neuron, influencing its excitability and ultimately leading to changes in its firing rate

Question 3

give examples of transmitter-gated ion channels

Answer 3

• Examples: nicotinic acetylcholine receptors (nAChRs) for fast synaptic transmission and muscle contraction, GABA receptors ( inhibitory synaptic transmission), AMPA receptors (excitatory synaptic transmission)

Question 3

explain G-protein coupled receptors (metabotropic receptors)

Answer 3

1. Neurotransmitter molecules bind to receptor proteins embedded in the postsynaptic membrane
2. The receptor proteins activate small proteins, called G-proteins, which are free to move along the intracellular face of the postsynaptic membrane
3. The activated G-proteins activate “effector” proteins

Question 4

what is receptor tyrosine kinases

Answer 4

Cell surface receptors that play a key role in signal transduction pathways. They are involved in long-term plasticity, learning, and memory by triggering intracellular signaling cascades.

Question 5

how does receptor tyrosine kinases trigger intracellular signaling cascades

Answer 5

1. Neurotransmitter binding: Neurotransmitters bind to specific sites on the RTK, causing a conformational change
2. Activation: This change activates the receptor’s tyrosine kinase activity
3. Auto-phosphorylation: The receptor phosphorylates its own tyrosine residues, creating docking sites for signaling proteins
4. Signaling cascades: Docking proteins bind and trigger downstream events, leading to changes in gene expression, protein synthesis, and synaptic strength

Question 6

examples of RTKs in synaptic plasticity

Answer 6

• EphB receptors: Involved in Hebbian learning and long-term potentiation (LTP)
• NMDA receptors: Important for LTP and long-term depression (LTD)
• Trk receptors: Facilitate neurotrophin signaling and synaptic plasticity

Question 7

inbalance in serotonin, dopamine or norepinephine signaling

Answer 7

depression

Question 8

reduced dopamine signaling due to neuron loss

Answer 8

parkison disease

Question 9

dysregulation of neurotransmitter systems

Answer 9

anxiety, addiction, schizophrenia

Question 10

function astrocytes

Answer 10

• Glutamate uptake and clearance: Prevents excitotoxicity by removing excess neurotransmitter
• Neurotransmitter regulation: Release and removal of neurotransmitters to maintain synaptic balance
• Synaptic plasticity: Release of neurotrophic factors like BDNF to promote neuron survival and synaptic strength
• Energy supply: Provide lactate and other energy substrates to meet neuronal energy demands

Question 11

astrocytes interaction with neurons

Answer 11

• Gap junctions: Facilitate direct communication between astrocytes and neurons through shared ions and signaling molecules
• Chemical signaling: Astrocytes release gliotransmitters like ATP and glutamate, modulating synaptic transmission and neuronal activity

Question 12

Stores and releases neurotransmitters into the synaptic cleft

Answer 12

Pre-synaptic terminal

Question 13

Contains receptors that bind neurotransmitters and initiate signaling cascades in the receiving neuron

Answer 13

Post-synaptic spine:

Question 14

function of adhesion molecules

Answer 14

• Anchor pre- and post-synaptic spines together for strong synaptic connections
• Regulate neurotransmitter release and reception
  o Maintain synaptic plasticity, learning, and memory
• Facilitate efficient synaptic transmission and proper receptor localization

Question 15

dysregulation of adhesion molecules is implicated in disorders like

Answer 15

alzheimer, autism spectrum disorder, and schizophrenia

Question 16

explain a bit about glut3 transporters

Answer 16

Glucose is metabolized via glycolysis and aerobic oxidation. Neuronal glucose uptake relies on GLUT3 transporters

Question 17

What are the stages of cellular respiration

Answer 17

1. Glycolysis: Conversion of glucose into pyruvate in the cytosol, generating ATP and NADH
2. Citric acid cycle (Krebs cycle): Pyruvate enters mitochondria, forming acetyl-CoA, which generates NADH, FADH₂, and CO₂
3. Oxidative phosphorylation: ATP is synthesized as electrons pass through the electron transport chain, driving the proton gradient

Question 17

mitochondrial dysfunction (neural disorders)

Answer 17

oNeurological disorders: Impaired function is linked to conditions like mitochondrial myopathies, Parkinson’s, and Alzheimer’s

Question 18

Increased reactive oxygen species (ROS) production

Answer 18

Excess ROS can damage cellular components like DNA, proteins, and lipids, exacerbating oxidative stress and mitochondrial dysfunction

Question 19

Impaired calcium homeostasis

Answer 19

Impaired calcium homeostasis: Mitochondria regulate intracellular calcium levels. Dysregulated calcium handling affects muscle contraction and relaxation, leading to weakness and fatigue

Question 20

Disrupted cellular signaling pathways

Answer 20

Mitochondria influence pathways involved in metabolism, apoptosis, and gene expression. Dysfunction can lead to abnormal cellular behavior

Question 21

Increased apoptosis

Answer 21

Impaired mitochondria can trigger programmed cell death, leading to tissue wasting and degeneration

Question 22

Mitophagy

Answer 22

Damaged mitochondria are usually removed via mitophagy. Impairment in this process can worsen mitochondrial dysfunction

Question 23

Epigenetic changes:

Answer 23

Dysfunction can cause DNA methylation and histone modifications, altering gene expression and contributing to disease

Question 24

Mitochondrial dynamics:

Answer 24

Normal mitochondrial fusion and fission maintain function. Disruption results in dysfunctional mitochondria and reduced ATP production

Question 25

 Impaired mitochondrial membrane potential: Essential

Answer 25

Essential for ATP production and electron transport chain function. Impairment leads to decreased ATP and increased ROS

Question 26

Mitochondrial-targeted therapies:

Answer 26

 Coenzyme Q10 (CoQ10): An antioxidant that supports mitochondrial energy production, improves ATP synthesis, and reduces oxidative stress  Nicotinamide adenine dinucleotide (NAD+): A coenzyme that enhances energy metabolism and mitigates oxidative stress  Ubiquinol: A reduced form of CoQ10 that directly targets mitochondria to boost energy production

Question 27

vitamin c

Answer 27

helps reduce oxidative stress and prevent mitochondrial damage

Question 28

vitamin E

Answer 28

protects against lipd peroxidation and mitochondrial damage

Question 29

alpha-lipoic acid

Answer 29

reduces oxidative stress and improves insulin sensetivity.