Biology 40 B

Thursday, May 2, 2024

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 . 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

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:

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 neuron 1.
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 modulation 1.

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 speed 2. 🧠💡

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.

Wednesday, May 1, 2024

Gamma-aminobutyric acid (GABA) is an inhibitory neurotransmitter in the central nervous system. Its effects on the post-synaptic cell depend on the type of GABA receptor and the specific context:

GABA-A Receptors:

Activation of GABA-A receptors typically leads to hyperpolarization of the post-synaptic cell.

GABA-A receptors are ligand-gated chloride channels. When GABA binds to these receptors, chloride ions flow into the cell, making the membrane potential more negative (hyperpolarized).

This hyperpolarization reduces the likelihood of action potential firing.

GABA-B Receptors:

Activation of GABA-B receptors can have more complex effects.

GABA-B receptors are metabotropic receptors coupled to G-proteins.

They can lead to hyperpolarization by opening potassium channels, allowing potassium ions to flow out of the cell.

However, they can also modulate other signaling pathways, affecting neuronal excitability in various ways.

Context Matters:

The overall impact of GABA depends on the specific brain region, cell type, and the balance between excitatory and inhibitory inputs.

In some cases, GABA can lead to depolarization due to the reversal potential of chloride ions being close to the resting membrane potential.

For example, during early development, GABA can be excitatory due to the high intracellular chloride concentration.

In summary, GABA can either hyperpolarize or depolarize the post-synaptic cell, depending on the receptor subtype and the cellular context. 🧠💡

quizz

Touch -Choose matching definition

light stimuli

physical or mechanical stimuli

causes depolarization

chemical senses

Taste and smell-Choose matching definition

Energy senses

Vestibular senses

Somatosenses

Chemical senses

Receiving information about the environment to gain input (conscious perception) about what is happening outside the body or inside the body Choose matching term

Autonomic Nervous System

Sensation

Electricity Parts

Repolarization

Basic function of nervous system-Choose matching definition

Dendrites And Cell Body

Sensation
Integration
Response

Causes Depolarization

Chemical Senses

Central Nervous System (CNS)

Central Nervous System (CNS)

CNS

Center of the nervous system

Brain & Spinal cord

Integrates sensory information and initiates motor responses

Includes ascending and descending neuron

2. PNS

Outside the CNS

Cranial nerves & Spinal nerves

Includes afferent and efferent neurons

3.Basic function of nervous system

Sensation

Integration

Response

4.Sensation

Receiving information about the environment to gain input (conscious perception) about what is happening outside the body or inside the body

5.Taste and smell

Chemical senses

6.Touch

physical or mechanical stimuli

7.Sight

light stimuli

8.Hearing

Sound waves

9.Where could sensory stimulus from inside the body come from?

Sensory stimuli from inside the body could be from stretch receptors in organ walls or from the blood concentration of certain ions

Steps of integration

-Received stimuli from the senses is communicated to the nervous system where the information is processed

-The stimuli are compared or integrated with: other stimuli, past stimuli, or the state of the person at the particular time

-Specific responses will be generated

Response

Production of a response on the basis of stimuli perceived by sensory structures

2 forms of response

2 Forms
Voluntary (Somatic Nervous System)
Involuntary (Autonomic Nervous System)

Voluntary

contraction of skeletal muscle

Involuntary

contraction of smooth muscle, regulation of cardiac muscle, activation of glands

Somatic nervous system

Conscious perception

Voluntary motor response: contraction of skeletal muscle

Includes reflexes that happen without conscious decision & motor responses that become automatic as a person learns motor skills

Autonomic nervous system

Involuntary control of the body, regulates the organs systems usually for the sake of homeostasis but can also be due to an emotional state

Sensory input can be internal or external

Motor output is from smooth & cardiac muscle, & glandular tissue

enteric nervous system

Controls smooth muscle and glandular tissue in the digestive system

Part of the autonomic nervous system & part of the PNS

Can operate independently of the CNS

Glial cells

variety of cells that support the neurons & their activities

Neurons

most functionally important cells

Contain a cell body (soma) & processes called axons & dendrites

Neurons pt.2

Conduct nerve impulses to communicate information about sensations, produce movements, & induce thoughts

Have extreme longevity

Cannot divide, so cannot be replaced

High metabolic rate, cannot survive without oxygen

Neurons cell body (soma)

synthesizes proteins (Nissl bodies), many mitochondria

Dendrites

conduct nerve signals to the cell body

Axon fibers

sometimes covered by a myelin sheath, conducts nerve impulses away from the cell body

Axon hillock

area between cell body & axon

Axon terminal

ending of axon branches, contain mitochondria & vesicles (with neurotransmitters)

synaptic end bulb

enlargement at end of axon terminal, connects with target cell at a synapse

input zone of neuron

Dendrites and cell body

Summation zone

axon hillock - incoming nerve impulses combine

Conduction zone

axon - contains many voltage-gated Na+ & K+ channels

Output zone

distal end of axon- contains many voltage-gated Ca2+ channels

Multipolar

Multipolar - single axon & many dendrites, most common (found in motor neurons)

Bipolar

Bipolar - 2 processes separated by cell body (rare: found in retina & olfactory mucosa)

Unipolar

Unipolar - 1 process with cell body off to the side, (found in sensory neurons of PNS)

4 major types of CNS

Astrocytes

Microglia

Ependymal cells

Oligodendrocytes

2 major types of PNS

Schwann cells

Satellite Cells

Oligodendrocytes

Found in the CNS

Hold nerve fibers together and produce the myelin sheath (phospholipid insulating cover)

1 cell myelinates many axons

Myelin sheath

Insulates, increases speed of action potentials, & holds neurons together

ONLY in the PNS, there are gaps in the myelin sheath: Nodes of Ranvier

Loss of myelin (demyelination) can cause a loss of sensation (numb) & motor control (paralyzed)

White matter

is myelinated

PNS: myelinated nerve

CNS: myelinated tract

Grey matter

cell bodies and dendrites are unmyelinated

PNS: ganglion (soma)

CNS: nucleus or ganglion (soma)

Astrocytes

Found in the CNS

Star shaped

Largest and most numerous

Connect to both neurons and capillaries, creating a frame-work

Transfer nutrients from the blood to the neurons

Trap leaked K+ & neurotransmitters

Form blood-brain barrier (BBB)

Repair damaged neural tissue

Microglia

Found in the in CNS

Least numerous and smallest glial cells

Phagocytic cells derived from monocytes

Small, usually stationary

In inflamed brain tissue, they enlarge move about and engulf pathogens, waste, & debris

Ependymal cell

Found in the CNS

Resemble epithelial cells

Form thin sheets, lining fluid-filled cavities (ventricles)

Aid in circulation of fluid with cilia

Shwann cells

Found in the PNS

Also called neurolemmocytes

Support nerve fibers and form myelin sheaths

Wrap around a portion of only one axon

Essential for nerve regrowth

Satellite cells

Cells that cover and support cell bodies (sensory & autonomic ganglia) that function like astrocytes but do not play a role in the BBB

Multiple Sclerosis (MS)

Autoimmune disease

Causes inflammation & destruction of myelin in the CNS

As the insulation (mylin sheath) is destroyed, scarring becomes obvious

"Multiple scars" are found in the white matter

Symptoms include both somatic & autonomic deficits in muscle control

Guillian-Barre Syndrome

Demyelinating disease of the PNS

Also an autoimmune reaction

Sensory & motor deficits are common

Autonomic failures can lead to heart rhythm changes, or drops in blood pressure, especially when standing up

Sensory receptor steps

If the stimulus is strong enough to reach threshold an action potential will travel down the axon

When it reaches the end bulbs it releases a neurotransmitter

The neurotransmitter binds to receptors on the target neuron, which then has its own action potential

The 2nd neuron synapses with a neuron in the thalamus, which then sends the information to the sensory cortex

Response to stimuli from brain

In cerebral cortex, information is processed (integrates the stimulus with your emotional state & memories)

A plan is developed & the motor cortex will send out a command to your skeletal muscles

An upper motor neuron synapses with a lower motor neuron

The lower motor neuron releases Ach onto the muscle fiber & the action potential begins the muscle contraction

Electricity parts

Current = Voltage

Resistance

Voltage is the potential difference

Ions differences create voltage

Resistance is provided by the plasma membrane

All living cells maintain a difference in the concentration of ions across their membranes

Protein channels

Channels are selective to which ions they allow through

Mechanically-gated:

open in response to physical deformation of receptor (sensory), when pressure is applied channels open & ions enter the cell

Chemically-gated (ligand-gated):

open when the right chemical binds, ions then cross the membrane changing its charge. Also called ionotropic receptors because it allows ions to enter or leave the cell.

Voltage -gated channels:

open and close in response to changes in membrane potential, Normally the inner portion is negative & when it becomes less negative ions cross the membrane

Leakage channels:

opens & closes at random, contribute to the resting membrane voltage of excitable membranes

Membrane potential

Potential = distribution of charges across a cell membrane

Measured in millivolts (mV)

Compares the inside charge to the outside charge

The membrane surface has a slight difference in ion charges & this allows neurons & muscle cells to generate electrical signals

Resting Membrane Potential (RMP)

Polarized Membrane:

plays most important role

Leaky channels allow K+ to leak out and lower amounts of Na+ to leak in

Magnitude of potential difference: measured in millivolts (-70mV)

Maintained by Na+/K+ pumps

sodium potassium pump

Pumps 3 Na+ out of cell & 2 K+ into cell

Works against concentration gradient

ATP required for energy to run pump

Cells become polarized

Depolarization

starts with the opening of Na+ channels

rushes into the cell, changing the membrane potential to become less negative

Membrane potential reaches +30mV

Repolarization

Na+ channels close & K+ channels open

leaves the cell, voltage moves back towards -70mV

Hyperpolarization

K+ channels are slow to close & the membrane potential go below -70mV

What initiates action potential

Ligand-gated channels open when a neurotransmitter binds to it

Mechanically-gated channels open when a physical stimulus affects a sensory receptor

Voltage-gated channels open when the membrane potential is -55mV

All of Nothing Principle

A stimulus either triggers an action potential or it does not

Once threshold is reached an action potential will occur!!

The magnitude is the same no matter how it reached threshold

absolute refractory period

when the membrane is depolarizing

Will not respond to a stimulus, no matter how strong

relative refractory period

when the membrane is repolarizing

Membrane will respond only to a very strong stimulus

Coding for stimulus intensity

All action potentials are alike

Strong stimuli generate impulses more often

Frequency gives strength not amplitude of individual impulses

Propagation of an action potential

Continuous conduction"

Action potential starts in the beginning of the axon

Contains a high density of Na+ channels, rapidly depolarizes

As depolarization spreads, more Na+ channels open & it travels down the axon

Never moves backward

Faster Speed: large diameter, presence of myelin sheath, & increased temperatures

Saltatory conduction

Occurs in myelinated axons

Action Potentials occur only at Nodes of Ranvier

Flow under myelin sheath to next node

"Leaps" from node to node

Faster & saves ATP (less surface area to pump Na+/K+ across)

graded potentials

Local changes in membrane potential

Usually occur in dendrites

Amount of change determined by the size of the stimulus

Can be either depolarizing or hyperpolarizing

or Ca2+ enter (depolarize) or

or Cl- leave the cell (hyperpolarize)

generator potential

Develop in dendrites

In sensory neurons:

Both free nerve endings & those that are encapsulated

receptor potential

Graded potentials in their membranes result in the release of neurotransmitters at synapses

In sensory neurons: Both taste cells & photoreceptors of the retina

Happens only in cells that act as receptors that communicate with sensory neurons

post synaptic potential

Graded potential in the dendrites of a neuron that is receiving synapses from other cells

Can be depolarizing or hyperpolarizing

EPSP) Excitatory post synaptic potential:

causes cell to move towards threshold

(IPSP) Inhibitory post synaptic potential:

causes cell to move away from threshold

Summation

Summate = add together

Occurs at the axon hillock (except for sensory neurons)

Combined effects of graded potentials

If membrane depolarizes, the membrane will reach threshold

Can be either spatial or temporal

electrical synapses

Cells joined by gap junctions

Allows electrical currents to flow between cells

Found in cardiac muscle & single-unit smooth muscle (shown)- remember, intercalated discs in cardiac muscle have gap junctions and desmosomes!

Chemical synapse

Involves the transmission of a chemical from one cell to another.

The release of acetylcholine is an example of a chemical synapse.

The synapse

connection between a neuron & its target cell

Ionotropic

ligand-gated

Metabotropic

involves a complex of proteins resulting in metabolic changes in the cell

nicotinic receptors

Causes depolarization

muscarinic receptors

Causes depolarization or hypopolarization

metabotropic receptors

Two common second messenger systems use cAMP and IP3 (inositol triphosphate)

Second messengers cause metabolic changes within the cell -hence the name metabotropic receptors

The effector protein catalyzes the second messenger

Alzheimer's disease

Progressive degenerative brain disorder that results in dementia

Due to misfolded proteins that form plaques & tangles that kill neurons

Brain shrinks

Parkinson's disease

Strikes mostly in the 50s & 60s

Degeneration of dopamine releasing neurons of the substantia nigra

Basal nuclei become overactive

Persistent tremor at rest, shuffling gait, & stiff facial expressions

Treated with L-dopa - but it becomes ineffective, deep brain stimulation can alleviate tremors

Huntington's disease

Fatal hereditary disorder

Strikes during middle age

Mutant protein accumulates in brain cells & the tissue dies

Massive degeneration of the basal nuclei & cerebral cortex

Produces "chorea" - wild, jerky, continuous flapping non-voluntary movements (hyperkinetic)

Disease is progressive & leads to mental deterioration

Usually fatal within 15 years

Huntington's Disease Chorea

Drugs used to treat it: block dopamine's effects

Creutzfeldt-Jakob disease

Human variant of prion disease - "mad cow disease"

What responses are generated by the nervous system when you run on a treadmill? Include an example of each type of tissue that is under nervous system control.

Running on a treadmill involves contraction of the skeletal muscles in the legs, increase in contraction of the cardiac muscle of the heart, and the production and secretion of sweat in the skin to stay cool.