Dopamine modulation neurons

Waszezak, B.L., and Walters, J.R. Dopamine modulation of the effects of y-aminobutyric acid on substantia nigra pars reticulata neurons. Science 220 218-221, 1983. 

It is widely accepted that Parkinson s disease primarily results from degeneration of pigmented neurons in the substantia nigra (Gibb 1998). This causes a loss of nigrostriatal projections and lack of dopamine modulation in the striatum. In addition to loss of neurons, many of the remaining neurons contain Lewy bodies. 

Like presynaptic dopamine autoreceptors, presynaptic histamine autoreceptors are activated by the released endogenous transmitter to inhibit further histamine release, as shown by the increase in histamine release caused by antagonists at H3 receptors a definite piece of physiology. Evidence has been presented recently that cardiac postganglionic sympathetic neurons of the guinea pig synthesize and release histamine as a co-transmitter (Li et al. 2003 2006). These noradrenaline-histamine neurons possess H3 autoreceptors which, when activated, depress the release of both noradrenaline and histamine - unlike the D2-like autoreceptors of dopamine-neurotensin neurons which modulate the release of the two cotransmitters in opposite direction (see Section 2.2). It would be of interest to see whether, conversely, activation of ot2-autoreceptors inhibits the release of histamine in the guinea pig heart. 

Davila NG, Blakemore LJ, Trombley PQ (2003) Dopamine modulates synaptic transmission between rat olfactory bulb neurons in culture. J Neurophysiol 90 395 104 Delgado A, Sierra A, Querejeta E, Valdiosera RF, Aceves J (2000) Inhibitory control of the GABAergic transmission in the rat neostriatum by D2 dopamine receptors. Neuroscience 95 1043-8... 

Kreitzer AC, Malenka RC (2005) Dopamine modulation of state-dependent endocannabinoid release and long-term depression in the striatum. J Neurosci 25(45) 10537—45 Kreitzer AC, Regehr WG (2001) Retrograde inhibition of presynaptic calcium influx by endogenous cannabinoids at excitatory synapses onto purkinje cells. Neuron 29 717-27 Kreitzer AC, Carter AG, Regehr WG (2002) Inhibition of interneuron firing extends the spread of endocannabinoid signaling in the cerebellum. Neuron 34 787-96... 

Seamans JK, Gorelova N, Durstewitz D, Yang CR. 2001a. Bidirectional dopamine modulation of GABAergic inhibition in prefrontal cortical pyramidal neurons. J Neurosci 21 3628-3638. 

We found that a GSH deficit reversed the direction of DA modulation of NMDA responses (Steullet et al., 2008). In control neurons, DA enhanced NMDA responses. But in neurons with a BSO-induced GSH deficit, DA decreased NMDA responses via activation of D2-type receptors. This decrease disappeared when normal GSH levels were restored by GSH-ethyl ester, a membrane-permeable GSH analog. The difference in dopamine modulation of NMDA responses in control neurons and in neurons with a GSH deficit was mostly explained by a differential modulation of L-type calcium channels. DA enhanced the function of these channels in control neurons, but decreased it in BSO-treated neurons. The redox-sensitive ryanodine receptors (RyRs), which were enhanced in BSO-treated neurons, played an essential role in altering DA signaling in neurons with a GSH deficit. These data suggest that enhancement of the function of RyRs in neurons with low GSH levels favors D2-type receptor-mediated and calcium-dependent pathways, causing a change in DA modulation of L-type calcium channels and ultimately in DA modulation of NMDA responses. 

Steullet P, Lavoie S, Kraftsik R, Guidi R, Gysin R, et al. 2008. A glutathione deficit alters dopamine modulation of L-type calcium channels via D2 and ryanodine receptors in neurons. Free Radical Biol Med 44 1042-1054. 

Greif GJ, Lin YJ, Liu JC, Freedman JE (1995) Dopamine-modulated potassium channels on rat striatal neurons specific activation and cellular expression. J Neurosci /5 4533 4544. 

Lin YJ, Chen X, Freedman JE (1998) U-37883A potently inhibits dopamine-modulated K+ channels on rat striatal neurons. Eur J Pharmacol 552 335-341. 

Among the catecholamines, dopamine has long been of interest to both chemists and neuroscientists. It is one of the most important neurotransmitters and is ubiquitous in the mammalian central nervous system[5]. It modulates many aspects of brain circuitry in a major system of the brain including the extra pyramidal and mesolimbic system, as well as the hypothalamic pituitary axis[6]. It also plays a crucial role in the functioning of the central nervous, cardiovascular, renal and hormonal systems[4], A loss of dopamine containing neurons or its transmission is also related to a number of illnesses and conditions including Parkinson s disease, schizophrenia, motivational habit, reward mechanisms and the regulation of motor functions and in the function of the central nervous, hormonal and cardiovascular system[5,18,19]. It is therefore of interest to measure dopamine in the extracellular fluid in animals to order to monitor neurotransmission processes and correlate neurochemistry with behavior[19]. 

Davila NG, Blakemore LJ, Trombley PQ. 2003. Dopamine modulates synaptic transmission between rat olfectory bulb neurons in culture. J Neurophysiol 90 395-404. 

The basal nuclei are a collection of paired structures that modulate motor pathways from the cerebral cortex and play a role in the fine control of movement. Part of this is a pathway from the substantia nigra in the midbrain to an area called the striatum in the basal nuclei. The neurotransmitter of this pathway is dopamine and loss of dopamine-containing neurons here causes Parkinson s disease (see page 212). 

Typioal antipsyohotic drugs act in both extrapyramidal and limbio brain regions at D2-type dopamine receptors that can be located postsynaptically (on cell bodies, dendrites, and nerve terminals of other neurons) as well as presynaptioally on dopamine neurons. Dopamine reoeptors looated presynaptically on dopamine cell bodies and nerve terminals are called autoreceptors and aot to negatively modulate neuronal firing and dopamine synthesis and release (Fig. 22.3) (24). Low concentrations of oertain ... 

Dopamine, serotonin, and endogenous enkephalins (opiates) modulate neuronal activity. If you drop dopamine on isolated neurons, transmission of neuronal impulses is inhibited. Dopamine and serotonin counteract the effect of the stimulatory monoamines, epinephrine and norepinephrine. 

Several classes of drugs modulate the firing rates or patterns of midbrain dopamine neurons by direct, monosynaptic, or indirect, polysynaptic, inputs to the cell bodies within the ventral mesencephalon (i.e., nicotine and opiates). In contrast, amphetamine, cocaine, and methylphenidate act at the level of the dopamine terminal interfering with normal processes of transmitter packaging, release, reuptake, and metabolism. 

Even more sophisticated control of neurotransmitter release is suggested by the possibility of heteroceptors . These receptors are thought to be located on the terminals of, and to modulate transmitter release from, one type of neuron, but are activated by transmitter released from a different type of neuron (Laduron 1985). For example, noradrenaline has been proposed to modulate release of a wide range of transmitters (e.g. dopamine, 5-HT and glutamate) through activation of a2-heteroceptors on the terminals of each of these different types of neuron. However, one factor that should be borne in mind is that most of the evidence for heteroceptors comes from studies of... 

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