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Forebrain ischemia triggers GABAergic system degeneration in substantia nigra at chronic stages in rats.

Lin B, Levy S, Raval AP, Perez-Pinzon MA, Defazio RA - Cardiovasc Psychiatry Neurol (2010)

Bottom Line: At day 56, the optical density of GAD67-, but not VGAT-, immunoreactivity in substantia nigra pars reticulata (SNR)-significantly decreased.CR-neurons concentrated in substantia nigra pars compacta (SNC) were reduced by 27% from day 3 (n = 5) to day 56 (n = 7, ANOVA, p < .01).Our results demonstrate delayed impairment of the GABAergic system components in SN and associated with movement deficits after global ischemia.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology (D4-5), Cerebral Vascular Disease Research Center, University of Miami Miller School of Medicine, P.O. Box 016960, Miami, FL 33101, USA.

ABSTRACT
The long-term consequences of forebrain ischemia include delayed Parkinson's syndrome. This study revealed delayed neurodegeneration in the substantia nigra 8 weeks after 12.5 minutes of global ischemia in rat brain. Following neuronal loss of 30-40% in central and dorsolateral striatum at day 3, neuronal damage in the substantia nigra (SN) was assessed at 4-8 weeks using immunohistochemistry for glutamate decarboxylase 67 (GAD67), vesicular GABA transporter (VGAT), and calretinin (CR). At day 56, the optical density of GAD67-, but not VGAT-, immunoreactivity in substantia nigra pars reticulata (SNR)-significantly decreased. CR-neurons concentrated in substantia nigra pars compacta (SNC) were reduced by 27% from day 3 (n = 5) to day 56 (n = 7, ANOVA, p < .01). Movement coordination was impaired at day 56, as evaluated using beam-walking test (time-to-traverse 5.6 ± 1.2 sec versus 11.8 ± 5.4 sec; sham versus ischemia, p < .05, n = 5, and 7, resp.). Our results demonstrate delayed impairment of the GABAergic system components in SN and associated with movement deficits after global ischemia.

No MeSH data available.


Related in: MedlinePlus

The number of normal (i.e., vital) neurons in the striatum decreases rapidly after global ischemia. Bar graph shows normal neurons (mean ± SD) significantly decreased in rat striatum at days 3–56 after 12.5 minutes of transient forebrain ischemia, per high-power (40 ×) microscopic field (*indicates the significant difference, ischemic versus sham groups, p ≤ .03, ANOVA, post hoc Tukey HSD).
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fig1: The number of normal (i.e., vital) neurons in the striatum decreases rapidly after global ischemia. Bar graph shows normal neurons (mean ± SD) significantly decreased in rat striatum at days 3–56 after 12.5 minutes of transient forebrain ischemia, per high-power (40 ×) microscopic field (*indicates the significant difference, ischemic versus sham groups, p ≤ .03, ANOVA, post hoc Tukey HSD).

Mentions: All rats showed mild necrosis in the dorsolateral striatum, and several rats had mild damage in the central striatum at days 3–7. No additional necrotic injury within the striatum was observed at days 28 and 56. Normal neurons significantly decreased in both dorsolateral and central striatum at days 3–56. The numbers were 60 ± 8 at day 3 (n = 5), 54 ± 12 at day 7 (n = 7), 70 ± 15 at day 28 (n = 6), 68 ± 4 at day 56 (n = 7) in dorsolateral striatum and 67 ± 15, 59 ± 16, 69 ± 8, and 66 ± 10 in central striatum while the numbers of normal neurons in sham rats (n = 4) were 104 ± 13 in dorsolateral striatum and 94 ± 5 in central striatum. The ischemia reduced the number of normal neurons in striatum (see Figure 1, mean ± S.D., ANOVA, p ≤ .01). Moderate-to-severe “spongy” changes (defined as empty spaces in histological sections) in striatum were present at day 56 in 5 of 7 rats (Figure 2(d)).


Forebrain ischemia triggers GABAergic system degeneration in substantia nigra at chronic stages in rats.

Lin B, Levy S, Raval AP, Perez-Pinzon MA, Defazio RA - Cardiovasc Psychiatry Neurol (2010)

The number of normal (i.e., vital) neurons in the striatum decreases rapidly after global ischemia. Bar graph shows normal neurons (mean ± SD) significantly decreased in rat striatum at days 3–56 after 12.5 minutes of transient forebrain ischemia, per high-power (40 ×) microscopic field (*indicates the significant difference, ischemic versus sham groups, p ≤ .03, ANOVA, post hoc Tukey HSD).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2957857&req=5

fig1: The number of normal (i.e., vital) neurons in the striatum decreases rapidly after global ischemia. Bar graph shows normal neurons (mean ± SD) significantly decreased in rat striatum at days 3–56 after 12.5 minutes of transient forebrain ischemia, per high-power (40 ×) microscopic field (*indicates the significant difference, ischemic versus sham groups, p ≤ .03, ANOVA, post hoc Tukey HSD).
Mentions: All rats showed mild necrosis in the dorsolateral striatum, and several rats had mild damage in the central striatum at days 3–7. No additional necrotic injury within the striatum was observed at days 28 and 56. Normal neurons significantly decreased in both dorsolateral and central striatum at days 3–56. The numbers were 60 ± 8 at day 3 (n = 5), 54 ± 12 at day 7 (n = 7), 70 ± 15 at day 28 (n = 6), 68 ± 4 at day 56 (n = 7) in dorsolateral striatum and 67 ± 15, 59 ± 16, 69 ± 8, and 66 ± 10 in central striatum while the numbers of normal neurons in sham rats (n = 4) were 104 ± 13 in dorsolateral striatum and 94 ± 5 in central striatum. The ischemia reduced the number of normal neurons in striatum (see Figure 1, mean ± S.D., ANOVA, p ≤ .01). Moderate-to-severe “spongy” changes (defined as empty spaces in histological sections) in striatum were present at day 56 in 5 of 7 rats (Figure 2(d)).

Bottom Line: At day 56, the optical density of GAD67-, but not VGAT-, immunoreactivity in substantia nigra pars reticulata (SNR)-significantly decreased.CR-neurons concentrated in substantia nigra pars compacta (SNC) were reduced by 27% from day 3 (n = 5) to day 56 (n = 7, ANOVA, p < .01).Our results demonstrate delayed impairment of the GABAergic system components in SN and associated with movement deficits after global ischemia.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology (D4-5), Cerebral Vascular Disease Research Center, University of Miami Miller School of Medicine, P.O. Box 016960, Miami, FL 33101, USA.

ABSTRACT
The long-term consequences of forebrain ischemia include delayed Parkinson's syndrome. This study revealed delayed neurodegeneration in the substantia nigra 8 weeks after 12.5 minutes of global ischemia in rat brain. Following neuronal loss of 30-40% in central and dorsolateral striatum at day 3, neuronal damage in the substantia nigra (SN) was assessed at 4-8 weeks using immunohistochemistry for glutamate decarboxylase 67 (GAD67), vesicular GABA transporter (VGAT), and calretinin (CR). At day 56, the optical density of GAD67-, but not VGAT-, immunoreactivity in substantia nigra pars reticulata (SNR)-significantly decreased. CR-neurons concentrated in substantia nigra pars compacta (SNC) were reduced by 27% from day 3 (n = 5) to day 56 (n = 7, ANOVA, p < .01). Movement coordination was impaired at day 56, as evaluated using beam-walking test (time-to-traverse 5.6 ± 1.2 sec versus 11.8 ± 5.4 sec; sham versus ischemia, p < .05, n = 5, and 7, resp.). Our results demonstrate delayed impairment of the GABAergic system components in SN and associated with movement deficits after global ischemia.

No MeSH data available.


Related in: MedlinePlus