Posted by jrbecker on December 12, 2005, at 10:36:25
In reply to Re: Anorgasmia and word substitution » med_empowered, posted by Dinah on December 11, 2005, at 15:37:02
I have experienced word recall problems on many different meds. Probably the worst offender for me was Lamictal. Second to that was selegiline and also Wellbutrin at higher doses. Both Cymbalta and Effexor are mild offenders at times but only at the higher doses. Ironically, both stimulants and benzos also exacerbate these problems, although it's probably that the latter causes general memory recall issues rather than the more specific issue of word recall. As for the stims, I think this is partly due to the "hyperfocus" effect that this has on some users. Also, I tend to have problems when coming off a dose rather than when its having full effects. When in combo with ADs, drinking too much caffeine can also bring on this effect. A recent study highlights this phenomenon...
http://news.bbc.co.uk/2/hi/health/3909085.stm
The problem probably involves multiple chemical pathways, but dopamine seems to be highly implicated. Recent studies have pointed to an optimal window of dopamine levels where memory would function effectively (not too high or too low)...
Under the curve: critical issues for elucidating D1 receptor function in working memory.
Neuroscience. 2005 Nov 24
Williams GV, Castner SA.
It has been postulated that spatial working memory operates optimally within a limited range of dopamine transmission and D1 dopamine receptor signaling in prefrontal cortex. Insufficiency in prefrontal dopamine, as in aging, and excessive transmission, as in acute stress, lead to impairments in working memory that can be ameliorated by D1 receptor agonist and antagonist treatment, respectively. Iontophoretic investigations of dopamine's influence on the cellular mechanisms of working memory have revealed that moderate D1 blockade can enhance memory fields in primate prefrontal pyramidal neurons while strong blockade abolishes them. The combined behavioral and physiological evidence indicates that there is a normal range of dopamine function in prefrontal cortex that can be described as an "inverted-U" relationship between dopamine transmission and the integrity of working memory. Both in vivo and in vitro studies have demonstrated a role for dopamine in promoting the excitability of prefrontal pyramidal cells and facilitating their N-methyl-d-aspartate inputs, while simultaneously restraining recurrent excitation and facilitating feedforward inhibition. This evidence indicates that there is a fine balance between the synergistic mechanisms of D1 modulation in working memory. Given the critical role of prefrontal function for cognition, it is not surprising that this balancing act is perturbed by both subtle genetic influences and environmental events. Further, there is evidence for an imbalance in these dopaminergic mechanisms in multiple neuropsychiatric disorders, particularly schizophrenia, and in related nonhuman primate models. Elucidating the orchestration of dopamine signaling in key nodes within prefrontal microcircuitry is therefore pivotal for understanding the influence of dopamine transmission on the dynamics of working memory. Here, we explore the hypothesis that the window of optimal dopamine signaling changes on a behavioral time-scale, dependent upon current cognitive demands and local neuronal activity as well as long-term alterations in signaling pathways and gene expression. If we look under the bell-shaped curve of prefrontal dopamine function, it is the relationship between neuromodulation and cognitive function that promises to bridge our knowledge between molecule and mind.
poster:jrbecker
thread:588001
URL: http://www.dr-bob.org/babble/20051211/msgs/588317.html