The supramammillary region of the cat sends substance P-like immunoreactive axons to the hippocampal formation and the entorhinal cortex

1988 ◽  
Vol 90 (3) ◽  
pp. 259-264 ◽  
Author(s):  
Tadashi Ino ◽  
Kazuo Itoh ◽  
Tetsuo Sugimoto ◽  
Takeshi Kaneko ◽  
Hiroto Kamiya ◽  
...  
2004 ◽  
Vol 92 (2) ◽  
pp. 1226-1235 ◽  
Author(s):  
Douglas A. Caruana ◽  
C. Andrew Chapman

Although a major output of the hippocampal formation is from the subiculum to the deep layers of the entorhinal cortex, the parasubiculum projects to the superficial layers of the entorhinal cortex and may therefore modulate how the entorhinal cortex responds to sensory inputs from other cortical regions. Recordings at multiple depths in the entorhinal cortex were first used to characterize field potentials evoked by stimulation of the parasubiculum in urethan-anesthetized rats. Current source density analysis showed that a prominent surface-negative field potential component is generated by synaptic activation in layer II. The surface-negative field potential was also observed in rats with chronically implanted electrodes. The response was maintained during short stimulation trains of ≤125 Hz, suggesting that it is generated by activation of monosynaptic inputs to the entorhinal cortex. The piriform cortex also projects to layer II of the entorhinal cortex, and interactions between parasubicular and piriform cortex inputs were investigated using double-site stimulation tests. Simultaneous activation of parasubicular and piriform cortex inputs with high-intensity pulses resulted in smaller synaptic potentials than were expected on the basis of summing the individual responses, consistent with the termination of both pathways onto a common population of neurons. Paired-pulse tests were then used to assess the effect of parasubicular stimulation on responses to piriform cortex stimulation. Responses of the entorhinal cortex to piriform cortex inputs were inhibited when the parasubiculum was stimulated 5 ms earlier and were enhanced when the parasubiculum was stimulated 20–150 ms earlier. These results indicate that excitatory inputs to the entorhinal cortex from the parasubiculum may enhance the propagation of neuronal activation patterns into the hippocampal circuit by increasing the responsiveness of the entorhinal cortex to appropriately timed inputs.


2010 ◽  
Vol 25 (12) ◽  
pp. 1720-1729 ◽  
Author(s):  
Rodrigo S Sestito ◽  
Lucas B Trindade ◽  
Rodrigo G de Souza ◽  
Lucila N Kerbauy ◽  
Melina M Iyomasa ◽  
...  

Reduced glutamatergic signaling may contribute to cognitive dysfunction in schizophrenia. Glutamatergic synapses might be the site of primary abnormalities in this disorder with the dopaminergic changes being secondary to altered glutamatergic transmission. Isolation rearing of rats from weaning has been used as an experimental model for affective disorders like schizophrenia. In this immunohistochemistry study we evaluate the changes in the expression of GluR1 and GluR2 AMPA receptors in the hippocampus, amygdala and entorhinal cortex induced by isolation rearing. Two groups of Wistar rats (grouped and isolated, n = 6/each) were used. Isolation rearing induced a significant decrease in GluR1- and GluR2-immunopositive cells in the hippocampus. For GluR1 the reduction was 31% in the hilus of dentate gyrus ( p = 0.02) and 47% in CA3 ( p = 0.002). For GluR2 the reduction was 52% in the hilus of dentate gyrus ( p < 0.0001) and 29% in CA1 ( p = 0.002). Isolation rearing induced a non-significant decrease in GluR1-immunopositive cells in the basolateral amygdala ( p = 0.066) while no alteration was found in the lateral nucleus ( p = 0.657). For GluR2 no changes were induced by isolation in both nuclei of the amygdala. In the entorhinal cortex no apparent difference was seen in GluR1- or GluR2-immunopositive cells when isolated reared rats were compared to grouped rats. The results suggest that isolation rearing from weaning induces changes on the expression of AMPA glutamate receptors in the hippocampus similar to those reported for postmortem human brains with schizophrenia. These findings also contribute to additional evidence for using isolation rearing of rats from weaning as an animal model for schizophrenia.


2016 ◽  
Vol 2 (4) ◽  
pp. 260-274
Author(s):  
Dajue Wang

With the fast-growing aging population, dementia has become a health priority. However, in the past, medicine was largely dealing with physical disorders, and not enough knowledge and experience have been accumulated for mental health. The main and first symptom of this disorder is the loss of memory; hence, understanding the hippocampal formation is the key to tackling dementia. In 2007, a milestone book titled “Hippocampus Book” was published. One of the authors/editors is the 2014 Nobel Laureate in Physiology and Medicine, Professor John O'Keefe. It is a MUST-READ encyclopedia about the hippocampal formation, for those who wish to commit themselves to helping the patients with dementia. The formation consists of the hippocampus, entorhinal cortex, subiculum, presubiculum, parasubiculum, and dentate gyrus. The hippocampus is further divided into CA1, CA2, and CA3. The entorhinal cortex is the gateway of receiving all sensory information from the neocortex, while the subiculum is the exit for the efferent projections to the neocortex. Memory is divided into short-term and long-term memory. The former does not require protein synthesis while the latter does. The electrophysiological activities of creating these memories are short-term potentiation and long-term potentiation respectively. In most cases, the entorhinal cortex is the first structure to be damaged, and even short-term memory cannot be created. However, all except spatial memory are stored in the neocortex. Damage to the hippocampal formation would not affect the storage and retrieval of memories. Hence, past memories may remain intact in the early phases of the disorder. This devastating progressive disease has no cure. However, the highly plastic hippocampal formation may offer us some hope. It is the responsibility of the pharmaceutical industries to develop new drugs. Clinicians should add their efforts to the endeavor. The author would suggest that they explore insulin-like growth factors, brain stimulation, cell transplantation, and animal-assisted therapy to find some innovative solutions to help patients with dementia. As the current status of neuroscience stands, the animal-assisted therapy seems to stand out among all methods. It alleviates symptoms and stabilizes the ailment.


1994 ◽  
Vol 345 (3) ◽  
pp. 321-344 ◽  
Author(s):  
Sonsoles De Lacalle ◽  
Chun Lim ◽  
Teresa Sobreviela ◽  
Elliott J. Mufson ◽  
Louis B. Hersh ◽  
...  

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