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Soma-dendritic autoreceptors

The dopamine-containing nigro-neostriatal dopaminergic neurons possess receptors for dopamine. These dopamine receptors occur on both the nerve terminals within the neostriatum (pre-synaptic autoreceptors) as well as on the soma and dendrites (soma-dendritic autoreceptors). Stimulation of either category of autoreceptor can regulate the synthesis, turnover and release of dopamine in the neostriatum but by different mechanisms. [Pg.132]

Systemical or intranigral application of dopamine receptor agonists depresses the firing of nigrostriatal dopamine cells by stimulating soma-dendritic autoreceptors in the zona compacta, an effect again antagonized by neuroleptics (110, 111, 112). ... [Pg.132]

Presynaptic H3 receptors also are uniform in their signal transduction. They couple to Gi/o proteins and decrease the depolarization-induced release of neurotransmitters by inhibiting multiple calcium channels (e.g., Arrang et al. 1985 Schlicker et al. 1994 Endou et al. 1994 Brown and Haas 1999 see Stark et al. 2004). For comparison, the signal transduction of soma-dendritic H3 autoreceptors in histamin-ergic neurons also involves a pertussis toxin-sensitive G-protein with subsequent inhibition of N- and P-type Ca2+ channels (Takeshita et al. 1998). The few exceptions to this signal transduction pathway are discussed in the corresponding subsections below (see Sections 3.1, 3.3, and 3.9). [Pg.306]

All G protein-coupled presynaptic 5-HT autoreceptors - there is no consistent evidence for 5-HT3 autoreceptors (Dorostkar and Boehm, this book) - are inhibitory. They belong mainly to the 5-HTi family and where subclassilied were 5-HTib or 5-HTid (Table 4). Non-5-HTi presynaptic autoreceptors, presumably 5-HTs and/or 5-HT7, replaced the 5-HTi-like receptors in 5-HTib knockout mice (Pineyro et al. 1995b see page 327 of Gothert and Schlicker 1997). Note that, as opposed to dopamine and histamine autoreceptors, 5-HT autoreceptors differ in the neurons terminal and soma-dendritic region in the latter, they are 5-HTia (Sprouse and Aghajanian 1986). [Pg.313]

As pointed out above (Section 4.2), 5-HTib agonists may dampen aggression via activation of 5-HTib autoreceptors. However, 5-HTib heteroreceptors may contribute (see Sari 2004). One hypothesis implicates inhibitory soma-dendritic 5-HTib receptors on vasopressin neurons in the anterior hypothalamus. Activity of these neurons promotes attacks and biting in rodents, hence inhibition of their activity leads to the opposite effect (Ferris et al. 1997). [Pg.323]

Autoreceptors (ARs) Interact with neurotransmitters produced by the same nerve, and consequently suppress or stimulate neurotransmitter release Into the synaptic cleft. They are located In the presynaptic nerve terminals or In the soma, dendrites, and axons of central nervous system neurons. [Pg.3]

Figure 17.4 The effect of neuroleptics on the activity of DA neurons. Although neuroleptics (DA antagonists) are used primarily to inhibit the postsynaptic effects of released DA they also increase the activity of the DA neuron itself since they (1) inhibit the effect of synaptic DA on nerve terminal autoreceptors and so increase DA release (2) block inhibitory DA autoreceptors on the soma of the DA neuron so that they cannot be stimulated by endogenous DA, possibly released from the neuron s own dendrites and (3) facilitate feedback excitation to the DA neuron from those neurons normally inhibited by distally released DA. All the DA receptors involved are D2 (or possibly D3). — Blocked by D2 antagonists (neuroleptics)... Figure 17.4 The effect of neuroleptics on the activity of DA neurons. Although neuroleptics (DA antagonists) are used primarily to inhibit the postsynaptic effects of released DA they also increase the activity of the DA neuron itself since they (1) inhibit the effect of synaptic DA on nerve terminal autoreceptors and so increase DA release (2) block inhibitory DA autoreceptors on the soma of the DA neuron so that they cannot be stimulated by endogenous DA, possibly released from the neuron s own dendrites and (3) facilitate feedback excitation to the DA neuron from those neurons normally inhibited by distally released DA. All the DA receptors involved are D2 (or possibly D3). — Blocked by D2 antagonists (neuroleptics)...
The 5-HTia receptor is located on the soma and the dendrites (somatodendritic autoreceptor) of 5-HT neurons, and at postsynaptic sites. Wang Aghajanian (1977), and Aghajanian Lakoski (1984) have shown that the somatodendritic autoreceptor mediates collateral inhibition, and that the ionic basis... [Pg.252]

G -protein-coupled receptors are often located on the presynaptic plasma membrane where they inhibit neurotransmitter release by reducing the opening of Ca2+ channels like inactivation and breakdown of the neurotransmitter by enzymes, this contributes to the neuron s ability to produce a sharply timed signal. An a2 receptor located on the presynaptic membrane of a noradrenaline-containing neuron is called an autoreceptor but, if located on any other type of presynaptic neuronal membrane (e.g., a 5-HT neuron), then it is referred to as a heteroreceptor (Langer, 1997). Autoreceptors are also located on the soma (cell body) and dendrites of the neuron for example, somatodendritic 5-HTia receptors reduce the electrical activity of 5-HT neurons. [Pg.23]

FIGURE 5—20. Both types of presynaptic alpha 2 autoreceptors are shown here. They are located either on the axon terminal, where they are called terminal alpha 2 receptors, or at the cell body (soma) and nearby dendrites, where they are called somatodendritic alpha 2 receptors. [Pg.161]

When the autoreceptor is located on the soma or dendrites of the nerrrone it is termed... [Pg.11]


See other pages where Soma-dendritic autoreceptors is mentioned: [Pg.323]    [Pg.135]    [Pg.323]    [Pg.135]    [Pg.360]    [Pg.334]    [Pg.225]    [Pg.298]    [Pg.310]    [Pg.282]    [Pg.282]    [Pg.300]    [Pg.300]    [Pg.183]    [Pg.169]    [Pg.16]    [Pg.160]   


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Autoreceptors

Autoreceptors soma-dendritic, stimulation

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