Discover the Surprising Differences Between EPSP and IPSP in Neuroscience – Boost Your Brain Knowledge Today!
Contents
- What is the role of neurotransmitter release in EPSP and IPSP?
- What is the depolarization effect in EPSP and how does it differ from IPSP?
- What are GABAergic neurons and their involvement in IPSP?
- How does hyperpolarization effect play a role in both EPSP and IPSP?
- Common Mistakes And Misconceptions
- Related Resources
What is the role of neurotransmitter release in EPSP and IPSP?
What is the depolarization effect in EPSP and how does it differ from IPSP?
What are GABAergic neurons and their involvement in IPSP?
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.