D1 receptor agonists reverse the subchronic phencyclidine (PCP)-induced novel object recognition (NOR) deficit in female rats

Translating the N-methyl-d-aspartate receptor antagonist model of schizophrenia to treatments for cognitive impairment in schizophrenia

“…Indeed, some treatments for some domains of cognition may impair other domains, e.g. over stimulation of dopamine (DA) D 1 receptors (Horiguchi et al, 2011a).…”

The Multicomponent Medication Lymphomyosot Improves the Outcome of Experimental Lymphedema

“…88,[93][94][95] In addition, several studies analyzing the effects of pharmacological or nonpharmacological treatments on cognitive function and memory revealed a stimulation with increasing doses up to a maximum, following an inhibition at higher doses. 90,91,96,97 In another example related to vaccine development, the authors observed a similar immune suppression effect at above threshold doses. 98 In the present study, we have shown that Lymphomyosot improves wound repair, modulates macrophage activity, and reduces acute lymphedema.…”

Pharmacotherapy of cognition in schizophrenia

“…The release of cortical and hippocampal DA and ACh, two neurotransmitters, in cortex and hippocampus, has been shown by microdialysis in freely moving rodents to be selectively enhanced by AAPDs, but not typical APDs [44]. It has been suggested that this produces cognitive enhancement, in part, through stimulation of D 1 , D 4 , nicotinic and muscarinic receptors [37,[44][45][46][47]. DA and ACh efflux may also overcome possible adverse effects of APD-induced D 2 or muscarinic receptor blockade, or both [12,44].…”

“…Unfortunately, like most CIS, studies, they did not report the percentages of patients who experience improvement that would be expected to be clinically significant, and beyond practice levels, 0.5 or 1.0 SD, respectively [36]. Similarly, the majority of CIS studies are 4-8 weeks in duration, which may be an insufficient length of time for significant benefit (see Ref [24 ]) because of the time needed for some of the emergent adaptive changes in synaptic function produced by AAPDs [37]. A test of the concepts advocated here to better evaluate the efficacy of AAPDs, as well as adjunctive treatments for AAPDs, would include as many of the following features as possible: random assignment of drug-free patients or patients taking typical APDs, to monotherapy with an AAPD which the patient had not recently received, a control group treated with typical APDs, treatment duration at least six months, no concomitant psychotropic medications, inclusion of only non-treatment resistant schizophrenia patients, and primary endpoints of proportions of subjects showing improvement 0.5 SD in each of the key domains of cognition.…”

“…A huge number of genes are involved in cognition [38], some of which, for example, COMT [39], those involved in growth factors such as BDNF processing and response [40], and neuregulin-1 [39], have been shown to affect severity of CIS and response to AAPDs. An example is the robust demonstration that COMT polymorphisms, which modulate the synaptic availability of DA in the cortex, affects working memory performance in patients with schizophrenia, first degree relatives and normal controls [37]. An interaction between COMT, enhanced cortical DA release by AAPDs, and the many other factors which affect DAergic function, including trace amines, expression of the D 1 receptor gene, and vesicular transport of DA, all of which have been reported to be abnormal in schizophrenia, would be expected to lead to AAPD-based improvement in working memory in some patients, and worsening in others, Clinical studies are consistent with this as a source of variance in response to treatment [24 ,26,27,28 ].…”