Behavioral and histopathological consequences of transient ischemic stroke in the Flinders Sensitive Line rat, a genetic animal model of depression.

Patients with depression have an increased risk for stroke, higher mortality rates following stroke and worse functional outcomes among survivors. Preclinical studies may help to better understand the underlying mechanisms linking these two diseases, but only a few animal studies have investigated the effects of prestroke depression. The present study investigates whether Flinders Sensitive Line (FSL) rats, a genetic depression model, respond differently to focal ischemic stroke compared to control strains (Flinders Resistant Line [FRL] and Sprague-Dawley [SD]).

The Kynurenine Pathway Is Upregulated by Methyl-deficient Diet and Changes Are Averted by Probiotics.

Scope: Probiotics exert immunomodulatory effects and may influence tryptophan metabolism in the host. Deficiency of nutrients related to C1 metabolism might stimulate inflammation by enhancing the kynurenine pathway. This study used Sprague Dawley rats to investigate whether a methyl-deficient diet (MDD) may influence tryptophan/kynurenine pathways and cytokines and whether probiotics can mitigate these effects.

Flinders sensitive line rats are resistant to infarction following transient occlusion of the middle cerebral artery.

Background: Depression is a common complication of stroke and increases the risk of mortality and disability. Pre-stroke depression is a possible risk factor for stroke and has also been linked to adverse outcomes. The underlying mechanisms linking depression and stroke remain unclear.

Effect of ischemic lesions in medial prefrontal cortex and nucleus accumbens on affective behavior in rats.

Post-stroke depression (PSD) and post-stroke anxiety (PSA) are usually undertreated and many cases may remain undiagnosed, indicating a need for a better understanding of the underlying mechanisms. Current animal models of PSD and PSA using the middle cerebral artery occlusion model may be associated with motor deficits that can interfere with behavioral tests of depression- and anxiety-like behavior. Unilateral lesions of the medial prefrontal cortex (mPFC) have been reported to induce a depression- and anxiety-like phenotype in mice.

Behavioral and metabolic effects of S-adenosylmethionine and imipramine in the Flinders Sensitive Line rat model of depression.

Depression is associated with dysregulation of methyl group metabolism such as low S-adenosylmethionine (SAM). We previously reported that Flinders Sensitive Line (FSL) rats, an animal model of depression, had lower concentrations of liver SAM than the control rats, Flinders Resistant Line (FRL) rats. The present study investigated if SAM supplementation may correct liver SAM and behavioral abnormalities in this model.

Effects of α7 Nicotinic Receptor Activation on Cell Survival in Rat Organotypic Hippocampal Slice Cultures.

Glutamatergic signaling via N-methyl-D-aspartate receptors (NMDARs) is important for physiological functioning, but can also induce cell death via excitotoxic mechanisms in many neuropathological diseases, such as stroke. Altering the cellular response to excitotoxic insults by modulating the downstream effects of NMDAR activation represents a promising therapeutic approach. For example, α7 nicotinic acetylcholine receptors (α7 nAChRs) signaling has been shown to be able to change NMDA-induced neurotoxicity in some models.

A method for objectively quantifying propidium iodide exclusion in organotypic hippocampal slice cultures.

Background: Organotypic hippocampal slice cultures (OHSCs) are an attractive in vitro model to examine mechanisms of neuronal injury, because the normal hippocampal architecture, function and cellular diversity are mostly preserved. The effects of exposure to excitotoxins such as N-methyl-d-aspartate (NMDA) on cell viability can be determined by propidium iodide (PI) staining.

New Method: We describe a simple method to objectively quantify cell death in NMDA exposed slice cultures using PI that provides a standardized means of quantifying cell death in hippocampal subfields without the need to induce maximal cell death in each slice.