Localization of Melanocortin 1 Receptor in the Substantia Nigra.

Recent findings have revealed that melanocortin 1 receptor (MC1R) deficiency leads to Parkinson's disease-like dopaminergic neurodegeneration in the substantia nigra (SN). However, its precise distribution and expressing-cell type in the SN remain unclear. Therefore, in this study, we analyzed the localization and characteristics of MC1R in the SN using histological methods, including in situ hybridization and immunohistochemistry.

Attractin deficiency causes metabolic and morphological abnormalities in slow-twitch muscle.

Skeletal muscle fibers are classified as slow-twitch and fast-twitch fibers, which have different reactive oxygen species (ROS) metabolism and mitochondrial biogenesis. Recently, Attractin (Atrn), which encodes secreted (sAtrn) and transmembrane (mAtrn)-type proteins, has been shown to be involved in free radical scavenging. Although Atrn has been found in skeletal muscle, little is known about the expression levels and function of Atrn in each muscle fiber type.

Microhemorrhage in a Rat Model of Neonatal Shaking Brain Injury: Correlation between MRI and Iron Histochemistry.

Previous studies have shown that neonatal shaking brain injury (SBI) causes transient microhemorrhages (MHs) in the gray matter of the cerebral cortex and hippocampus. Iron deposits and iron-uptake cells are observed surrounding MHs in this SBI model, suggesting local hypoxic-ischemic conditions. However, whether the shaken pups suffered systemic hypoxic-ischemic conditions has remained uncertain.

Neonatal shaking brain injury changes psychological stress-induced neuronal activity in adult male rats.

Neonatal shaking brain injury (SBI) leads to increases in anxiety-like behavior and altered hormonal responses to psychological stressors as adults. These abnormalities are hypothesized to be due to a change in sensitization in neuronal circuits as a consequence of neonatal SBI. We examined the effects of neonatal SBI on neuronal activity in the anxiety- and/or stress-related areas of adult rats using Fos immunohistochemistry.

Behavioral, hormonal, and neurochemical outcomes of neonatal repeated shaking brain injury in male adult rats.

It is well known that an abusive environment in childhood is related to individual anxiety behavior in adulthood. Though an imbalance of adrenocorticosteroid receptors and a dysfunction of monoaminergic neuron systems have been proposed, the underlying mechanisms are not fully understood. To address these problems, we recently developed a new model of shaking brain injury (SBI) in neonatal rats.

Repeated mild shaking of neonates induces transient cerebral microhemorrhages and anxiety-related behavior in adult rats.

Growing evidence suggests that neonatal cerebral microhemorrhages (MHs) are implicated in neuropsychiatric diseases in adults. Although animal studies have identified the progression of the underlying mechanisms of MHs, few studies have investigated the histopathology and behavioral outcomes. In this study, we created an experimental rat model of MHs using a new experimental device for repeated mild shaking brain injury (SBI) in the neonatal period and examined temporal changes in MHs using susceptibility weighted imaging (SWI) and iron histochemistry.

Role of neuronal nitric oxide synthase in slowly progressive dopaminergic neurodegeneration in the Zitter rat.

Neuronal nitric oxide synthase (nNOS) is involved in nigrostriatal dopaminergic (DA) neurodegeneration. However, little is known about the distribution patterns and functions of nNOS in slowly progressive DA neurodegeneration. Here we describe the spatiotemporal change in nNOS expression over the course of neurodegeneration and the effect of short- or long-term treatment with the nNOS inhibitor, 7-nitroindazole (7-NI), in zitter (zi/zi) rats.

Tyrosine hydroxylase afferents to the interstitial nucleus of the posterior limb of the anterior commissure are neurochemically distinct from those projecting to neighboring nuclei.

The interstitial nucleus of the posterior limb of the anterior commissure (IPAC) is exclusively innervated by tyrosine hydroxylase-immunoreactive (TH-IR) fibers as observed in the other nuclei of the rat forebrain such as the striatum and nucleus accumbens. Distinguishing TH-IR afferents to the IPAC from those projecting to neighboring nuclei has been difficult. However, we previously showed that the TH-IR fibers projecting to the IPAC were invulnerable to neurodegeneration in zitter mutant rats, whereas almost all TH-IR afferents fibers to the dorsolateral striatum were lost, indicating that these two groups of TH-IR afferents have distinct neurochemical properties.

Age-related behavioral, morphological and physiological changes in the hippocampus of zitter rats.

Convulsive seizure is known to be associated with hippocampal abnormalities, such as hilar cell degeneration, abnormal mossy fiber sprouting in the dentate gyrus (DG) and abnormal expression of immediate early genes. However, whether these morphological changes are a cause or consequence of convulsive seizures has remained contentious. Zitter (zi/zi) rats carry a mutation of the attractin gene and display spongiform degeneration of the brain.

Effects of environmental enrichment on the activity of the amygdala in micrencephalic rats exposed to a novel open field.

Environmental enrichment (EE) mediates recovery from sensory, motor, and cognitive deficits and emotional abnormalities. In the present study, we examined the effects of EE on locomotor activity and neuronal activity in the amygdala in control and methylazoxymethanol acetate (MAM)-induced micrencephalic rats after challenge in a novel open field. Control rats housed in EE (CR) showed reduced locomotor activity compared to rats housed in a conventional cage (CC), whereas hyperactivity was seen in MAM rats housed in a conventional cage (MC) and in MAM rats housed in EE (MR).

Neuroprotective effects of melatonin on the nigrostriatal dopamine system in the zitter rat.

Melatonin has ubiquitous actions, both as a direct free-radical scavenger and as an indirect anti-oxidant. The present study examined in vivo neuroprotective effects of melatonin on the nigrostriatal dopaminergic system in zitter (zi/zi) rat, which displays abnormal metabolism of superoxide leading to age-related degeneration of the dopaminergic system. For up to 9 months after weaning, zi/zi rats had ad libitum access to drinking water containing melatonin.

A rhythmic change of vesicular glutamate transporter (VGLUT) 2 expression in the rat pineal gland.

The pineal gland secretes melatonin under circadian control via nocturnal noradrenergic stimulation, and expresses vesicular glutamate transporter (VGLUT) 1, VGLUT2 and a VGLUT1 splice variant (VGLUT1v). Although we previously reported that VGLUT2 mRNA level of rat pineal gland at postnatal day 21 is higher in the nighttime than in daytime, questions remained as to the time of postnatal onset of this phenomenon and a 24-h change in the mRNA or protein level at postnatal days. The day-night difference in VGLUT2 mRNA level was evident 14 days after birth.

Temporally distinct expression of vesicular glutamate transporters 1 and 2 during embryonic development of the rat olfactory system.

To study the development of glutamatergic neurons during the main olfactory bulb morphogenesis in rats, we examined the expression of vesicular glutamate transporters 1 (VGLUT1) and 2 (VGLUT2). On VGLUT1, expressions of mRNA and immunoreactivity were first detected in the mitral cell layer on embryonic day (E) 17.5 and E18.

Application of Fluoro-Jade C in acute and chronic neurodegeneration models: utilities and staining differences.

Recent neuropathological studies have shown that Fluoro-Jade C (FJC), an anionic fluorescent dye, is a good marker of degenerating neurons. However, those studies have mostly examined acute rather than chronic models of neurodegeneration. We therefore compared FJC staining using the intrastriatal 6-hydroxydopamine (6-OHDA)-injected rat as an acute model and the zitter rat as a chronic model, as both show dopaminergic (DA) neurodegeneration.