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Neuron axon hillock

The primary role of the sodium channels is to generate action potentials in excitable cells. In case of neurons, the sodium channel density is high at axon hillocks or axon initial segment where action potentials start to propagate. The sodium channels are also present in dendrites. The sodium channels contribute to amplifying synaptic inputs (particularly those distally located) and are actively involved in back propagation of action potentials into dendrites. Subtle differences in properties of sodium channels influence the dendritic processes of synaptic integration in and complex ways. [Pg.1305]

The transient change in the transmembrane potential upon excitation. An action potential cycle consists of a transient depolarization of the cell membrane of an excitable cell (such as a neuron) as a result of increased permeability of ions across the membrane, followed by repolarization, hyperpolarization, and finally a return to the resting potential. This cycle typically lasts 1-2 milliseconds and travels along the axon from the cell body (or, axon hillock) to the axonal terminus at a rate of 1-100 meters per second. See Membrane Potential... [Pg.25]

De Zeeuw Cl, Ruigrok TJH, Holstege JC, Schalekamp MPA, Voogd J (1990c) Intracellular labeling of neurons in the medial accessory olive of the cat III. Ultrastructure of axon hillock and initial segment and their GABAergic innervation. J. Comp. Neurol., 300, 495-510. [Pg.324]

A postsynaptic neuron generates an action potential only when the plasma membrane at the axon hillock is depolarized to the threshold potential by the summation of small depolarizations and hyperpolarlzatlons caused by activation of multiple neuronal receptors (see Figure 7-48). [Pg.295]

So how does the cell potential reach the threshold voltage The junction between two neurons is called a synapse, and this junction is usually located at the terminus of a presynaptic neuron and the axon hillock of the postsynaptic neuron. The axon hillock is the location where the axon joins the neuronal cell body, and it is here that the action potential begins. A signal coming from the presynaptic neuron can trigger an action potential in the postsynaptic neuron by causing the cell potential of the postsynaptic neuron to reach threshold voltage. [Pg.201]

Akhough they cannot fcmn an action potential, the dendrites can influence the cell potential at the axon hillock, and thus raise or lower the neuronal sensitivity to action potential formation. They do this by sununing other inputs from other neurons that, again, may be either excitatory inhitntory. [Pg.201]

The function of the central neurons is still more complex. These cells may have hundreds and even thousands of excitatory and inhibitory synaptic inputs. The greater part of their membrane, which can be covered by synapses, has to integrate all the excitatory and inhibitory impulses arriving at the cell. Only if this integration results in the depolarization of the membrane potential in the region of the axon-hillock up to the threshold level is a spike generated. [Pg.234]

Fig. 4 Fluorescent double labeling using the A 3 antibody 4G8 red and APP reeri in heat+FA pretreated sections from 1.5-month-old APP/PS1 Kl mice. The 4G8 antibody (1 10,000) mainly labeled larger granules at the axon hillock of cortical neurons and did not co-localize with APP staining. Blue counterstaining of nuclei in the merged pictures was performed with DAPI. Scale bar 10 pm (color figure online)... Fig. 4 Fluorescent double labeling using the A 3 antibody 4G8 red and APP reeri in heat+FA pretreated sections from 1.5-month-old APP/PS1 Kl mice. The 4G8 antibody (1 10,000) mainly labeled larger granules at the axon hillock of cortical neurons and did not co-localize with APP staining. Blue counterstaining of nuclei in the merged pictures was performed with DAPI. Scale bar 10 pm (color figure online)...
Using the protocol described in Sect. 3.4 with a combination of heat and FA pretreatment, the Ap antibody 4G8 predominantly labeled granular structures at the axon hillock of cortical neurons, not showing any co-localization with APP (Fig. 4). [Pg.189]


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