Hippocampus memory

COX-2 expression was also found in brain areas related to memory (hippocampus, cortex) in patients with Alzheimer s disease (Ho et al., 1999, Yasojima et al., 1999). These findings together with clinical data suggest new options for the use of COX-2 inhibitors in this indication. 

The euphoric feelings associated with Cannabis use are thus ascribable to the interaction of A -THC with CBj receptors on presynaptic nerve terminals. However, CB receptors are also present in other areas of CNS, and thus, the same cannabinoids also cause impairment of cognition and memory (hippocampus) [43], involuntary movements and partial loss of motor control (basal ganglia and cerebellum) [44], and a beneficial and potential therapeutically useful inhibition of emesis [45], especially of the chemotherapy-induced emesis. It is still unclear whether the CB receptors are responsible for all of the centrally mediated actions of the cannabinoids. 

AVP is excitatory in the ventral hippocampus, either directly or by potentiation of glutamatergic responses. An inhibitory effect has been observed in AVP may be involved in the formation of long-term potentiation and thus learning and memory. However, AVP is proconvulsive, may augment the formation of dmg tolerance and dependence, and affects cardiovascular regulatory processes. 

Alzheimer s disease (AD) 2. In the hippocampus of p-amylo id-treated rats, an animal model of AD, 2-AG levels are elevated and exert neuroprotection but also participate in memory retention loss 2. Inhibitors of cellular re-uptake or CB-, antagonists, possibly depending on the phase of the disorder... 

The hippocampus, which got its name from the Greek word for seahorse, due to its form, is a nucleus in the depth of the temporal lobe. The hippocampus is important for the integration of sensory information, for spatial orientation and for memory formation. The hippocampal formation contains the CA (cornu ammonis) regions, the dentate gyms and the subiculum. 

Collection of interconnected subcortical and cortical brain structures (including hypothalamus, amygdala, and hippocampus) integrating multimodal intero- and exteroceptive information to produce coherent neuroendocrine and behavioral output, and to support memory functions. 

The temporal lobe is the inferior middle portion of the cerebral cortex of both hemispheres. The temporal lobes are involved in the analysis of visual and acoustic information and in memory formation. The hippocampus is part of the inner, medial side of the temporal lobes. 

Even if there is a link between the presence of tangles and plaques and the emergence of AzD, it is by no means certain how those markers could be responsible for all the symptoms. They do not seem to be sufficiently numerous or widely spread to disrupt brain function to the extent that eventually occurs in AzD, although their preferential location in the hippocampus and the known association of that area with memory processing could explain the loss of that faculty. 

So if ACh is involved in memory function, what does it do Any attempt to answer that question has to follow some consideration of how memory is thought to be processed. Many neuroscientists believe that memory is achieved by changes in the strength of synaptic connections (activation) between neurons and that increases in such synaptic activity somehow reinforce the pattern of neuronal activity during the memorising of an event so that it can be more easily restored later. One form of such plasticity is longterm potentiation (LTP), which has been mostly studied in the hippocampus where, as in other areas associated with memory, there is the appropriate complex synaptic morphology. 

That the hippocampus is important for memory is generally accepted. This is not because it is a site of major degeneration in AzD, that finding can only be used to account for the memory loss if memory is known to be dependent on the hippocampus, but because lesions of that region are known to impair memory. Case reports in the medical literature are rightly mistrusted but few people have felt inclined to disregard the evidence presented by one 27-year-old male mechanic who underwent bilateral hippocampal removal for intractable epilepsy in Montreal in 1953. While that condition was improved the operation has not been repeated because memory loss was almost total, so while he appeared to behave reasonably normally (and still does), he cannot remember where he lives, what he has just eaten or the person he met a few minutes previously. 

The pathologic hallmarks of the disease in the brain include neurofibrillary tangles and neuritic plaques made up of various proteins, which result in a shortage of the neurotransmitter acetylcholine. These are primarily located in brain regions involved in learning, memory, and emotional behaviors such as the cerebral cortex, hippocampus, basal forebrain, and amygdala.11... 

The total human complement of neurons is laid down around birth, and if they die they cannot be replaced - unlike most cells in our body. However, this central dogma of neuroscience has been challenged by the recent finding that neurogenesis can occur in the adult rat hippocampus, and these new cells seem to be required for at least one type of memory (Shors et al., 2001). Whether this will also be the case in... 

Cannabinoid receptors are expressed throughout the cerebral cortex and the hippocampus, and a subpopulation of these cells appear to show an unusually high level of activity. It is possible that cells in these areas modulate the sensory effects of cannabis, particularly the effects on perception, task performance and memory. In addition, the anticonvulsant properties of cannabis are believed to be mediated here. Parts of the hypothalamus show high levels of receptor sites for cannabinoids this may be related to hypothermia effects. High levels in the cerebellum may be related to mediating the property of cannabinoids that produces the reduction in ataxic (muscle co-ordination) symptoms in certain disorders (Herkenham et al., 1991). 

Veng LM, Mesches MH and Browning MD (2003). Age-related working memory impairment is correlated with increases in the L-type calcium channel protein alD (Cavl.3) in area CA1 of the hippocampus and both are ameliorated by chronic nimodipine treatment. Molecular Brain Research, 110, 193-202. 

White AM, Matthews DB and Best PJ (2000). Ethanol, memory, and hippocampal function a review of recent findings. Hippocampus, 10, 88-93. 

Hippocampus Spatial resolution, learning, memory autobiographical events... 

Lanahan A et al. Selective alteration of long-term potentiation-induced transcriptional response in hippocampus of aged, memory-impaired rats. J Neurosci 1997 17 2875-2885. 

Studies reveal that a homozygous GlyT-1 (-/-) knockout in mice is neonatally lethal. However heterozygous GlyT-1 (+/-) mice survive to adulthood and display enhanced NMDA receptor function in the hippocampus, better memory retention, and no disruption in sensory gating when dosed with amphetamine [15]. 

THE NEURONAL PATHWAYS OF THE HIPPOCAMPUS ARE ESSENTIAL STRUCTURES FOR MEMORY FORMATION 272... 

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