Final Neuro Study Guide 2

Class 2:
- Drug action vs. drug effects

Drug action: specific molecular changes produced by a drug when it binds to a particular target site or receptor

Drug effects: molecular changes that lead to more widespread alterations in physiological or psychological function

- Modes of drug administration and the barriers that drugs encounter when on their
way to a target receptor

Modes of administration

1. intravenous

2. inhalation

3. subcutaneous

4. intramuscular

   Pharmacokinetics vs. Pharmacodynamics- Understand the different ways these
   two variables factor in to drug concentrations and actions in the body. What are
   we measuring with each of these?

Pharmacokinetics: what the body does to a drug

Pharmacodynamics: what a drug does to the body
- Efficacy vs. Potency- What are the terms used to describe each and what do
they mean.

Efficacy: the maximum effect which can be expected from a drug

Potency: the concentration or dose of a drug necessary to produce a given effect
Class 3:
- Different cell-types found in the nervous system and their functions

Neurons: transmit and process information

1. GABA - inhibitory

2. Glutamate - excitatory

Glia: support neurons, modulate neuronal activity, development, clean up
- Membranes as insulators

The lipid bilayer of biological membranes is an oily barrier that cannot solvate ions

• an insurmountable barrier for ions

  
  - The role of the sodium/potassium ATPase (Na+/K+ pump)

the sodium potassium pump uses ATP to actively exchange extracellular potassoum for intracellular sodium - if it stops working the

- Be able to name the different parts of the action potential (AP) waveform and the
ions that are responsible for producing them. Where is the AP generated, where
is it regenerated, how does the neuron ensure AP propagation (movement) along
the axon

The different parts of the action potential waveform: Different parts of the action potential waveform include specific phases that represent changes in membrane potential due to ionic movements. These phases are produced primarily by voltage-gated ion channels and influence how action potentials propagate along the axon.

- Voltage-gated ion channels- How they gate (open/close), how they contribute to
APs, where they are concentrated in the neuron.

Voltage gated ion channels open and close based on changes in membrane potential

they allow ions to flow across the membrane, and are

Class 4&5:
- Understand how a pre-synaptic action potential leads to a post-synaptic change
in membrane potential.

o Postsynaptic response is dependent upon presynaptic voltage

o Postsynaptic response is dependent upon extracellular [Ca2+]

o Neurotransmitter is released in discrete quanta **Voltage-Gated Ion Channels:** These are specialized proteins embedded in the neuron’s membrane that open or close in response to changes in membrane potential. They are essential for generating action potentials (APs) by allowing specific ions to cross the membrane, particularly sodium (Na+) and potassium (K+). These channels are predominantly located at critical points in the neuron, such as the axon hillock and nodes of Ranvier, where they facilitate rapid signal transmission. **Class 4&5 Overview:** The action of a presynaptic neuron firing an action potential leads to a change in the electrical charge of the postsynaptic cell's membrane. This postsynaptic response is significantly influenced by two main factors: the voltage present in the presynaptic neuron and the concentration of calcium ions ([Ca2+]) in the extracellular environment. The presence of calcium ions is crucial because, during depolarization of the presynaptic neuron, calcium enters the cell and triggers the release of neurotransmitters. These neurotransmitters are released in quantal packets, meaning they are stored in small vesicles and released in discrete amounts, allowing for precise communication between neurons.

o Vesicles exist in the presynaptic terminal and appear to be storage
vesicles for neurotransmitters

o How calcium enters the presynaptic terminal during depolarization, can
trigger release, and affects the extent of release

o What happens to vesicles after fusing with the membrane.

- Understand concepts of inhibitory vs. excitatory inputs into post-synaptic cells
including spatial vs. temporal summation

**Vesicles in the Presynaptic Terminal:** Vesicles are specialized membrane-bound structures found in the presynaptic terminal of neurons. They serve as storage containers for neurotransmitters, which are essential for transmitting signals across synapses. - **Calcium Entry and Neurotransmitter Release:** During the depolarization of the presynaptic neuron, voltage-gated calcium channels open in response to changes in membrane potential. Calcium ions (Ca2+) flood into the presynaptic terminal from the extracellular space, significantly affecting the synaptic transmission process. The influx of calcium is crucial as it binds to proteins on the vesicle membrane, facilitating the fusion of neurotransmitter-filled vesicles with the presynaptic membrane. This fusion triggers the release of neurotransmitters into the synaptic cleft via a process known as exocytosis. The extent of neurotransmitter release can be modulated by the concentration of calcium ions that enter during depolarization—higher calcium ion concentrations lead to greater neurotransmitter release. - **Fate of Vesicles Post-Fusion:** After fusing with the presynaptic membrane and releasing their contents, vesicles are generally recycled through a process called endocytosis. The membrane of the fused vesicle is retrieved, and it can either be repurposed to create new vesicles or recycled for other cellular functions. This recycling process is vital for maintaining synaptic strength and ensuring that sufficient neurotransmitter storage is available for subsequent neuronal signaling. - **Inhibitory vs. Excitatory Inputs into Postsynaptic Cells:** It is essential to understand the distinction between inhibitory and excitatory inputs faced by postsynaptic neurons. Excitatory inputs typically promote depolarization and increase the likelihood of an action potential in the postsynaptic neuron by allowing positive ions (such as Na+) to enter the cell. Conversely, inhibitory inputs lead to hyperpolarization, decreasing the likelihood of an action potential by allowing negative ions (such as Cl-) to flow into the cell or by causing potassium ions (K+) to exit. - **Spatial vs. Temporal Summation:** The concepts of spatial and temporal summation are also crucial in understanding how postsynaptic cells integrate incoming signals. Spatial summation refers to the process where multiple excitatory or inhibitory signals from different presynaptic neurons converge on a single postsynaptic neuron, collectively influencing its potential. Temporal summation, on the other hand, occurs when multiple signals are received in quick succession from a single presynaptic neuron, which can accumulate and lead to a significant change in membrane potential. Both summation mechanisms are essential for determining whether a postsynaptic neuron will fire an action potential in response to synaptic inputs. ### Vesicles in the Presynaptic Terminal Vesicles are specialized, membrane-bound structures located in the presynaptic terminal of neurons. These vesicles serve as storage containers for neurotransmitters, which are essential chemical messengers for transmitting signals across synapses between neurons. The release of neurotransmitters from these vesicles is a fundamental step in neuronal communication. - **Calcium Entry and Neurotransmitter Release:** During the depolarization of the presynaptic neuron, voltage-gated calcium channels open in response to a change in membrane potential. Calcium ions (Ca²⁺) flood into the presynaptic terminal from the extracellular environment. This influx of calcium is critical for the synaptic transmission process, as it binds to proteins on the vesicle membrane and triggers the fusion of neurotransmitter-filled vesicles with the presynaptic membrane. The resulting release of neurotransmitters into the synaptic cleft occurs through exocytosis, a process characterized by the vesicles merging with the membrane and spilling their contents into the space between neurons. - **Influence of Calcium Ion Concentration:** The extent of neurotransmitter release is directly influenced by the concentration of calcium ions that enter during depolarization—higher concentrations lead to a greater release of neurotransmitters, facilitating more effective signaling between neurons. - **Fate of Vesicles Post-Fusion:** After the vesicles fuse with the presynaptic membrane and release their neurotransmitter contents, they typically undergo a recycling process known as endocytosis. This process involves the retrieval of the vesicle membrane and its repurposing to form new vesicles or to be recycled for other cellular functions. This recycling mechanism is essential for maintaining synaptic efficacy and ensuring an adequate supply of neurotransmitters for future neuronal signaling. ### Inhibitory vs. Excitatory Inputs into Postsynaptic Cells Understanding the types of inputs that postsynaptic neurons receive is crucial for comprehending neuronal signaling: - **Excitatory Inputs:** Excitatory neurotransmitters promote depolarization in the postsynaptic neuron, increasing the likelihood of generating an action potential. This usually occurs through the entry of positive ions, such as Na⁺, which causes the membrane potential to become less negative. - **Inhibitory Inputs:** In contrast, inhibitory neurotransmitters lead to hyperpolarization of the postsynaptic neuron. This can happen via the entry of negative ions (such as Cl⁻) or the exit of positive ions (such as K⁺), making the membrane potential more negative and reducing the chances of an action potential firing. ### Spatial vs. Temporal Summation These concepts describe how postsynaptic neurons integrate incoming signals: - **Spatial Summation:** This occurs when multiple excitatory or inhibitory signals from different presynaptic neurons converge on a single postsynaptic neuron, collectively influencing its membrane potential. This summation can amplify the overall signal received by the postsynaptic cell. - **Temporal Summation:** This occurs when multiple signals arrive in quick succession from a single presynaptic neuron. The rapid firing rate allows for the accumulation of signals, potentially leading to a significant change in membrane potential due to the summation of their effects over time. Both forms of integration are crucial for determining whether a postsynaptic neuron will fire an action potential in response to its inputs.

Voltage-Gated Ion Channels: These specialized channels open and close based on changes in membrane potential. They play a crucial role in generating action potentials (APs) by allowing ions to flow across the membrane, and are primarily concentrated at the axon hillock and nodes of Ranvier in neurons.

Class 4&5 Overview: A presynaptic action potential can initiate a change in the membrane potential of a postsynaptic cell. The response in the postsynaptic cell depends on the voltage changes occurring in the presynaptic cell as well as the concentration of extracellular calcium ions ([Ca2+]). This relationship is vital for the transmission of signals between neurons.