bio 20300 anatomy and physiology unit 18 study guides

Key Concepts

• Synapses are specialized junctions that allow neurons to communicate with each other and with other cells
• Synaptic transmission involves the release of neurotransmitters from the presynaptic neuron, which bind to receptors on the postsynaptic cell
• Neurotransmitters are chemical messengers that carry signals across the synaptic cleft
• Synaptic plasticity refers to the ability of synapses to strengthen or weaken over time, which is crucial for learning and memory
• Disorders and dysfunctions of synaptic transmission can lead to various neurological and psychiatric conditions
• Understanding synaptic structure and function is essential for developing targeted therapies and interventions

Synapse Structure

• Synapses consist of three main components: the presynaptic terminal, the synaptic cleft, and the postsynaptic membrane
• The presynaptic terminal contains synaptic vesicles filled with neurotransmitters and mitochondria for energy production
  • Synaptic vesicles are small, membrane-bound organelles that store and release neurotransmitters
• The synaptic cleft is a narrow gap between the presynaptic and postsynaptic membranes, typically 20-40 nm wide
• The postsynaptic membrane contains receptors that bind to specific neurotransmitters released from the presynaptic terminal
  • Receptors can be ionotropic (directly open ion channels) or metabotropic (activate second messenger systems)
• Synapses can be axodendritic (between an axon and a dendrite), axosomatic (between an axon and a cell body), or axoaxonic (between two axons)
• The structure of synapses varies depending on the type of neurotransmitter and the function of the synapse

Types of Synapses

• Chemical synapses are the most common type, where neurotransmitters are released from the presynaptic terminal and bind to receptors on the postsynaptic membrane
  • Examples of chemical synapses include glutamatergic (excitatory) and GABAergic (inhibitory) synapses
• Electrical synapses are less common and involve direct communication between neurons through gap junctions
  • Gap junctions allow ions and small molecules to pass directly between cells, enabling rapid and synchronous communication
• Neuromuscular junctions are specialized synapses between motor neurons and skeletal muscle fibers
  • Acetylcholine is the primary neurotransmitter at neuromuscular junctions, binding to nicotinic acetylcholine receptors on the muscle fiber
• Central synapses are found in the brain and spinal cord, while peripheral synapses are located outside the central nervous system
• Excitatory synapses increase the likelihood of the postsynaptic neuron firing an action potential, while inhibitory synapses decrease this likelihood

Neurotransmitters

• Neurotransmitters are chemical messengers that carry signals across the synaptic cleft
• Common neurotransmitters include glutamate (excitatory), GABA (inhibitory), acetylcholine (excitatory and modulatory), dopamine (modulatory), serotonin (modulatory), and norepinephrine (modulatory)
• Neurotransmitters are synthesized in the presynaptic terminal and stored in synaptic vesicles
• Once released into the synaptic cleft, neurotransmitters can bind to specific receptors on the postsynaptic membrane
• Neurotransmitters are cleared from the synaptic cleft by reuptake into the presynaptic terminal or degradation by enzymes
  • Reuptake is mediated by specific transporter proteins (e.g., serotonin transporter, dopamine transporter)
• Imbalances in neurotransmitter levels or function can contribute to various neurological and psychiatric disorders (e.g., depression, Parkinson's disease, schizophrenia)

Synaptic Transmission Process

• Synaptic transmission begins with the arrival of an action potential at the presynaptic terminal
• The action potential triggers the opening of voltage-gated calcium channels, allowing calcium ions to enter the presynaptic terminal
• Calcium influx causes synaptic vesicles to fuse with the presynaptic membrane and release neurotransmitters into the synaptic cleft (exocytosis)
• Neurotransmitters diffuse across the synaptic cleft and bind to specific receptors on the postsynaptic membrane
• Binding of neurotransmitters to receptors can lead to the opening of ion channels (ionotropic receptors) or activation of second messenger systems (metabotropic receptors)
  • Opening of ion channels can result in depolarization (excitatory postsynaptic potential, EPSP) or hyperpolarization (inhibitory postsynaptic potential, IPSP) of the postsynaptic membrane
• The postsynaptic response depends on the type of neurotransmitter, the receptor subtype, and the overall balance of excitatory and inhibitory inputs
• Synaptic transmission is terminated by the removal of neurotransmitters from the synaptic cleft through reuptake or enzymatic degradation

Synaptic Plasticity

• Synaptic plasticity refers to the ability of synapses to strengthen or weaken over time in response to activity and experience
• Long-term potentiation (LTP) is a form of synaptic plasticity that involves a long-lasting increase in synaptic strength
  • LTP is thought to be a cellular mechanism underlying learning and memory formation
• Long-term depression (LTD) is a form of synaptic plasticity that involves a long-lasting decrease in synaptic strength
• Synaptic plasticity is mediated by changes in the number and properties of neurotransmitter receptors, as well as structural changes in synapses (e.g., growth of new dendritic spines)
• Hebbian plasticity is a type of synaptic plasticity based on the principle that "cells that fire together, wire together"
  • This means that synapses between neurons that are active at the same time are strengthened, while those that are not active together are weakened
• Synaptic plasticity is influenced by various factors, including neurotransmitter release, postsynaptic receptor activation, and intracellular signaling cascades
• Disruptions in synaptic plasticity mechanisms can contribute to cognitive impairments and neurological disorders (e.g., Alzheimer's disease, autism spectrum disorders)

Disorders and Dysfunctions

• Synaptic dysfunction can lead to various neurological and psychiatric disorders
• Alzheimer's disease is characterized by the accumulation of amyloid-beta plaques and tau tangles, which disrupt synaptic function and lead to cognitive decline
• Parkinson's disease involves the degeneration of dopaminergic neurons in the substantia nigra, leading to motor symptoms such as tremor and rigidity
• Schizophrenia is associated with abnormalities in dopaminergic and glutamatergic neurotransmission, which can lead to positive (e.g., hallucinations) and negative (e.g., social withdrawal) symptoms
• Depression is linked to imbalances in serotonergic, noradrenergic, and dopaminergic neurotransmission, as well as alterations in synaptic plasticity
• Autism spectrum disorders are associated with disruptions in synaptic development and function, particularly in glutamatergic and GABAergic signaling
• Epilepsy involves abnormal synchronous firing of neurons, which can be caused by imbalances in excitatory and inhibitory neurotransmission
• Addiction is associated with long-lasting changes in synaptic plasticity in reward-related brain circuits, particularly those involving dopamine

Clinical Applications

• Understanding synaptic structure and function is crucial for developing targeted therapies and interventions for neurological and psychiatric disorders
• Medications that modulate neurotransmitter levels or receptor function are commonly used to treat various conditions
  • Examples include selective serotonin reuptake inhibitors (SSRIs) for depression, dopamine agonists for Parkinson's disease, and antipsychotics for schizophrenia
• Deep brain stimulation (DBS) is a surgical intervention that involves implanting electrodes in specific brain regions to modulate synaptic activity
  • DBS is used to treat conditions such as Parkinson's disease, essential tremor, and obsessive-compulsive disorder
• Transcranial magnetic stimulation (TMS) is a non-invasive brain stimulation technique that can modulate synaptic plasticity and treat conditions such as depression and chronic pain
• Gene therapy approaches aim to correct synaptic dysfunction by delivering therapeutic genes or modulating gene expression in specific neural circuits
• Stem cell therapies hold promise for replacing lost or damaged neurons and restoring synaptic function in neurodegenerative disorders
• Cognitive behavioral therapy (CBT) and other psychotherapeutic interventions can induce synaptic plasticity changes that underlie improvements in mental health conditions
• Developing novel biomarkers and imaging techniques to assess synaptic function and plasticity can aid in the diagnosis and monitoring of neurological and psychiatric disorders