thank you for your clarifying post.
if what you've posted is correct, then the 'ramp-architecture' discussion of
AoK must be reworked to integrate the 'ramp architecture' stuff within the
discussion of hippocampal 'intermediate-'level' supersystem configuration'
dynamics... with specific respect to =fornix= lesions and resultant
anterograde 'memory' deficits.
Sincerely, K. P. Collins (ken)
Sturla Molden wrote in message <7n9mts$gaf$1 at kopp.stud.ntnu.no>...
>John <johnhkm at netsprintxxxx.net.au> wrote:
>>: I don't know why the finding the brain cyst solved the puzzle of this
case.
>: Okay, in memory area, but that's not explaining anything.
>>: Can anyone help me with this???
>>A fimbria/fornix lesion acts as a functional hippocampus
>lesion because it prevent colineriginc inervation from
>the medial septum to reach its targets in the hippocampus.
>This has consequnces for the theta and gamma osciallations
>(J. Neurosci., 1999, 30, 3223-3237; Nature, 1998, 394, 186-189).
>A 'cheap' way to produce hippocampal lesions in rats is
>to transect the fornix, however, the effects of fornix damage
>and hippocampus lesions is not 100% similar. For example,
>fornix lesions affect path-integration and delayed
>nonmatching-to-sample, which is unaffected by hippocampal
>ablation. Hippocampal lesions affect latent inhibition,
>which is unaffected by fornix lesions. Cerebral ischemia,
>which produce amnesia, affects delayed nonmatching-to-sample
>as well.
>>The article on the website says nothing about the exact
>nature of the amnesia. A complete fornix lesion produce
>anterograde amnesia, however, there are no indications
>of this in the article. It could be a form of temporally
>graded retrograde amnesia (a 'time laps'). 'Mistaking the
>present for the past' is a poor behavioural diagnosis, I
>don't think it makes much sence at all.
>>>Sturla Molden
