Expression of a heroin contextually conditioned immune effect in male rats requires CaMKIIα-expressing neurons in dorsal, but not ventral, subiculum and hippocampal CA1

Our recent study revealed that photobiomodulation (PBM) inhibits delayed neuronal death by preserving mitochondrial dynamics and function following global cerebral ischemia (GCI). In the current study, we clarified whether PBM exerts effective roles in endogenous neurogenesis and long-lasting neurological recovery after GCI. Adult male rats were treated with 808 nm PBM at 20 mW/cm2 irradiance for 2 min on cerebral cortex surface (irradiance ∼7.0 mW/cm2, fluence ∼0.8 J/cm2 on the hippocampus) beginning 3 days after GCI for five consecutive days. Cognitive function was evaluated using the Morris water maze. Neural stem cell (NSC) proliferation, immature neurons, and mature neurons were examined using bromodeoxyuridine (BrdU)-, doublecortin (DCX)-, and NeuN-staining, respectively. Protein expression, such as NLRP3, cleaved IL1β, GFAP, and Iba1 was detected using immunofluorescence staining, and ultrastructure of astrocyte and microglia was observed by transmission electron microscopy. The results revealed that PBM exerted a markedly neuroprotective role and improved spatial learning and memory ability at 58 days of ischemia/reperfusion (I/R) but not at 7 days of reperfusion. Mechanistic studies revealed that PBM suppressed reactive astrocytes and maintained astrocyte regeneration at 7 days of reperfusion, as well as elevated neurogenesis at 58 days of reperfusion, as evidenced by a significant decrease in the fluorescence intensity of GFAP (astrocyte marker) but unchanged the number of BrdU-GFAP colabeled cells at the early timepoint, and a robust elevation in the number of DCX-NeuN colabeled cells at the later timepoint in the PBM-treated group compared to the GCI group. Notably, PBM treatment protected the ultrastructure of astrocyte and microglia cells at 58 days but not 7 days of reperfusion in the hippocampal CA1 region. Furthermore, PBM treatment significantly attenuated the GCI-induced immunofluorescence intensity of NLRP3 (an inflammasome component), cleaved IL1β (reflecting inflammasome activation) and Iba1, as well as the colocalization of NLRP3/GFAP or cleaved IL-1β/GFAP, especially in animals subjected to I/R at 58 days. Taken together, PBM treatment performed postischemia exerted a long-lasting protective effect on astrocytes and promoted endogenous neurogenesis in the hippocampal CA1 region, which might contribute to neurological recovery after GCI.

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Distribución hipocampal del Neuropeptido Y (NPY) en un modelo animal de demencia senil del tipo Alzheimer inducido por estreptozotocina

Revista ECIPeru ◽

10.33017/reveciperu2011.0041/ ◽

2019 ◽

pp. 172-175

Keyword(s):

Neuropeptide Y ◽

Rat Model ◽

Male Rats ◽

Mammalian Brain ◽

Amino Acid Peptide ◽

Ca1 Region ◽

Hippocampal Ca1 Region ◽

Hippocampal Ca1 ◽

Dementia Of Alzheimer’S Type ◽

De Medicina

Distribución hipocampal del Neuropeptido Y (NPY) en un modelo animal de demencia senil del tipo Alzheimer inducido por estreptozotocina Hippocampal distribution of neuropeptide Y in rat model of streptozotocin-induced experimental dementia of Alzheimer’s type Ariza A, Andrade R, Aguilar LA Laboratorio de Neurociencia y Comportamiento, Facultad de Medicina “Alberto Hurtado’’, Universidad Peruana Cayetano Heredia, Lima 31, Perú. DOI: https://doi.org/10.33017/RevECIPeru2011.0041/ RESUMEN La distribución de numerosos neuropéptidos en el cerebro humano sugiere que los sistemas peptidérgicos pueden contribuir a la patogénesis del déficit cognitivo en el envejecimiento patológico tal como trastornos de demencia. El neuropéptido Y (NPY) es un péptido de 36 aminoácidos y además es el neuropéptido conocido más abundante en el cerebro de mamíferos. La estructura primaria del NPY ha sido bien preservada durante la evolución haciendo a este neuropéptido uno de los neuropéptidos mas conservados entre especies. A pesar de que algunos datos divergentes se encuentran disponibles en la bibliografía científica, la mayor parte de las evidencias sugiere que los niveles del NPY en la corteza, hipocampo, ganglio basal y líquido cefalorraquídeo son contradictorios. La inyección intracerebroventricular de estreptozotocina causa insuficiencia de la glucosa cerebral y metabolismo energético junto con el daño oxidativo y disfunción colinérgica, y provee un modelo relevante para la enfermedad de Alzheimer. El presente estudio examinó la presencia de cuerpos celulares inmunoreactivos conteniendo NPY en un modelo animal para la enfermedad de Alzheimer. Ratas machos fueron inyectados bilateralmente con estreptozotocina (0.5mg/kg), mientras que las ratas controles recibieron el mismo volumen del vehículo, luego las ratas fueron sacrificadas para los análisis inmunocitoquímicos. Un mes después de la inyección de estreptozotocina una alta densidad de células inmunoreactivas para NPY fueron encontradas en las regiones CA1, CA2 y CA3 del hipocampo y en el giro dentado (DG). Además, astrocitos activados fueron vistos en el hipocampo y en la corteza. La distribución del NPY indica que el neuropéptido estudiado puede estar involucrado en múltiples funciones como neuroprotección en el cerebro de las ratas. Estos datos sugieren que el neuropéptido Y puede tener funciones importantes en la progresión de la enfermedad de Alzheimer. Descriptores: Selenito de sodio, NPY, estreptozotocina, demecia senil del tipo alzheimer ABSTRACT Distribution of numerous neuropeptides in the human brain suggests that peptidergic systems may contribute to the pathogenesis of cognitive impairment in pathological aging such as dementia disorders. Neuropeptide Y (NPY) is a 36-amino acid peptide and it is the most abundant neuropeptide presently known in the mammalian brain. The primary structure of NPY has been well preserved during evolution making this peptide one of the most conserved among species. Although some divergent data are available, the bulk of evidence suggests that NPY levels in cortex, hippocampus, basal ganglia and cerebrospinal fluid are contradictory. Intracerebroventricular-streptozotocin (ICV-STZ) in rats causes impairment of brain glucose and energy metabolism along with oxidative damage and cholinergic mdysfunction, and provides a relevant model for Alzheimer’s disease (AD). The present study examined the presence of inmmunoreactive cell bodies containing NPY in a rat model of AD. Male rats were injected bilaterally with ICV-STZ (0.5mg/kg), while sham rats received the same volume of vehicle, then rats were sacrificed for immunocytochemical assays. One month after STZ injection a high density of NPY-immunoreactive perikarya was found in the hippocampal CA1 region, CA2 region, CA3 region and dentate gyrus (DG). In addition, activated astrocytes were seen in the hippocampus and in the cortex. This NPY distribution indicates that the neuropeptide studied might be involved in multiple functions like neuroprotection in the rat brain. These finding suggest that NPY may have important roles in the progression of AD. Keywords: Sodium selenite, NPY, Streptozotocin, Sporadic dementia of Alzheimer's type.

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Chewing Prevents Stress-Induced Hippocampal LTD Formation and Anxiety-Related Behaviors: A Possible Role of the Dopaminergic System

BioMed Research International ◽

10.1155/2015/294068 ◽

2015 ◽

Vol 2015 ◽

pp. 1-7 ◽

Cited By ~ 7

Author(s):

Yumie Ono ◽

So Koizumi ◽

Minoru Onozuka

Keyword(s):

Dopaminergic System ◽

Ventral Hippocampus ◽

Male Rats ◽

Ca1 Region ◽

Hippocampal Ca1 Region ◽

Hippocampal Ca1 ◽

Plus Maze ◽

And Control

The present study examined the effects of chewing on stress-induced long-term depression (LTD) and anxiogenic behavior. Experiments were performed in adult male rats under three conditions: restraint stress condition, voluntary chewing condition during stress, and control condition without any treatments except handling. Chewing ameliorated LTD development in the hippocampal CA1 region. It also counteracted the stress-suppressed number of entries to the center region of the open field when they were tested immediately, 30 min, or 60 min after restraint. At the latter two poststress time periods, chewing during restraint significantly increased the number of times of open arm entries in the elevated plus maze, when compared with those without chewing. Thein vivomicrodialysis further revealed that extracellular dopamine concentration in the ventral hippocampus, which is involved in anxiety-related behavior, was significantly greater in chewing rats than in those without chewing from 30 to 105 min after stress exposure. Development of LTD and anxiolytic effects ameliorated by chewing were counteracted by administering the D1 dopamine receptor antagonist SCH23390, which suggested that chewing may activate the dopaminergic system in the ventral hippocampus to suppress stress-induced anxiogenic behavior.

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