Dopamine In Corpus Striatum Research Articles

Effects of ethanol on brain monoamine content of spontaneously hypertensive rats (SHR).

Spontaneously hypertensive rats (SHR) were administered either 2.4 g/kg ethanol or an isocaloric glucose daily for 4 weeks and the levels of norepinephrine (NE), epinephrine (EP), dopamine (DA), serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) in different brain regions were determined. Results indicated a 3-fold increase in NE level in brain stem and hypothalamus and more than 2-fold increase in DA in corpus striatum in alcohol-treated rats as compared to controls. There was a significant increase in the level of DA in the corpus striatum but the levels in cerebral cortex, brain stem and hippocampus were decreased instead. Decreases in 5-HT levels were found in hypothalamus, brain stem, cortex and cerebellum of alcohol-treated brain as compared to untreated controls. These results indicate alterations of the biogenic amine contents in different regions of the SHR brain after chronic ethanol ingestion. Since stimulated release of biogenic amines in the SHR brain has been implicated in the regulation of blood pressure, changes due to ethanol ingestion may be a risk factor in hypertensive patients.

Ontogeny of dopaminergic function in the rat midbrain tegmentum, corpus striatum and frontal cortex

Ontogenic development of the dopaminergic system in rat brain was investigated. This was accomplished by monitoring changes in postsynaptic dopamine receptor formation and presynaptic dopamine content in the midbrain tegmentum, frontal cortex and corpus striatum from the 18th day of gestation through adulthood. The dopamine antagonist spiperone was used as the binding ligand to quantitate receptor number while dopamine content was measured chromatographically. [ 3H]Spiperone binding kinetics in adult animals revealed that the maximum number of receptor sites ( B max) was 160, 900 and 597 fmol/mg protein in midbrain tegmentum, frontal cortex and corpus striatum, respectively, while the corresponding equilibrium constant ( K d) values were 0.15, 0.52 and 0.15 nM. During the course of development, the affinity for spiperone binding in corpus striatum and frontal cortex did not change significantly, while in midbrain tegmentum the binding affinity in younger animals was significantly lower. Results from competitive inhibition experiments using various serotonergic and dopaminergic antagonists suggested that at all ages dopamine D 2-receptors were responsible for spiperone binding in corpus striatum and midbrain tegmentum. In frontal cortex, binding properties consistent with D 2-receptors were observed in non-adult animals; by the time adulthood was reached, however, spiperone binding characteristics were altered and appeared to correspond to serotonin sites. The developmental patterns of the dopaminergic markers were different in all 3 tissues. Adult receptor levels were achieved very early in midbrain tegmentum, while increases in receptor number continued in corpus striatum and frontal cortex, at different rates, throughout the postnatal period. A marked increase in dopamine in corpus striatum occurred during the second and third postnatal weeks and the transmitter content remained relatively constant after this time. Transient fluctuations in endogenous dopamine during the postnatal period were observed in midbrain tegmentum and frontal cortex. A general feature of the ontogenic pattern in all tissues appeared to be increases in dopamine receptor preceding increases in dopamine synthesis. A hypothesis on the developmental regulation of dopamine neurons was derived.

Nonaminergic striatal neurons convert exogenous L-dopa to dopamine in parkinsonism.

In intact striatum, the enzyme dopa decarboxylase is localized predominantly in dopaminergic nerve terminals. In Parkinson disease, loss of dopaminergic neurons is associated with massive depletion of striatal decarboxylase activity. Nevertheless, efficacy of exogenous L-dopa in parkinsonism is generally believed to result from its enzymatic decarboxylation to dopamine in the corpus striatum. It has previously been suggested that, after degeneration of nigrostriatal pathways, decarboxylation of administered L-dopa may occur mainly at such striatal sites as surviving dopaminergic terminals, serotonergic neurons, or capillaries; but currently available data do not favor these hypotheses. Recent experimental studies indicate that a substantial amount of decarboxylase activity is localized in striatal interneurons or efferent neurons that may not normally synthesize monoamines. We propose that after depletion of dopaminergic terminals, these nonaminergic striatal neurons may contain a large fraction of residual dopa decarboxylase activity and may represent an important locus for conversion of administered dopa to functional dopamine in the parkinsonian corpus striatum.

The effect of X-irradiation on the amount of dopamine in corpus striatum of the rat

The effect of ionizing radiation on the amount of dopamine in corpus striatum was investigated in rats exposed to 650 or 850 R of X-rays. The amount of dopamine in the corpus striatum was measured fluorimetrically in various periods of time after irradiation. It was found that, irrespective of the dose applied, the ionizing radiation caused a significant depletion of dopamine in the striatum.

Investigations of the mechanism of central action of kinins.

The effects of kinins on the level of norepinephrine, dopamine, and serotonin and on their metabolites, i.e., normetanephrine, homovanillic acid, and 5-hydroxyindoloacetic acid in the brain tissue divided into cerebellum, corpus striatum, cortex, hippocampus, hypothalamus, medulla oblongata, and midbrain were investigated. It was shown that bradykinin in a dose of 4 mug decreased the content of norepinephrine in corpus striatum, midbrain, and cerebellum. It also decreased the level of dopamine in corpus striatum but increased the level of serotonin in corpus striatum and midbrain. Similar changes were observed with 100 Mu/kg of kallikrein. It was that changed levels of investigated neuromediators are accompanied by changed levels of their metabolites. Bradykinin, in a dose of 4 mug, decreased the level of normetanephrine in corpus striatum, hippocampus, and midbrain and the level of homovanillic acid in corpus striatum, and increased the level of 5-hydroxyindoloacetic acid in corpus striatum and hippocampus. It was also shown that bradykinin increased norepinephrine uptake by the blood platelets when its level in the platelets was low, and released the absorbed norepinephrine into the medium when the level of norepinephrine was higher. The above results confirm the existence of an interaction of kinins with neuromediators in the central nervous system.

The nigrostriatal pathway: A correlative study based on neuroanatomical and neurochemical criteria in the cat and the monkey

Localized lesions of the corpus striatum result in a regional cell loss in the ipsilateral substantia nigra. Unilateral lesions of the ventromedial tegmental area (Tsaï) in the upper midbrain or caudal hypothalamus result in a complete cell loss in the corresponding substantia nigra and nucleus parabrachialis pigmentosus. The latter morphological changes are associated with a decreased concentration of dopamine in the ipsilateral corpus striatum. Lesions of the rostrolateral hypothalamus involving the region of the medial forebrain bundle (MFB) produce similar morphological and chemical changes. Caudolateral lesions of the substantia nigra result in a decreased concentration of dopamine in the laterocaudal part of the corpus striatum corresponding to the caudal putamen. The interruption of the striatonigral fibers does not produce any cell change in the substantia nigra. Lesions of the entopeduncular nucleus or of the ventral thalamus do not produce any cell change in the substantia nigra and are associated with a normal concentration of dopamine in the corpus striatum. These results suggest that the nigrostriatal fibers establish a topographical relationship between corresponding regions of the substantia nigra and the corpus striatum similar to that disclosed in the striatonigral pathway. This striato-nigro-striatal loop represents a peculiar mechanism involved in the synthesis of striatal dopamine.