Guiding Questions week 3

Action Potentials

Differentiate between graded potentials and action potentials.

Where in the neuron do action potentials occur?

How does the strength of the stimulus effect the amplitude of the action potential? Why are they all-or-none?

increasing the stimulus strength causes an increase in the frequency of an action potential.

Explain how ion permeability changes during the rising phase and falling phase of an action potential.

What is the stimulus for opening EACH of the channels used during an action potential?

A stimulus from a sensory cell or another neuron causes the target cell to depolarize toward the threshold potential. If the threshold of excitation is reached, all Na⁺ channels open and the membrane depolarizes. At the peak action potential, K⁺ channels open and K⁺ begins to leave the cell.

What is the order of stimulus, opening and closing of all of these channels?

How is the resting membrane potential reestablished after an action potential?

Hint, we did this for our in-class activity! Can you visualize what’s happening with each of the channels?

Voltage gated Na+ channels in the axon contain two gates. What are they? How are they triggered?

What are the absolute and relative refractory periods?

How does the inactivation gate on the Na+ channel cause the absolute refractory period?

What causes the relative refractory period?

How are action potentials conducted along the length of the neuron?

Why don’t action potentials lose amplitude along the length of the axon?

If action potentials all have the same amplitude, how do action potentials transmit the intensity of the signal (to phrase it a different way, how do neurons alter the amount of neurotransmitter release based on the size of the stimulus?)?

Explain how myelin increases conduction speed down the length of an axon.

Explain the mechanism of salutatory conduction

What is the effect of demyelination? What are the symptoms of demyelination diseases (multiple sclerosis).

 

Synaptic Transmission

Draw and label the components of a synapse. Be sure to label the following structures: presynaptic cell, axon terminal, synaptic cleft, and postsynaptic cell (either neuronal or non neuronal)

What is the difference between a chemical and electrical synapse?

What is the trigger for neurotransmitter release from a synapse? Outline the steps of synaptic transmission.

How is neurotransmitter release terminated?

How is synaptic activity terminated (be sure to talk about all three mechanisms)?

Differentiate between “FAST” receptors and “SLOW” receptors on a post synaptic cell.

Explain how neurotransmitter binding to a fast receptor might cause an EPSP in the post synaptic cell. How about and IPSP?

Explain how a neurotransmitter binding to a slow receptor might cause an EPSP in the post synaptic cell. How about an IPSP?

activity 4

 

Opioids

 Opioids can also be classified according to their effect at opioid receptors. In this manner opioids can be considered as agonists, partial agonists and antagonists. Agonists interact with a receptor to produce a maximal response from that receptor (analgesia following morphine administration is an example).

clozapine

 The mechanism of action of clozapine as an anti-suicidal agent is unknown, but apparently it is not related to greater efficacy in refractory psychosis, being more linked to a direct antidepressant action and an indirect effect mediated by an improvement in cognitive functions [51].

cocaine bind and inhibit the dopamine reuptake transporter that removes dopamine from the synaptic cleft dopamine release increase or decrease

 cocaine bind and inhibit the dopamine reuptake transporter that removes dopamine from the synaptic cleft dopamine release increase or decrease

Copilot

Certainly! Let’s delve into the fascinating effects of cocaine on dopamine release. Cocaine primarily exerts its behavioral effects by enhancing dopaminergic neurotransmission, which involves amplifying dopamine-encoded sensorimotor integration. The presumed mechanism for this effect is the inhibition of the dopamine transporter, which blocks dopamine uptake and prolongs the duration of dopamine in the extracellular space1.

Here’s how cocaine affects dopamine release:

Dopamine Uptake Inhibition: Cocaine binds to and inhibits the dopamine reuptake transporter (DAT). By doing so, it prevents the removal of dopamine from the synaptic cleft, leading to an accumulation of dopamine in the extracellular space. This prolonged presence of dopamine enhances its signaling to receiving neurons.

Enhanced Dopamine Release: Interestingly, there is growing evidence that cocaine can also augment dopamine release. Even after depleting the readily releasable pool of dopamine, cocaine remains capable of elevating dopamine levels. How does it achieve this? Cocaine mobilizes a reserve pool of dopamine-containing synaptic vesicles. These vesicles are not part of the immediate release pool but can be recruited when needed. Cocaine taps into this reserve pool, further increasing dopamine levels1.

In summary, cocaine both inhibits dopamine reuptake (by blocking DAT) and increases dopamine release (by mobilizing reserve vesicles). This intricate interplay contributes to the drug’s psychostimulant effects. If you have more questions or need further clarification, feel free to ask! 😊1.

Alcohol has complex effects on synaptic activity in the brain. Let’s explore these effects:

 Alcohol has complex effects on synaptic activity in the brain. Let’s explore these effects:

https://sites.duke.edu/apep/module-2-the-abcs-of-intoxication/content-alcohol-disrupts-the-communication-between-neurons/

Depression of Neuronal Function: Alcohol acts as a general depressant of the central nervous system. It inhibits the function of neurons by reducing their ability to transmit electrical impulses. These impulses carry essential information for normal brain function. Essentially, alcohol dampens neuronal communication1.

Interaction with Receptors:

GABA Receptors: Alcohol can bind to GABA receptors, holding the ion channels open longer. This increases the entry of chloride ions (negative charges) into neurons.

Glutamate Receptors: Alcohol also binds to glutamate receptors, decreasing the entry of sodium and calcium (positive charges) into neurons2.

Endocannabinoid System: Alcohol exposure affects the endocannabinoid (eCB) system, which plays a role in synaptic function. Brain region-specific effects include altering the synthesis of endocannabinoids (such as anandamide and 2-AG), their precursors, and the density and coupling efficacy of CB1 receptors. These alterations impact synaptic function, including neuronal excitability and postsynaptic conductance3.

In summary, alcohol disrupts synaptic communication, affecting neurotransmitter release and receptor activity. The overall inhibitory effect on the brain resembles that produced by other sedative drugs. If you have more questions or need further details, feel free to ask! 😊

Initially, alcohol consumption increases dopamine levels, contributing to the pleasurable effects of drinking.

 Alcohol has a powerful effect on dopamine activity in the brain. When we drink, the brain’s so-called reward circuits are flooded with dopamine. This flood of dopamine produces euphoric feelings, which we recognize as feeling “buzzed.” Additionally, dopamine activates memory circuits in other parts of the brain, creating a pleasant experience that leaves us thirsting for more. However, the long-term impact of alcohol on dopamine levels is more complex.

Initial Boost: Initially, alcohol consumption increases dopamine levels, contributing to the pleasurable effects of drinking.

Adaptation and Depletion: With continued alcohol use, the brain adapts to this dopamine overload. It starts producing less dopamine, reduces the number of dopamine receptors, and increases dopamine transporters (which remove excess dopamine between brain cells). As a result, dopamine levels plummet, affecting mood.

Craving and Addiction: People with alcohol addiction may unconsciously consume more alcohol to boost their dopamine levels and regain that initial spark1.

In summary, alcohol both releases dopamine initially and depletes dopamine over time, contributing to the cycle of craving and addiction. If you have further questions or need more information, feel free to ask! 

cocaine amount of dopamine release( increase decrease of no change )

 Cocaine primarily exerts its behavioral effects by enhancing dopaminergic neurotransmission, amplifying dopamine-encoded sensorimotor integration. The presumed mechanism for this effect is inhibition of the dopamine transporter, which blocks dopamine uptake and prolongs the duration of dopamine in the extracellular space. However, there is growing evidence that cocaine can also augment dopamine release1. Let’s break it down:

Dopamine Uptake Inhibition: Cocaine blocks the removal of dopamine from the synapse, leading to an accumulation of dopamine and an amplified signal to the receiving neurons2.

Enhanced Dopamine Release: Cocaine enhances dopamine release by mobilizing a reserve pool of dopamine-containing synaptic vesicles. Even after depleting the readily releasable pool of dopamine, cocaine can still elevate dopamine levels by tapping into this reserve pool1.

In summary, cocaine both inhibits dopamine reuptake and increases dopamine release, contributing to its psychostimulant effects. The intricate interplay between these mechanisms plays a crucial role in the drug’s impact on the brain and behavior. If you have any more questions or need further clarification, feel free to ask! 😊

Draw label and component of synapse

https://www.khanacademy.org/science/biology/human-biology/neuron-nervous-system/a/the-synapse?redirected-from-mobile-app=1 

Certainly! Let’s explore the difference between chemical and electrical synapses:

1. Chemical Synapse:

   • A chemical synapse is a gap between two neurons where information is transmitted chemically using neurotransmitter molecules.
   • It involves two plasma membranes: the pre-synaptic membrane (in the pre-synaptic cell) and the post-synaptic membrane (in the post-synaptic cell).
   • The synaptic cleft is the space between these membranes.
   • When an action potential reaches the terminal of the pre-synaptic membrane, voltage-gated calcium channels open.
   • Calcium ions move from the synaptic cleft into the pre-synaptic nerve cell through these channels.
   • This increased calcium concentration inside the pre-synaptic cell triggers synaptic vesicles to fuse with the pre-synaptic membrane, releasing neurotransmitters into the synaptic cleft via exocytosis.
   • These neurotransmitters diffuse across the synaptic cleft and bind to receptors on the post-synaptic membrane, inducing an action potential in the post-synaptic neuron1.

2. Electrical Synapse:

   • An electrical synapse occurs between two neurons through gap junctions, which directly connect the two plasma membranes.
   • In electrical synapses, the transmission of nerve impulses occurs via ions.
   • The synaptic cleft in electrical synapses is small compared to chemical synapses.
   • Unlike chemical synapses, where neurotransmitters are involved, electrical synapses allow the electrical signal to move straight through the synapse.
   • As a result, electrical synapses are much faster than chemical synapses.
   • However, chemical synapses offer greater flexibility and modulation1.

In summary:

• Chemical synapses rely on neurotransmitters for signal transmission, while electrical synapses use gap junctions for direct electrical communication between cells.
• Chemical synapses provide flexibility, while electrical synapses prioritize speed2. 🧠💡

If you have any more questions or need further clarification, feel free to ask! 

chapter 12.5

 Local changes in the membrane potential are called graded potentials and are usually associated with the dendrites of a neuron.

Graded potentials can be of two sorts, either they are depolarizing or hyperpolarizing.