Abstract
Acquisition of the trace-conditioned eye blink response (CR) is mediated by a variety of brain structures, including the cerebellum, the hippocampus, and brain stem nuclei. We examined the effects of a neuronal sodium channel antagonist (lamotrigine) on the ability of rabbits to acquire an eye blink CR after 6.5 min of cerebral ischemia. New Zealand white rabbits (n = 31) were randomly assigned to sham (S), normothermic ischemia (N), hypothermic (30°C) ischemia(H), or lamotrigine (50 mg/kg) treated (L) groups. In the N, H, and L groups, 6.5 min of global cerebral ischemia was produced using an inflatable neck tourniquet. Trace conditioning was started on the 7th postischemic day. The conditioned stimulus consisted of a tone (85 dB, 6 kHz) presented for 100 ms. The unconditioned stimulus was an air puff (150 ms duration) directed at the cornea. The interval between the end of the conditioned stimulus and the start of the unconditioned stimulus (the trace interval, TI) was 300 ms in duration. A trace-conditioned response was defined as an eye blink that was initiated during the TI. Eighty trials were delivered daily for 15 days. Neurologic deficits were greatest in the N group, and these animals had fewer CRs (149 ± 157) than animals in the S (509 ± 214) or H (461 ± 149) groups (P < 0.05 by analysis of variance). Animals in the L group had a total number of CRs (380 ± 253) that was intermediate between the S and N groups. Histologic evidence of neural injury was greatest in the N group. This study demonstrates that a brief episode of cerebral ischemia results in the impairment of this test of neurobehavioral function. Both hypothermia and lamotrigine were able to attenuate the impairment of eye blink trace- conditioned responses produced by cerebral ischemia.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 105-113 |
| Number of pages | 9 |
| Journal | Experimental Neurology |
| Volume | 159 |
| Issue number | 1 |
| DOIs | |
| State | Published - Sep 1999 |
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Keywords
- Brain
- Conditioned response
- Hypothermia
- Ischemia
- Lamotrigine
- Rabbits
ASJC Scopus subject areas
- Neurology
- Neuroscience(all)
Cite this
Effects of hypothermia and lamotrigine on trace-conditioned learning after global cerebral ischemia in rabbits. / Kwon, Jae Young; Bacher, Andreas; Deyo, Donald J.; Grafe, Marjorie R.; Disterhoft, John F.; Uchida, Tatsuo; Zornow, Mark H.
In: Experimental Neurology, Vol. 159, No. 1, 09.1999, p. 105-113.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effects of hypothermia and lamotrigine on trace-conditioned learning after global cerebral ischemia in rabbits
AU - Kwon, Jae Young
AU - Bacher, Andreas
AU - Deyo, Donald J.
AU - Grafe, Marjorie R.
AU - Disterhoft, John F.
AU - Uchida, Tatsuo
AU - Zornow, Mark H.
PY - 1999/9
Y1 - 1999/9
N2 - Acquisition of the trace-conditioned eye blink response (CR) is mediated by a variety of brain structures, including the cerebellum, the hippocampus, and brain stem nuclei. We examined the effects of a neuronal sodium channel antagonist (lamotrigine) on the ability of rabbits to acquire an eye blink CR after 6.5 min of cerebral ischemia. New Zealand white rabbits (n = 31) were randomly assigned to sham (S), normothermic ischemia (N), hypothermic (30°C) ischemia(H), or lamotrigine (50 mg/kg) treated (L) groups. In the N, H, and L groups, 6.5 min of global cerebral ischemia was produced using an inflatable neck tourniquet. Trace conditioning was started on the 7th postischemic day. The conditioned stimulus consisted of a tone (85 dB, 6 kHz) presented for 100 ms. The unconditioned stimulus was an air puff (150 ms duration) directed at the cornea. The interval between the end of the conditioned stimulus and the start of the unconditioned stimulus (the trace interval, TI) was 300 ms in duration. A trace-conditioned response was defined as an eye blink that was initiated during the TI. Eighty trials were delivered daily for 15 days. Neurologic deficits were greatest in the N group, and these animals had fewer CRs (149 ± 157) than animals in the S (509 ± 214) or H (461 ± 149) groups (P < 0.05 by analysis of variance). Animals in the L group had a total number of CRs (380 ± 253) that was intermediate between the S and N groups. Histologic evidence of neural injury was greatest in the N group. This study demonstrates that a brief episode of cerebral ischemia results in the impairment of this test of neurobehavioral function. Both hypothermia and lamotrigine were able to attenuate the impairment of eye blink trace- conditioned responses produced by cerebral ischemia.
AB - Acquisition of the trace-conditioned eye blink response (CR) is mediated by a variety of brain structures, including the cerebellum, the hippocampus, and brain stem nuclei. We examined the effects of a neuronal sodium channel antagonist (lamotrigine) on the ability of rabbits to acquire an eye blink CR after 6.5 min of cerebral ischemia. New Zealand white rabbits (n = 31) were randomly assigned to sham (S), normothermic ischemia (N), hypothermic (30°C) ischemia(H), or lamotrigine (50 mg/kg) treated (L) groups. In the N, H, and L groups, 6.5 min of global cerebral ischemia was produced using an inflatable neck tourniquet. Trace conditioning was started on the 7th postischemic day. The conditioned stimulus consisted of a tone (85 dB, 6 kHz) presented for 100 ms. The unconditioned stimulus was an air puff (150 ms duration) directed at the cornea. The interval between the end of the conditioned stimulus and the start of the unconditioned stimulus (the trace interval, TI) was 300 ms in duration. A trace-conditioned response was defined as an eye blink that was initiated during the TI. Eighty trials were delivered daily for 15 days. Neurologic deficits were greatest in the N group, and these animals had fewer CRs (149 ± 157) than animals in the S (509 ± 214) or H (461 ± 149) groups (P < 0.05 by analysis of variance). Animals in the L group had a total number of CRs (380 ± 253) that was intermediate between the S and N groups. Histologic evidence of neural injury was greatest in the N group. This study demonstrates that a brief episode of cerebral ischemia results in the impairment of this test of neurobehavioral function. Both hypothermia and lamotrigine were able to attenuate the impairment of eye blink trace- conditioned responses produced by cerebral ischemia.
KW - Brain
KW - Conditioned response
KW - Hypothermia
KW - Ischemia
KW - Lamotrigine
KW - Rabbits
UR - http://www.scopus.com/inward/record.url?scp=0345425741&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0345425741&partnerID=8YFLogxK
U2 - 10.1006/exnr.1999.7130
DO - 10.1006/exnr.1999.7130
M3 - Article
C2 - 10486179
AN - SCOPUS:0345425741
VL - 159
SP - 105
EP - 113
JO - Experimental Neurology
JF - Experimental Neurology
SN - 0014-4886
IS - 1
ER -