In excitatory postsynaptic potentials, an excitatory response is generated.

This phenomenon is known as an excitatory postsynaptic potential (EPSP).

Electrical stimuli to the auditory nerve evoke a graded excitatory postsynaptic potential in the octopus cells.

This depolarization is called the excitatory postsynaptic potential (EPSP).

Action potentials are most commonly initiated by excitatory postsynaptic potentials from a presynaptic neuron.

Population spikes often reflect synaptically induced firing and therefore, they can be classified as a type of field excitatory postsynaptic potentials.

In addition, NO increases the frequency of miniature excitatory postsynaptic potentials (e.p.s.ps) in hippocampal cultures.

The DS ganglion cells respond to their preferred direction with a large excitatory postsynaptic potential followed by a small inhibitory response.

Sometimes this can be due to a phenomenon caused by inhibition called shunting, which is the decreased conductance of excitatory postsynaptic potentials.

In particular, norepinephrine decreases glutamatergic excitatory postsynaptic potentials by the activation of α-adrenergic receptors.

Depressed excitatory postsynaptic potentials (EPSPs) result from this particular stimulation pattern.

On the other hand, they respond to their null direction with a simultaneous small excitatory postsynaptic potential and a large inhibitory postsynaptic potential.

These neurotransmitters are "captured" by cell surface receptors, which generate an excitatory postsynaptic potential, in order to transmit the impulse again to another cell.

In many cases the excitatory postsynaptic potential (EPSP) will not reach the threshold for eliciting an action potential.

Those that are excitatory are referred to as excitatory postsynaptic potential (EPSP).

The initial term I represents the current arriving from external sources, such as excitatory postsynaptic potentials from the dendrites or a scientist's electrode.

If the cell is receiving two excitatory postsynaptic potentials, they combine so that the membrane potential is depolarized by the sum of the two changes.

The neurotransmitter glutamate, for example, is predominantly known to trigger excitatory postsynaptic potentials (EPSPs).

These neurons displayed a higher frequency and larger amplitudes of miniature excitatory postsynaptic potentials (mEPSP).

An excitatory postsynaptic potential (EPSP) opens the channels, thus generating a LTS.

This is an excitatory postsynaptic potential (EPSP), as it brings the neuron's potential closer to its firing threshold (about -50mV).

AMPA generates fast excitatory postsynaptic potentials (EPSP).

The most typical functional change in chromatolytic motor neurons is the significant reduction in size of the monosynaptic excitatory postsynaptic potentials (EPSPs).

On the other hand, norepinephrine appears to inhibit glutamatergic excitatory postsynaptic potentials (EPSPs) in the central nervous system by the activation of alpha-1 adrenergic receptors.

Increased NT-3/trkC binding results in larger monosynaptic excitatory postsynaptic potentials (EPSPs) and reduced polysynaptic components.

EPSP(excitatory post-synaptic potential)

Gil et al. (1997) applied the cholinergic agonist muscarine to neocortical layers and found that excitatory post-synaptic potentials between intracortical synapses were depressed.

Looking more closely at electrotonic coupling, gap junctions permit the diffusion of current across linked cells and result in higher resistance to action potential induction since excitatory post-synaptic potentials must to diffuse across a greater membrane area.

It has been determined from electrophysiological data that excitatory synapses on proximal apical dendrites of prefrontal cortex pyramidal neurons serve to amplify excitatory post-synaptic potential (EPSP) signals generated in distal apical dendrites.

One hypothesis suggests that in the frontal cortex, 5HT promotes late asynchronous excitatory post-synaptic potentials, a process antagonized by serotonin itself through 5HT which may explain why SSRI's and other serotonin-affecting drugs do not normally cause a patient to hallucinate.