Purpose: to examine the effects of psychological stress on symptom outcomes of depression and biological mechanisms of DA, 5-HT, and α-synuclein Sample: male C57BL/6 mice (); MPTP/probenecid induction
“Cage tilting, damp sawdust, placement in empty cage, group housing, placement in empty cage with water on the bottom, placement of a foreign object in cage, inversion of light/dark cycle, food or water deprivation, lights on for a short period of time during the dark phase, and switching cages” (p. 3)
Biological mechanisms: DA, 5-HT, TH, DAT, VMAT-2, α-synuclein levels in nigrostriatal (substantia nigra and striatum) and nonnigrostriatal tissues (hippocampus, cortex, and cerebellum) Symptom outcomes: depression as measured by behavioral deficits and anhedonia using the (a) open filed test; (b) narrow beam walking test; and (c) sucrose intake test
Biological mechanisms: increased depletion of DA, 5-HT, TH, DAT, and VMAT-2 was identified in stress-treated lesioned subjects. Stress exaggerated the expression of nigrostriatal and nonnigrostriatal α-synuclein. Symptom outcomes: stress increased behavioral deficits and anhedonia in stress-treated lesioned subjects.
Purpose: to examine the effects of psychological stress on motor symptom outcomes and biological mechanisms associated with loss of DA neurons Sample: rats (sample size/gender not provided); 6-OHDA induction
Chronic variable stress (protocol not provided)
Biological mechanisms: TH cell counts in the SNc Symptom outcomes: forelimb asymmetry tests (not defined)
Biological mechanisms: stress was associated with significantly lower TH cell counts in the SNc in lesioned subjects. Symptom outcomes: stress was associated with significant forelimb asymmetry in lesioned subjects.
Purpose: to examine the effects of psychological stress and corticosterone administration on motor symptom outcomes and biological mechanisms of DA neurodegeneration Sample: female rats (); 6-OHDA induction
Restraint in Plexiglas tubes
Biological mechanisms: plasma concentrations of corticosterone and TH positive cells, Fluoro-Jade B cells, and GFAP immunoreactivity in the MTA, VTA, and SNc Symptom outcomes: skilled forelimb reaching, skilled walking, open field behavior, and apomorphine-induced rotations
Biological mechanisms: in stress- and corticosterone-treated lesioned subjects, the loss of TH positive cells was associated with significant increases in Fluor-Jade B cells in the SNc. Significant reductions in Nissl-positive cells in the VTA and SNc and enhanced GFAP immunoreactivity in the SNc were also demonstrated in stress-and corticosterone-treated lesioned subjects. Symptom outcomes: stress and elevated corticosterone levels impaired skilled limb reaching and limb coordination, impeded spontaneous recovery, and altered exploratory behavior in lesioned subjects.
Purpose: to examine the effects of psychological stress on the neuroprotective effects of voluntary exercise on motor symptom outcomes and biological mechanisms of dopaminergic neurodegeneration Sample: male rats (); 6-OHDA induction
Running wheel immobilization and shifting light/dark cycles
Biological mechanisms: TH positive cells in the SNc Symptom outcomes: number of running wheel revolutions and apomorphine-induced rotations
Biological mechanisms: stressed runners demonstrated lower TH positive cells in the SNc. Symptom outcomes: stressed runners demonstrated a significant increase in rotational behavior.
Purpose: to examine the extent to which psychological stress affects motor symptom outcomes and biological mechanisms specific to DA concentrations Sample: male rats (sample size not provided); 6-OHDA
Tail-shock stress
Biological mechanisms: extracellular striatal DA, DOPAC, and HVA levels in vivo and in brain tissue specimens Symptom outcomes: akinesia defined as latency to move all four paws when placed on a flat surface within 120 seconds and catalepsy defined as latency to return all four paws to table surface within 120 seconds
Biological mechanisms: subjects exposed to tail-shock stress demonstrated significantly increased striatal extracellular DA, DOPAC, and HVA levels. In all but one subject, these levels did not reach levels comparable to those demonstrated in nonlesioned animals following tail-shock stress. Symptom outcomes: no consistent pattern was demonstrated between stress and akinetic and cataleptic motor behaviors. A significant negative correlation was shown between poststress latencies for catalepsy and extracellular DA concentrations, with a similar trend identified for akinesia.
Purpose: to examine the effects of psychological stress on motor symptom outcomes and biological mechanisms involving DA Sample: male rats ; MPTP induction
Immobilization in water kept at 25°C for 15 consecutive hours
Biological mechanisms: striatal DA content, DOPAC and HVA levels, and DA indices (DOPAC + HVA/DA) in brain tissue specimens Symptom outcomes: locomotor activity (not defined)
Biological mechanisms: striatal DA content was significantly lower in stress-treated lesioned subjects. Striatal DA indices were significantly elevated in both the stress-treated lesioned and control groups. No significant difference was demonstrated in the DA metabolites DOPAC or HVA. Symptom outcomes: in lesioned subjects, stress was associated with more pronounced but transient decreases in locomotor activity.
Purpose: to examine the effects of psychological stress on motor symptom outcomes of akinesia and biological mechanisms involving DA and norepinephrine levels Sample: male rats (); 6-OHDA induction
Glucodeprivation while withholding food, osmotic diuresis while withholding water, cold exposure, and tail shock
Biological mechanisms: DA and norepinephrine content in brain tissue specimens Symptom outcomes: akinesia defined as latency to move of greater than 60 seconds during the following two tests: (a) movement of all four paws when placed on a flat surface and (b) return of front or rear paws to the ground after being elevated on a Styrofoam block
Biological mechanisms: stress was associated with DA deficiencies in the striatum. Symptom outcomes: striatal DA deficiencies were more predictive of stress-induced akinesias than in other areas of the brain. There was no consistent relationship between hippocampal norepinephrine levels and stress-induced akinesia.
