Dopamine midbrain

Dopamine Midbrain (substantia nigra) Neuronal synapse Neuronal connections in cerebral striatum... 

Both psychostimulants D-amphetamine and cocaine elevate extracellular dopamine concentrations in the terminal region of midbrain dopamine neurons,... 

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. 

Chiodi, LA and Bunney, BS (1983) Typical and at q)ical neuroleptics differential effects of chronic administration on the activity of A9 and AlO midbrain dopamine neurones. J. Neurosci. 3 1607-1619. 

The motor activation produced by psychomotor stimulants has been long associated with the midbrain dopamine systems. While focused stereotyped behavior produced by high doses of indirect sympathomimetics is blocked by removal of dopamine terminals in the corpus striatum (Creese and Iversen 1975), the locomotor activation produced by low doses of indirect sympathomimetics is blocked by removal of dopamine terminals in the region of the nucleus accumbens (Kelly et al. 1975). This dopaminergic substrate for psychostimulant effects appears selective for the indirect sympathomimetics in that dopamine lesions to the region of the nucleus... 

Freeman, A.S., and Bunney, B.S. The effects of phencyclidine and N-allylnormetazocine on midbrain dopamine neuronal activity. 

The extrapyramidal motor system controls muscle movement through a system of pathways and nerve tracts that connect the cerebral cortex, basal ganglia, thalamus, cerebellum, reticular formation, and spinal neurons. Patients with PD lose dopamine neurons in the substantia nigra, which is located in the midbrain within the brain stem. The substantia... 

Figure 7.3 Interspike interval (ISI) histograms of midbrain dopamine neural firing in behaving rats (reproduced with permission from (Miller et al. 1983)). Note the nearly identical mean intervals, consistent with reported mean firing rate similarities between SWS and REM sleep, as opposed to the broader ISI range observed in REM sleep, reflective of the burst firing in a significant subpopulation of neurons (contrast the widths of the dashed bars above the histograms).

Some less obvious phenomena of catecholamine transport and biosynthesis further illustrate the complexities of deciphering how efferents from midbrain dopamine neurons contribute to sleep-wake regulation. The plasma membrane norepinephrine transporter (NET), which is responsible for the uptake of extracellular noradrenaline, can also readily transport dopamine, and does so in vivo. This... 

Blackburn T., Suzuki K, Ashby C., Jr. (2006). The acute and chronic administration of the 5-HT (2B/2C) receptor antagonist SB-200646A significantly alters the activity of spontaneously active midbrain dopamine neurons in the rat an in vivo extracellular single cell study. Synapse. 59, 502-12. 

Georges F., Aston-Jones G. (2001). Potent regulation of midbrain dopamine neurons by the bed nucleus of the stria terminalis. J. Neurosci. 21(16), RC160. 

Grenhoff J., North R., Johnson S. (1995). Alpha 1-adrenergic effects on dopamine neurons recorded intracellularly in the rat midbrain slice. Eur. J. Neurosci. 7, 1707-13. 

Olijslagers J., Werkman T., McReary A. et al. (2004). 5-HT2 receptors differentially modulate dopamine-mediated auto-inhibition in A9 and A10 midbrain areas of the rat. Neuropharmacology 46, 504 10. 

The neural structures involved in the promotion of the waking (W) state are located in the (1) brainstem [dorsal raphe nucleus (DRN), median raphe nucleus (MRN), locus coeruleus (LC), laterodorsal and pedunculopontine tegmental nuclei (LDT/PPT), and medial-pontine reticular formation (mPRF)] (2) hypothalamus [tuberomammillary nucleus (TMN) and lateral hypothalamus (LH)[ (3) basal forebrain (BFB) (medial septal area, nucleus basalis of Meynert) and (4) midbrain ventral tegmental area (VTA) and substantia nigra pars compacta (SNc) (Pace-Schott Hobson, 2002 Jones, 2003). The following neurotransmitters function to promote W (1) acetylcholine (ACh LDT/PPT, BFB) (2) noradrenaline (NA LC) (3) serotonin (5-HT DRN, MRN) (4) histamine (HA TMN) (5) glutamate (GLU mPRF, BFB, thalamus) (6) orexin (OX LH) and (7) dopamine (DA VTA, SNc) (Zoltoski et al, 1999 Monti, 2004). 

Ochi, J. Shimizu, K. (1978). Occurrence of dopamine-containing neurons in the midbrain raphe nuclei. Neurosci. Lett. 8, 317-20. 

Sulzer, D., Maidment, N.T., and Rayport, S., Amphetamine and other weak bases act to promote reverse transport of dopamine in ventral midbrain neurons, J. Neurochem., 60, 527, 1993. 

Wu, X. and French, E.D., Effects of chronic delta9-tetrahydrocannabinol on rat midbrain dopamine neurons an electrophysiological assessment, Neuropharmacology, 39, 391, 2000. 

Dani, J.A., Radcliffe, K.A., Pidoplichko, V.I. Variations in desensitization of nicotinic acetylcholine receptors from hippocampus and midbrain dopamine areas. Eur. J. Pharmacol. 393 31, 2000. 

Wooltorton, J.R., Pidoplichko, V.I., Broide, R.S., Dani, J. A. Differential desensitization and distribution of nicotinic acetylcholine receptor subtypes in midbrain dopamine areas. J. Neurosci. 23 3176, 2003. 

Wu, J., George, A.A., Schroeder, K.M. et al. Electrophysiological, pharmacological, and molecular evidence for alpha7-nicotinic acetylcholine receptors in rat midbrain dopamine neurons. J. Pharmacol. Exp. Ther. 311 80, 2004. 

Pidoplichko, V.I., DeBiasi, M., Williams, J.T., Dani, J.A. Nicotine activates and desensitizes midbrain dopamine neurons. Nature. 390 401, 1997. 

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