CA1 Field Of Dorsal Hippocampus Research Articles

IL-1β increases necrotic neuronal cell death in the developing rat hippocampus after status epilepticus by activating type I IL-1 receptor (IL-1RI)

Interleukin-1β (IL-1β) is associated with seizure-induced neuronal cell death in the adult brain. The contribution of IL-1β to neuronal injury induced by status epilepticus (SE) in the immature brain remains unclear. In the present study, we investigated the effects of IL-1β administration on hippocampal neuronal cell death associated with SE in the immature brain, and the role of the type I receptor of IL-1β (IL-1RI). SE was induced with lithium–pilocarpine in 14-days-old (P14) rat pups. Six hours after SE onset, pups were i.c.v. injected in the right ventricle with IL-1β (0, 0.3, 3, 30, or 300ng), 30ng of IL-1RI antagonist (IL-1Ra) alone, or 30ng of IL-1Ra plus 3ng of IL-1β. As control groups, pups without seizures were injected with 3ng of IL-1β or vehicle. Twenty-four hours after SE onset, neuronal cell death in the CA1 field of dorsal hippocampus was assessed by hematoxylin–eosin, Fluoro-Jade B and in vivo propidium iodide (PI) staining; expression of active caspase-3 (aCas-3) was also determined, using immunohistochemistry. The concentration–response curve of IL-1β showed a bell-shape. Only pups injected with 3ng of IL-1β after SE showed a significant increase in the number of cells with eosinophilic cytoplasm and pyknotic nuclei, as well as F-JB positive cells with respect to the vehicle group. This effect was prevented when IL-1β was injected with IL-1Ra. Injection of 3ng of IL-1β increased the number of PI-positive cells in CA1 area after SE. Injection of 3ng of IL-1β did not produce hippocampal cell death in rats without seizures. Active caspase-3 expression was not observed after treatments in hippocampus. The activation of the IL-1β/IL-1RI system increases necrotic neuronal cell death caused by SE in rat pups.

CNS Dopamine Transmission Mediated by Noradrenergic Innervation

The presynaptic source of dopamine in the CA1 field of dorsal hippocampus is uncertain due to an anatomical mismatch between dopaminergic terminals and receptors. We show, in an in vitro slice preparation from C57BL/6 male mice, that a dopamine (DA) D1 receptor (D1R)-mediated enhancement in glutamate synaptic transmission occurs following release of endogenous DA with amphetamine exposure. It is assumed DA is released from terminals innervating from the ventral tegmental area (VTA) even though DA transporter (DAT)-positive fibers are absent in hippocampus, a region with abundant D1Rs. It has been suggested this results from a lack of DAT expression on VTA terminals rather than a lack of these terminals per se. Neither a knockdown of tyrosine hydroxylase (TH) expression in the VTA by THsiRNA, delivered locally, by adeno-associated viral vector, nor localized pharmacological blockade of DAT to prevent amphetamine uptake into DA terminals, has any effect on the D1R synaptic, enhancement response to amphetamine. However, either a decrease in TH expression in the locus ceruleus (LC) or a blockade of the norepinephrine (NE) transporter prevents the DA-mediated response, indicating LC terminals can release both NE and DA. These findings suggest noradrenergic fibers may be the primary source of DA release in hippocampus and corresponding DA-mediated increase in synaptic transmission. Accordingly, these data imply the LC may have a role in DA transmission in the CNS in response to drugs of abuse, and potentially, under physiological conditions.

Neuronal response in the CA1 field of the cat dorsal hippocampus to visual stimuli

Responses of 46 neurons of the CA1 field, of the dorsal hippocampus to visual stimuli were investigated during acute experiments on awake cats following pretrigeminal brainstem action. The receptive field was small in size in 71% of hippocampal neurons. The cells responded both tonically (34%) and phasically (66%) to the presentation of immobile stimuli. All the test cells of the CA1 field of the dorsal hippocampus responded to moving visual stimuli and 27% of these neurons were directionally tuned. A group of 7% of the neurons displayed particular sensitivity to the movement of a dark spot across the receptive field; these cells frequently reacted more to a moving dark spot than to a bar. Findings indicate the presence of highly specific sensory neurons within the hippocampus.

Hippocampal unit activity to tonal stimuli during arousal from sleep and in awake rats

Single cell activity was recorded from electrodes chronically implanted in fascia dentata and the CA-1 field of dorsal hippocampus in unrestrained rats during presentations of tonal stimuli. In the first experiment 32% of the cells showed reliable decreases in activity to the tonal stimuli and 26% showed reliable increases. Most of these cells (73%) habituated under rapid tone presentation. The second experiment showed that tonal stimuli caused changes in activity in more cells when the tones aroused the animal from sleep (75% affected) than when the tone was presented to an awake animal (18% affected). In both experiments all affected fascia dentata cells were inhibited. However, 36% of the affected CA-1 cells were augmented. The data indicate that the hippocampus undergoes dramatic changes during arousal from sleep, and that previously found changes in hippocampal activity during conditioning might be due to conditioned changes in the capability of stimuli to arouse the animal from sleep.