Catecholamine alterations in experimental hydrocephalus

Miyake, Hirohisa; Eghwrudjakpor, Patrick O.; Sakamoto, Takashi; Mori, Koreaki

doi:10.1007/bf00300789

Cited by 11 publications

(5 citation statements)

References 21 publications

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“…In the present study, striatal TH level was not affected by hydrocephalus (Fig. 7 A, B), in accord with earlier reports that striatal dopamine level remained steady in experimental hydrocephalic rats and rabbits [ 11 , 39 , 41 ]. In the striatum, dopamine binds to DR1 and DR2, expressed preferentially on d and i-MSNs respectively.…”

Section: Discussionsupporting

confidence: 93%

Modulation of striatal glutamatergic, dopaminergic and cholinergic neurotransmission pathways concomitant with motor disturbance in rats with kaolin-induced hydrocephalus

Chen

Tseng

2022

Fluids Barriers CNS

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Background Hydrocephalus is characterized by abnormal accumulation of cerebrospinal fluid in the cerebral ventricles and causes motor impairments. The mechanisms underlying the motor changes remain elusive. Enlargement of ventricles compresses the striatum of the basal ganglia, a group of nuclei involved in the subcortical motor circuit. Here, we used a kaolin-injection juvenile rat model to explore the effects of acute and chronic hydrocephalus, 1 and 5 weeks post-treatment, respectively on the three major neurotransmission pathways (glutamatergic, dopaminergic and cholinergic) in the striatum. Methods Rats were evaluated for motor impairments. Expressions of presynaptic and postsynaptic protein markers related to the glutamatergic, dopaminergic, and cholinergic connections in the striatum were evaluated. Combined intracellular dye injection and substance P immunohistochemistry were used to distinguish between direct and indirect pathway striatal medium spiny neurons (d and i-MSNs) for the analysis of their dendritic spine density changes. Results Hydrocephalic rats showed compromised open-field gait behavior. However, male but not female rats displayed stereotypic movements and compromised rotarod performance. Morphologically, the increase in lateral ventricle sizes was greater in the chronic than acute hydrocephalus conditions. Biochemically, hydrocephalic rats had significantly decreased striatal levels of synaptophysin, vesicular glutamate transporter 1, and glutamatergic postsynaptic density protein 95, suggesting a reduction of corticostriatal excitation. The expression of GluR2/3 was also reduced suggesting glutamate receptor compositional changes. The densities of dendritic spines, morphological correlates of excitatory synaptic foci, on both d and i-MSNs were also reduced. Hydrocephalus altered type 1 (DR1) and 2 (DR2) dopamine receptor expressions without affecting tyrosine hydroxylase level. DR1 was decreased in acute and chronic hydrocephalus, while DR2 only started to decrease later during chronic hydrocephalus. Since dopamine excites d-MSNs through DR1 and inhibits i-MSNs via DR2, our findings suggest that hydrocephalus downregulated the direct basal ganglia neural pathway persistently and disinhibited the indirect pathway late during chronic hydrocephalus. Hydrocephalus also persistently reduced the striatal choline acetyltransferase level, suggesting a reduction of cholinergic modulation. Conclusions Hydrocephalus altered striatal glutamatergic, dopaminergic, and cholinergic neurotransmission pathways and tipped the balance between the direct and indirect basal ganglia circuits, which could have contributed to the motor impairments in hydrocephalus.

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Section: Discussionsupporting

confidence: 93%

Modulation of striatal glutamatergic, dopaminergic and cholinergic neurotransmission pathways concomitant with motor disturbance in rats with kaolin-induced hydrocephalus

Chen

Tseng

2022

Fluids Barriers CNS

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“…In another study, levels of norepinephrine in the brain were unchanged in experimental hydrocephalus, but activity of norepinephrine neurons was decreased after stimulation [100]. However, kaolin-induced hydrocephalus in rats did not increase brain levels of dopamine [100]. In an experimental adult rat model of hydrocephalus norepinephrine levels were increased in the brain [60].…”

Section: Cerebral Cortex and Basal Gangliamentioning

confidence: 96%

“…Overexpression of transforming growth factor ~1 (TGF-~l) in the brain has been related to the induction of hydrocephalus in mice [41,138]. In another study, levels of norepinephrine in the brain were unchanged in experimental hydrocephalus, but activity of norepinephrine neurons was decreased after stimulation [100]. Norepinephrine neuronal pathways show a reduction of Cerebral Cortex and Basal Ganglia 71 norepinephrine levels [36].…”

Section: Cerebral Cortex and Basal Gangliamentioning

confidence: 99%

Pathophysiology of Hydrocephalus

Silva

2005

Pediatric Hydrocephalus

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Hydrocephalus is a pathological entity that has been known since Hippocrates and Galen [33]. It is one of the most common disorders treated by neurosurgeons. The overall incidence and prevalence of the disease can be difficult to estimate, as it can occur as an isolated entity or in association with other neurological disorders. Congenital hydrocephalus is present in 3 of 1000 live births [97]. Aside from the congenital etiology, hydrocephalus can result from a series of neurological conditions such as head trauma, intracranial hemorrhage, tumor, or infection of the central nervous system at any time during life.Whatever its cause, the symptomatology of hydrocephalus is remarkably similar among patients. The radiological appearance is also deceptively alike for most age groups. However, age is an important factor in determining the clinical picture. Hydrocephalus due to a congenital infection of the central nervous system in a neonate is a different disorder from the normal-pressure hydrocephalus of the adult, despite the fact that both are morphologically represented by ventriculomegaly. Like the etiology, the specific damage caused by hydrocephalus is also strongly influenced by the age at onset of the disease.The pathophysiology of hydrocephalus is much more complex than its clinical or radiological presentation, going beyond the ventricular dilatation and mantle thinning obvious at first inspection. Together with gross macroscopic changes, hydrocephalus leads to alterations of the normal physiology, biochemistry, and ultrastructure of the brain. Three factors are basic for the determination of the severity of the injuries caused by hydrocephalus and the ultimate outcome. They are: age at onset, etiology, and the duration of the disease.The stage of maturation of the brain afflicted by hydrocephalus must be taken into account when discussing pathophysiology. Development is a fundamental aspect of the physiology of the brain in young immature animals and humans: metabolic pathways are maturing, neuronal activity is greatly increased, biosynthetic activity is intense, and myelination proceeds at a

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“…This method could also allow us to better evaluate if there are any rostrocaudal differences in the LC concerning the effects of kaolin injection. In hydrocephalus models, decreases in surrogate markers of NA levels were reported at the cortex and hippocampus [ 35 , 36 ], whereas the opposite was shown at the striatum [ 35 , 37 ]. Since the LC is the main source of noradrenergic fibers in the brain, it will be important to ascertain if there are changes in noradrenaline transport in the brain during hydrocephalus [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

Pain Modulation from the Locus Coeruleus in a Model of Hydrocephalus: Searching for Oxidative Stress-Induced Noradrenergic Neuroprotection

Louçano

Oliveira

Martins

et al. 2022

IJMS

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Pain transmission at the spinal cord is modulated by noradrenaline (NA)-mediated actions that arise from supraspinal areas. We studied the locus coeruleus (LC) to evaluate the expression of the cathecolamine-synthetizing enzyme tyrosine hydroxylase (TH) and search for local oxidative stress and possible consequences in descending pain modulation in a model of hydrocephalus, a disease characterized by enlargement of the cerebral ventricular system usually due to the obstruction of cerebrospinal fluid flow. Four weeks after kaolin injection into the cisterna magna, immunodetection of the catecholamine-synthetizing enzymes TH and dopamine-β-hydroxylase (DBH) was performed in the LC and spinal cord. Colocalization of the oxidative stress marker 8-OHdG (8-hydroxyguanosine; 8-OHdG), with TH in the LC was performed. Formalin was injected in the hindpaw both for behavioral nociceptive evaluation and the immunodetection of Fos expression in the spinal cord. Hydrocephalic rats presented with a higher expression of TH at the LC, of TH and DBH at the spinal dorsal horn along with decreased nociceptive behavioral responses in the second (inflammatory) phase of the formalin test, and formalin-evoked Fos expression at the spinal dorsal horn. The expression of 8-OHdG was increased in the LC neurons, with higher co-localization in TH-immunoreactive neurons. Collectively, the results indicate increased noradrenergic expression at the LC during hydrocephalus. The strong oxidative stress damage at the LC neurons may lead to local neuroprotective-mediated increases in NA levels. The increased expression of catecholamine-synthetizing enzymes along with the decreased nociception-induced neuronal activation of dorsal horn neurons and behavioral pain signs may indicate that hydrocephalus is associated with alterations in descending pain modulation.

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Catecholamine alterations in experimental hydrocephalus

Cited by 11 publications

References 21 publications

Modulation of striatal glutamatergic, dopaminergic and cholinergic neurotransmission pathways concomitant with motor disturbance in rats with kaolin-induced hydrocephalus

Modulation of striatal glutamatergic, dopaminergic and cholinergic neurotransmission pathways concomitant with motor disturbance in rats with kaolin-induced hydrocephalus

Pathophysiology of Hydrocephalus

Pain Modulation from the Locus Coeruleus in a Model of Hydrocephalus: Searching for Oxidative Stress-Induced Noradrenergic Neuroprotection

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