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Excitatory Postsynaptic Potential (EPSP) vs. Inhibitory Postsynaptic Potential (IPSP) (Neuroscience Tips)

Discover the Surprising Differences Between EPSP and IPSP in Neuroscience – Boost Your Brain Knowledge Today!

Step Action Novel Insight Risk Factors
1 Understand the difference between EPSP and IPSP EPSP is a depolarization effect that increases the likelihood of an action potential, while IPSP is a hyperpolarization effect that decreases the likelihood of an action potential None
2 Know the types of neurons involved in EPSP and IPSP Excitatory signal transmission is mediated by glutamatergic neurons, while inhibitory signal transmission is mediated by GABAergic neurons None
3 Understand the mechanism of EPSP and IPSP EPSP is caused by the opening of ion channels that allow positively charged ions to enter the cell, while IPSP is caused by the opening of ion channels that allow negatively charged ions to enter the cell or positively charged ions to leave the cell None
4 Know the role of neurotransmitter release in EPSP and IPSP Glutamate is the primary neurotransmitter involved in EPSP, while GABA is the primary neurotransmitter involved in IPSP None
5 Understand the importance of the action potential threshold The action potential threshold is the level of depolarization required to trigger an action potential. EPSPs can bring the membrane potential closer to the threshold, while IPSPs can move the membrane potential further away from the threshold None

Contents

  1. What is the role of neurotransmitter release in EPSP and IPSP?
  2. What is the depolarization effect in EPSP and how does it differ from IPSP?
  3. What are GABAergic neurons and their involvement in IPSP?
  4. How does hyperpolarization effect play a role in both EPSP and IPSP?
  5. Common Mistakes And Misconceptions
  6. Related Resources

What is the role of neurotransmitter release in EPSP and IPSP?

Step Action Novel Insight Risk Factors
1 The presynaptic neuron releases neurotransmitters into the synaptic cleft. Neurotransmitter binding affinity determines the strength of the EPSP or IPSP. Overstimulation of excitatory neurotransmitters can lead to neuronal damage or death.
2 The neurotransmitters bind to receptors on the postsynaptic membrane. Receptor activation threshold must be reached for an action potential to be initiated. Inhibition of inhibitory neurotransmitters can lead to overexcitation and seizures.
3 Ion channels on the postsynaptic membrane open, allowing ions to flow in or out. Excitatory neurotransmitters cause membrane depolarization, while inhibitory neurotransmitters cause hyperpolarization. Inhibition of inhibitory neurotransmitters can lead to overexcitation and seizures.
4 The postsynaptic membrane potential changes, either becoming more positive (EPSP) or more negative (IPSP). The sum of all EPSPs and IPSPs determines whether an action potential is initiated. Overstimulation of excitatory neurotransmitters can lead to neuronal damage or death.
5 If the sum of EPSPs reaches the action potential initiation threshold, an action potential is initiated. Neural circuit integration and synaptic plasticity regulation allow for neuronal network modulation. Overstimulation of excitatory neurotransmitters can lead to neuronal damage or death.

What is the depolarization effect in EPSP and how does it differ from IPSP?

Step Action Novel Insight Risk Factors
1 Define EPSP and IPSP EPSP is an excitatory postsynaptic potential that occurs when an excitatory neurotransmitter binds to a receptor on the postsynaptic neuron, causing sodium influx and depolarization of the membrane potential. IPSP is an inhibitory postsynaptic potential that occurs when an inhibitory neurotransmitter binds to a receptor on the postsynaptic neuron, causing potassium efflux and hyperpolarization of the membrane potential. None
2 Explain depolarization effect in EPSP Depolarization is the process of making the membrane potential less negative, bringing it closer to the action potential threshold. In EPSP, depolarization occurs due to the influx of positively charged sodium ions, which makes the postsynaptic neuron more likely to fire an action potential. None
3 Compare depolarization effect in EPSP and IPSP In IPSP, depolarization does not occur. Instead, the membrane potential becomes more negative due to the efflux of positively charged potassium ions or the influx of negatively charged chloride ions. This makes the postsynaptic neuron less likely to fire an action potential. None

What are GABAergic neurons and their involvement in IPSP?

Step Action Novel Insight Risk Factors
1 GABAergic neurons are neurons that release the neurotransmitter GABA. GABAergic neurons are the main source of IPSP in the brain. Overactivation of GABAergic neurons can lead to excessive inhibition and cause neurological disorders.
2 GABA receptor activation by GABA released from GABAergic neurons leads to the opening of chloride ion channels in the postsynaptic membrane. Chloride ion channels allow negatively charged chloride ions to enter the neuron, leading to hyperpolarization of the neuron. Malfunctioning chloride ion channels can lead to neurological disorders such as epilepsy.
3 Hyperpolarization of the neuron decreases the likelihood of the neuron firing an action potential, leading to a decrease in neuronal excitability. GABAergic neurons play a crucial role in regulating the balance between excitation and inhibition in neural networks. Dysregulation of GABAergic neurons can lead to anxiety and mood disorders.
4 GABAergic neurons and their involvement in IPSP make them a target for epilepsy treatment. GABAA receptors, which are the main type of GABA receptors, are the target of many sedative-hypnotic drugs. Modulation of GABAergic neurotransmission can have therapeutic potential for various neurological disorders.

How does hyperpolarization effect play a role in both EPSP and IPSP?

Step Action Novel Insight Risk Factors
1 EPSP When a neuron receives a signal, ion channels open and allow positively charged sodium ions to enter the cell, causing depolarization. This depolarization can lead to an excitatory postsynaptic potential (EPSP), which increases the likelihood of neuron firing. If too many EPSPs occur too quickly, it can lead to overexcitation and potential damage to the neuron.
2 IPSP Alternatively, ion channels can allow negatively charged chloride ions to enter the cell or positively charged potassium ions to leave the cell, causing hyperpolarization. This hyperpolarization can lead to an inhibitory postsynaptic potential (IPSP), which decreases the likelihood of neuron firing. If too many IPSPs occur, it can lead to underexcitation and potential inhibition of necessary neural processes.
3 Hyperpolarization Hyperpolarization plays a role in both EPSP and IPSP because it determines the threshold potential required for neuron firing. The threshold potential is the minimum level of depolarization required for an action potential to occur. Hyperpolarization can either increase or decrease the distance between the resting state and the threshold potential, making it easier or harder for an action potential to occur. If hyperpolarization occurs too frequently or for too long, it can lead to a decrease in overall neural activity and potential disruptions in neural communication.

Common Mistakes And Misconceptions

Mistake/Misconception Correct Viewpoint
EPSP and IPSP are the same thing. EPSP and IPSP are two different types of postsynaptic potentials that have opposite effects on the neuron‘s membrane potential. EPSPs depolarize the membrane, while IPSPs hyperpolarize it.
Only one type of postsynaptic potential can occur at a time in a neuron. Both EPSPs and IPSPs can occur simultaneously in a neuron, depending on which neurotransmitters are released by presynaptic neurons onto its dendrites or cell body. The net effect of these potentials determines whether an action potential will be generated or not.
All neurotransmitters cause either EPSP or IPSP responses in neurons. Different neurotransmitters can cause either excitatory or inhibitory responses in neurons, depending on their receptors’ subtypes and locations on the postsynaptic membrane. For example, glutamate is usually an excitatory neurotransmitter, but it can also activate inhibitory receptors such as GABA(B) receptors under certain conditions. Similarly, GABA is typically an inhibitory transmitter but has been shown to produce excitation through ionotropic (GABA(A)) receptor activation under specific circumstances.
The strength of an EPSP/IPSP depends only on the amount of neurotransmitter released by presynaptic neurons. The strength of an EPSC/IPSC also depends on other factors such as the distance between synapses and dendrites/cell bodies, synaptic efficacy (i.e., how well presynaptic activity correlates with postsynaptic firing), and neuromodulation (i.e., how other signaling molecules modulate synaptic transmission). These factors contribute to shaping neuronal circuits’ plasticity and information processing capabilities.

Related Resources

  • Fast hyperpolarization following an excitatory postsynaptic potential in cat bladder parasympathetic neurons.
  • Simultaneous expression of excitatory postsynaptic potential/spike potentiation and excitatory postsynaptic potential/spike depression in the hippocampus.
  • Changes in field excitatory postsynaptic potential shape induced by tetanization in the CA1 region of the guinea-pig hippocampal slice.
  • Differential and selective antagonism of the slow-inhibitory postsynaptic potential and slow-excitatory postsynaptic potential by gallamine and pirenzepine in the superior cervical ganglion of the rabbit.
  • Modulation of action potential during the late slow excitatory postsynaptic potential in bullfrog sympathetic ganglia.
  • Age-related decrease in the N-methyl-D-aspartateR-mediated excitatory postsynaptic potential in hippocampal region CA1.
  • N-methyl-D-aspartate receptors mediate a slow excitatory postsynaptic potential in the rat midbrain dopaminergic neurons.
  • Composite nature of the monosynaptic excitatory postsynaptic potential.
  • Fluctuations in pyramid-pyramid excitatory postsynaptic potentials modified by presynaptic firing pattern and postsynaptic membrane potential using paired intracellular recordings in rat neocortex.
  • Bidirectional plasticity of excitatory postsynaptic potential (EPSP)-spike coupling in CA1 hippocampal pyramidal neurons.
  • Backpropagation of the delta oscillation and the retinal excitatory postsynaptic potential in a multi-compartment model of thalamocortical neurons.
  • 17beta-Estradiol reduces excitatory postsynaptic potential (EPSP) amplitude in rat basolateral amygdala neurons.
  • Somatostatin regulates excitatory amino acid receptor-mediated fast excitatory postsynaptic potential components in vagal motoneurons.
  • Frequency dependent activation of a slow N-methyl-D-aspartate-dependent excitatory postsynaptic potential in turtle cerebellum by mossy fibre afferents.
  • Adenosine inhibits the NMDA receptor-mediated excitatory postsynaptic potential in the hippocampus.
  • Serotonin attenuates a slow inhibitory postsynaptic potential in rat hippocampal neurons.
  • Differential and selective antagonism of the slow-inhibitory postsynaptic potential and slow-excitatory postsynaptic potential by gallamine and pirenzepine in the superior cervical ganglion of the rabbit.
  • Current hypotheses for the slow inhibitory postsynaptic potential in sympathetic ganglia.
  • Phaclofen inhibition of the slow inhibitory postsynaptic potential in hippocampal slice cultures: a possible role for the GABAB-mediated inhibitory postsynaptic potential.
  • A dopaminergic inhibitory postsynaptic potential mediated by an increased potassium conductance.
  • On the properties and origin of the GABAB inhibitory postsynaptic potential recorded in morphologically identified projection cells of the cat dorsal lateral geniculate nucleus.
  • Glutamate mediates an inhibitory postsynaptic potential in dopamine neurons.
  • Electrogenesis of the slow inhibitory postsynaptic potential in bullfrog sympathetic ganglia.
  • The slow inhibitory postsynaptic potential in rat hippocampal CA1 neurones is blocked by intracellular injection of QX-314.
  • Serotonin-mediated inhibitory postsynaptic potential in guinea-pig prepositus hypoglossi and feedback inhibition by serotonin.
  • Effects of methylphenidate on the inhibitory postsynaptic potential in rat locus coeruleus neurons.
  • The pathway for the slow inhibitory postsynaptic potential in bullfrog sympathetic ganglia.
  • The serotonergic inhibitory postsynaptic potential in prepositus hypoglossi is mediated by two potassium currents.
  • Effects of milnacipran on the inhibitory postsynaptic potential in neurons of the rat locus coeruleus.
  • A chloride-dependent inhibitory postsynaptic potential in cat trochlear motoneurons.
  • Monosynaptic muscarinic activation of K+ conductance underlies the slow inhibitory postsynaptic potential in sympathetic ganglia.