Posted by JohnX2 on March 23, 2002, at 0:24:09
In reply to Re: treatment resistant depressionSLS » petters, posted by SLS on March 21, 2002, at 10:55:52
I want lithium because of its neuroprotective and neurotrophic potential. It is supposed to promote plasticity. Maybe this would help to restore the size and function of the hippocampus. What do you think? Depression has greatly impaired my memory.
>Scott,
Sorry to budge in on your thread. I'm interested on your comment about lithium and its effects on plasticity in the hippocampus? Can you direct me to any information on this?
BTW, memantine has been shown to improve memory and cognition by improving ltp in the hippocampus.
I included some areas of application from the PDR
which they sent me translated into english, and a few abstracts I dug up (this was in demented patients, which you are not, but it does show clinical efficacy, i believe).(Hope the cut and paste doesn't suck).
Regards,
John--------------------------------------------------------------------------------
Akatinol Memantine Tablets/Drops (German Translated PDR)
4. Areas of Application
For the treatment of mild and moderate cerebral performance disorders with the following cardinal symptoms: concentration and memory disorders, loss of interest and drive, premature fatigue, reduced self-maintanance, motoricity disorders in routine activities and depressive mood (dementia syndrome) as well as in diseases which an increase in attention and alertness (vigilance) is required.
Cerebral and spinal spasticity such as , for example, as a result of infantile cerebral injury, craniocerebral trauma, multiple sclerosis, parapalegia, cerebral ischemia.
Parkinson and parkinson-like diseases (Parkinson syndrome).-----------------------------------------------------------------
ABSTRACTEffects of the uncompetitive NMDA receptor antagonist memantine on hippocampal long-term potentiation, short-term exploratory modulation and spatial memory in awake, freely moving rats. Eur J Neurosci 1996 Mar;8(3):565-71 (ISSN: 0953-816X) Barnes CA; Danysz W; Parsons CG
Arizona Research Laboratories Division of Neural Systems, Memory and Aging, University of Arizona, Tucson 85724, USA. Chronic treatment of adult male F-344 rats (9-12 months old) with therapeutically relevant doses of memantine (30 mg/kg/day in chow for > 8 weeks) increased the maintenance of long-term potentiation of field excitatory postsynaptic potentials from perforant path-granule cell hippocampal synapses recorded in the fascia dentata in vivo. In contrast, there was no effect of memantine on baseline synaptic responses or population spikes. Likewise, short-term exploratory modulation of these hippocampal evoked responses was not different between memantine-treated and control rats. Both groups of rats were able to learn the spatial version of the Morris water task equally well, but the memantine-treated group showed a strong tendency to show more selective spatial search patterns in the training quadrant of the water pool during a final probe trial. As such, these studies provide the first electrophysiological evidence that memantine can increase the durability of synaptic plasticity and provide preclinical confirmation of the cognitive improvement seen with memantine in the treatment of demented patients.-------------------------------------------------------------------------------------------
ABSTRACT
Memantine restores long term potentiation impaired by tonic N-methyl-D-aspartate (NMDA) receptor activation following reduction of Mg2+ in hippocampal slices. Neuropharmacology 1999 Sep;38(9):1253-9 (ISSN: 0028-3908) Frankiewicz T; Parsons CG
Department of Pharmacology, Merz and Co., Frankfurt am Main, Germany. This study compared the ability of memantine and (+)MK-801 to counteract deficits in the induction of long term potentiation (LTP) following reduction of Mg2+ in hippocampal slices--a model of increased synaptic noise due to tonic N-methyl-D-aspartate (NMDA) receptor activation. Decreasing Mg2+ from 1 mM to 10 microM for 60 min enhanced baseline field excitatory post-synaptic potential (fEPSP) slopes (87.2 +/- 10.6% above control) and impaired LTP (-4.1 +/- 9.8% compared to pre-tetanic levels). Long pre-incubations with memantine (1 microM), a concentration achieved in the CSF of dementia patients, almost fully restored the induction of LTP (to 43.4 +/- 8.4%) without changing the enhancement of baseline fEPSP slopes (84.1 +/- 11.6%). Memantine (10 microM) fully restored the induction of LTP (61.5 +/- 5.3%) and also decreased the enhancement of baseline fEPSP slopes (30.1 +/- 4.9%). In contrast, although (+)MK-801 (0.01, 0.1 and 1 microM) caused a concentration-dependent reduction in the low Mg2+ -induced enhancement of baseline fEPSP slopes, it was not able to restore the induction of LTP (3.0 +/- 9.8%, 16.3 +/- 5.7% and 4.8 +/- 6.7% respectively). These data indicate that memantine could produce symptomatological improvement in learning under conditions of tonic NMDA receptor activation such as those occurring in chronic neurodegenerative diseases whereas (+)MK-801 is likely to have only negative effects.
poster:JohnX2
thread:98310
URL: http://www.dr-bob.org/babble/20020322/msgs/99589.html