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Effects of chronic lead exposure on [3H]MK-801 binding in the brain of rat
64
T. Ma et al. / Toxicology Letters 92 (1997) 59–66
Table 2 (continued) Region
Temporal, area 1, layer V and VI
Hippocampal formation CA1
CA2
CA3
Dentate gyrus
Superficial gray layer superior colliculus
Central gray
Interpeduncular nuclei
Medial geniculate nuclei
Substantia nigra
PN (days)
[3H]MK-801 binding (fmol/mg tissue)a
(% of control)
Control
Lead-treated
28 56 112
97.5 93.8 95.09 13.8 106.0 93.8
91.3 96.3 128.7 9 22.6* 127.5 91.0*
94 136 120
28 56 112 28 56 112 28 56 112 28 56 112 28 56 112 28 56 112 28 56 112 28 56 112 28 56 112
151.2910.1 249.9 930.1 204.9 92.6 228.7 96.3 259.9 9 38.0 254.9 910.1 196.2 91.3 352.3 947.6 269.9 96.3 193.7 911.3 299.8 9 35.1 273.6 98.8 62.5 93.8 95.0 95.1 75.09 3.8 20.8 9 1.3 21.1 91.3 15.1 91.4 28.89 2.6 33.8 9 1.4 18.1 9 0.7 97.5 9 3.8 135.0 9 15.1 116.3 9 3.8 13.891.4 47.6 98.8 16.3 91.0
136.2 9 1.4 304.8 947.6* 267.4 926.0* 198.7 97.6 366.0 9 36.3* 332.3 9 7.6* 184.9 916.3 408.5 9 2.6 313.6 93.8 183.7 9 15.1 336.0 937.6 351.0 9 3.8* 57.6 91.0 110.0 927.6 86.3 91.4 22.6 9 1.3 23.8 9 1.3 13.8 90.5 27.6 91.3 37.6 92.6 20.1 91.3 100.0 91.0 152.5 9 20.1 131.2 97.6 12.6 9 1.4 55.0 93.8 18.8 90.5
90 122 131 87 141 130 94 116 116 95 112 128 92 116 115 108 113 91 96 111 111 103 113 113 91 116 115
The coronal brain sections from control and lead-treated rats were incubated for 120 min in an incubation solution which contained 50 mM Tris – acetate buffer (pH 7.4), 8 nM [3H]MK-801, 30 mM L-glutamic acid and 10 mM glycine. Other details were described in Section 2. Values are expressed as mean9S.E.M. from five rats. * Significantly different from control (PB0.05).
Changes in [3H]MK-801 binding were also found in entorhinal, occipital and temporal cortical areas, suggesting the cerebral cortex is also a target site for lead. The hippocampal formation and the limbic association cortex, including the entorhinal and temporal pole, work together in cognition, including memory. Doubtless, any factor-induced damage in the limbic association cortex may also result in behavioral disruptions and memory deficits.
It is generally considered that the young are more sensitive to lead-induced neurotoxicity than adults. However, no change at PN 28, and increase at PN 56 and PN 112, in [3H]MK-801 binding following lead exposure was found in the present study. No significant changes in [3H]MK801 binding at PN 28 may reflect a shorter duration of lead exposure and lower lead concentration. The blood lead concentration was about 1.6-fold higher at PN 56 and PN 112 than
T. Ma et al. / Toxicology Letters 92 (1997) 59–66
Table 2 (continued) Region
Temporal, area 1, layer V and VI
Hippocampal formation CA1
CA2
CA3
Dentate gyrus
Superficial gray layer superior colliculus
Central gray
Interpeduncular nuclei
Medial geniculate nuclei
Substantia nigra
PN (days)
[3H]MK-801 binding (fmol/mg tissue)a
(% of control)
Control
Lead-treated
28 56 112
97.5 93.8 95.09 13.8 106.0 93.8
91.3 96.3 128.7 9 22.6* 127.5 91.0*
94 136 120
28 56 112 28 56 112 28 56 112 28 56 112 28 56 112 28 56 112 28 56 112 28 56 112 28 56 112
151.2910.1 249.9 930.1 204.9 92.6 228.7 96.3 259.9 9 38.0 254.9 910.1 196.2 91.3 352.3 947.6 269.9 96.3 193.7 911.3 299.8 9 35.1 273.6 98.8 62.5 93.8 95.0 95.1 75.09 3.8 20.8 9 1.3 21.1 91.3 15.1 91.4 28.89 2.6 33.8 9 1.4 18.1 9 0.7 97.5 9 3.8 135.0 9 15.1 116.3 9 3.8 13.891.4 47.6 98.8 16.3 91.0
136.2 9 1.4 304.8 947.6* 267.4 926.0* 198.7 97.6 366.0 9 36.3* 332.3 9 7.6* 184.9 916.3 408.5 9 2.6 313.6 93.8 183.7 9 15.1 336.0 937.6 351.0 9 3.8* 57.6 91.0 110.0 927.6 86.3 91.4 22.6 9 1.3 23.8 9 1.3 13.8 90.5 27.6 91.3 37.6 92.6 20.1 91.3 100.0 91.0 152.5 9 20.1 131.2 97.6 12.6 9 1.4 55.0 93.8 18.8 90.5
90 122 131 87 141 130 94 116 116 95 112 128 92 116 115 108 113 91 96 111 111 103 113 113 91 116 115
The coronal brain sections from control and lead-treated rats were incubated for 120 min in an incubation solution which contained 50 mM Tris – acetate buffer (pH 7.4), 8 nM [3H]MK-801, 30 mM L-glutamic acid and 10 mM glycine. Other details were described in Section 2. Values are expressed as mean9S.E.M. from five rats. * Significantly different from control (PB0.05).
Changes in [3H]MK-801 binding were also found in entorhinal, occipital and temporal cortical areas, suggesting the cerebral cortex is also a target site for lead. The hippocampal formation and the limbic association cortex, including the entorhinal and temporal pole, work together in cognition, including memory. Doubtless, any factor-induced damage in the limbic association cortex may also result in behavioral disruptions and memory deficits.
It is generally considered that the young are more sensitive to lead-induced neurotoxicity than adults. However, no change at PN 28, and increase at PN 56 and PN 112, in [3H]MK-801 binding following lead exposure was found in the present study. No significant changes in [3H]MK801 binding at PN 28 may reflect a shorter duration of lead exposure and lower lead concentration. The blood lead concentration was about 1.6-fold higher at PN 56 and PN 112 than