ライフサイエンスコーパス: lesioned animal

1 ree M. bovis strains were recovered from non-lesioned animals.

2 rats and in the intact hemispheres of 6-OHDA-lesioned animals.

3 m or in the unlesioned hemispheres of 6-OHDA-lesioned animals.

4 ic activity were observed only in the 6-OHDA lesioned animals.

5 patterns in forebrain regions of intact and lesioned animals.

6 ion patterns in the forebrains of intact and lesioned animals.

7 lent levels of True Blue label in intact and lesioned animals.

8 putamen, thalamus, and amygdala of the MPTP-lesioned animals.

9 nimals, and CDP improving the performance of lesioned animals.

10 nding appeared by day 15 in both control and lesioned animals.

11 into the lateral ventricle of fimbria-fornix lesioned animals.

12 ffect on impaired performance in hippocampal lesioned animals.

13 de was collected from a random sample of non-lesioned animals.

14 on in REM sleep time was observed in the SOM-lesioned animals.

15 of correlations at large time scales in SCN-lesioned animals.

16 t as severe as those shown by the dorsal CA1 lesioned animals.

17 ocations relative to control and ventral CA1 lesioned animals.

18 both D2R and D3R relative to vehicle-treated lesioned animals.

19 y was not observed in either the LMN- or DTN-lesioned animals.

20 trast, LTD was preserved in nicotine-treated lesioned animals.

21 duced in BLA-lesioned animals but not in CeA-lesioned animals.

22 ess, a small day/night rhythm was present in lesioned animals.

23 s mild compared with cells recorded from PoS-lesioned animals.

24 re likely to choose the LR arm than the sham-lesioned animals.

25 essed relative to that in the shell- or sham-lesioned animals.

26 mRNA, but NPY mRNA was reduced in the ARC of lesioned animals.

27 anges in DA similar to those seen in the non-lesioned animals.

28 al root ganglion (DRG) neurons in intact and lesioned animals.

29 iate in low-lesioned, and smallest in highly lesioned animals.

30 atic induction of c-Fos in the CPu in 6-OHDA-lesioned animals.

31 ng) was quantified by autoradiography in DRN-lesioned animals.

32 representations in PoS-lesioned, but not ADN-lesioned, animals.

33 At 1 month after surgery, successfully lesioned animals (3 or less forelimb akinesia score, and

34 n throughout the dorsal striatum of neonatal lesioned animals, a response not observed within the int

35 Lesioned animals also showed diminished activity at base

36 Only 2 of 11 lesioned animals and 6% of slices from cortex exposed to

37 control groups consisted of a group of sham lesioned animals and a group of animals that had unilate

38 mmatory responses were similar in normal and lesioned animals and the acetylcholinesterase inhibitor,

39 formation relative to control and dorsal CA1 lesioned animals, and a mild deficit for the temporal or

40 binding was evident in the striatum of MPTP lesioned animals as compared with the control group.

41 oxylase mRNA increased in 2 and 12-month-old lesioned animals both 3 and 10 days post-treatment.

42 VC lesions produced behavior similar to VLF-lesioned animals but did not significantly affect tcMMEP

43 after training were severely reduced in BLA-lesioned animals but not in CeA-lesioned animals.

44 oral arrest could be reconstituted in fornix-lesioned animals by inducing synchronous activity in the

45 In lesioned animals, chronic amitriptyline (AMI; 5 mg/kg) t

46 in neocortical areas of both hemispheres of lesioned animals compared with protein levels of sham-op

47 e, was significantly impaired in hippocampus-lesioned animals compared with sham control animals.

48 Some DTN-lesioned animals contained cells whose firing rates were

49 Unlike acutely lesioned animals, continuously infused rats revealed no

50 ntly altered, suggesting that smaller CPs in lesioned animals could be largely attributable to greate

51 Nonetheless, OFC-lesioned animals could still approximate choice-outcome

52 ransplanting fetal SCN into the brain of the lesioned animal, demonstrating the first two of the esse

53 Although place cells from lesioned animals did not differ from controls on many pl

54 The performance of lesioned animals did not differ significantly from sham-

55 pattern to avoid the satiated food, whereas lesioned animals did not, suggesting that neonatal hippo

56 nucleus (VPL) in thalamic brain slices from lesioned animals displayed an increased probability of b

57 In contrast, hippocampal-lesioned animals displayed impairments across all spatia

58 Hearing-lesioned animals displayed tinnitus with a pitch in the

59 administration of apomorphine to the 6-OHDA lesioned animal evoked a robust and long-lasting excitat

60 When re-tested four weeks later, sham-lesioned animals exhibited long-term memory; in contrast

61 mpaired in BLA-lesioned animals, whereas CeA-lesioned animals exhibited only mild deficits.

62 ANFs from successfully lesioned animals exhibited significant pathophysiology c

63 An alternative hypothesis is that AM-lesioned animals fail to acquire certain fear CRs simply

64 ippocampal deafferentation in both groups of lesioned animals failed to prevent the accumulation of G

65 Additional cells were recorded from lesioned animals for up to 3 weeks after the lesion.

66 UNI lesioned animals from 6-36 days post-lesion showed no ne

67 Thus, in lesioned animals, Galpha(olf) upregulation is critical f

68 As compared with control animals, amygdala-lesioned animals had blunted responding to both positive

69 Lesioned animals had increased food intake in light and

70 Lesioned animals had reductions in 5-HT in the NA, and D

71 HD cells from lesioned animals had similar firing properties compared

72 tion of nerve growth factor (NGF) to aged or lesioned animals has been shown to reverse the atrophy o

73 The absence of sensitization in lesioned animals implies that, before physiological func

74 i.p.) improved passive avoidance behavior in lesioned animals in a mecamylamine-sensitive manner.

75 Residual Fos induction seen in lesioned animals in response to higher doses of LPS prov

76 b in the food-restricted, methyl bromide gas-lesioned animals indicates that the mechanisms that guid

77 In NBM-lesioned animals, k* was elevated significantly (by up t

78 Lesioned animals learned normally after multiple shocks,

79 nerve fiber (ANF) recordings were made from lesioned animals, lesion shams, and normal controls.

80 Further, cells from lesioned animals maintained a stable preferred firing di

81 spatial correlates of complex spike cells in lesioned animals may rely on a more limited set of senso

82 e of CS preexposure), Novelty in hippocampal lesioned animals might be larger, equal, or smaller (cor

83 In the 6-hydroxydopamine-lesioned animal model of Parkinson's disease, 5 altered

84 uced by apomorphine in the 6-hydroxydopamine-lesioned animal models of Parkinson's disease were studi

85 ibited long-term memory; in contrast, the TA-lesioned animals no longer showed target quadrant prefer

86 Lesioned animals not receiving Fluoro-Gold exhibited the

87 animals with mPFC lesions compared with sham-lesioned animals on the first day of retesting in all fi

88 Hippocampal lesioned animals performed poorly on the task and inject

89 DP in the septal lesioned subjects, with the lesioned animals performing worse than control animals,

90 ral asymmetries (compared to nonimmobilized, lesioned animals), presumably attributable to mild disus

91 to the increased locomotion observed in non-lesioned animals, rats pretreated with 6-OHDA showed no

92 Separate groups of sham and lesioned animals received either 50% or 25% reinforcemen

93 FGF-2 and compared it with that observed in lesioned animals receiving infusate controls.

94 elay-discounting curves was observed in wOFC-lesioned animals relative to shams--differences that dis

95 resentation of CS alone), onset responses in lesioned animals returned to their preconditioning firin

96 was identical to that of the experimentally lesioned animals revealed a bilateral ischemic lesion re

97 However, the same amygdala-lesioned animals showed a complete blockade of fear-pote

98 The lesioned animals showed a delay in the onset of desensit

99 -term memory was examined, both sham- and TA-lesioned animals showed a significant preference for the

100 following conditioned fear stress, habenula-lesioned animals showed decreased PPI which normalized w

101 Pretrained HCX-lesioned animals showed deficits similar to those of HIP

102 The nBM-lesioned animals showed initial acquisition impairment i

103 by damage to the auditory nerve, because the lesioned animals showed intact compound action potential

104 Pretrained HIPP-lesioned animals showed marked delay-dependent deficits

105 The OBs of lesioned animals showed marked expansions of 2A4(+)ORN b

106 In contrast, hippocampal-lesioned animals showed normal (slowed) learning.

107 In addition, HD cells from lesioned animals showed normal responses to two environm

108 However, lesioned animals showed reduced cocaine-seeking during c

109 In contrast, BI lesioned animals showed severe spatial learning deficits

110 TA-lesioned animals still exhibited a deficit in long-term

111 In the lesioned animals, striatal DA ipsilateral to 6-OHDA infu

112 In the non-lesioned animals, striatal DA was reduced and striatal D

113 l dopamine release from synaptosomes of MPTP-lesioned animals, suggesting that nicotine treatment had

114 Although fields from ADN-lesioned animals tended to have less landmark control th

115 r-expression of both D2R and D3R compared to lesioned animals that received blank vector.

116 The lesioned animals that received BMP7 pretreatment, as com

117 alysis experiments indicated that only those lesioned animals that received the mixture of MD-TH and

118 ies, revealed important factors operating in lesioned animals that were either absent or insignifican

119 tral forelimb area compared with that in the lesioned animals that were not rehabilitated.

120 A subset of these lesioned animals then had a cast applied for 7 d to the

121 alamic nucleus HD cells was still present in lesioned animals; thus, this property cannot be attribut

122 of ventrolateral PFC and the failure of LPFC-lesioned animals to disengage from the immediately prece

123 Another group of HIPP- and HCX-lesioned animals trained on the tasks after the lesion s

124 2 activation was confirmed in vivo in 6-OHDA-lesioned animals treated systemically with SKF38393.

125 tic assumptions of decision theory, the mOFC-lesioned animals' value comparisons were no longer indep

126 rection remained stable across days when the lesioned animal was placed into a novel environment.

127 halamic nucleus, c-fos mRNA induction in the lesioned animals was abolished in the bed nucleus of the

128 read of visual corticopontine connections in lesioned animals was greatly increased relative to unles

129 he performance of both the lesioned and sham-lesioned animals was impaired by the presentation of a v

130 In addition, the responding of amygdala-lesioned animals was insensitive to the omission of the

131 g followed by surgery, it was found that all lesioned animals were able to remember the sequence.

132 The responses of the amygdala-lesioned animals were compared with a group of age-match

133 quisition and overall response rates in core-lesioned animals were depressed relative to that in the

134 simultaneous olfactory discrimination; PRER-lesioned animals were dramatically and persistently impa

135 roximately 3 weeks of age, lesioned and sham-lesioned animals were either tested for the display of p

136 Lesioned animals were exposed to moderate doses of ethan

137 Lesioned animals were highly impaired in recall and acqu

138 ment with our prediction, postsurgery, VLPFC lesioned animals were impaired in performing a series of

139 In contrast, OFC lesioned animals were impaired regardless of whether the

140 Surprisingly, place cells from lesioned animals were more likely modulated by the direc

141 ndmark cue showed that place fields from PoS-lesioned animals were not controlled by the cue and shif

142 e third and fourth days of retraining, these lesioned animals were performing at a level comparable t

143 preferred direction drifted when HD cells in lesioned animals were recorded in the dark.

144 e assessed for neuronal differentiation, and lesioned animals were tested for amphetamine-induced rot

145 ition) in unlesioned rats and in cortices of lesioned animals were unaffected by priming.

146 In contrast, lesioned animals were unimpaired when responding on a pr

147 responses were significantly impaired in BLA-lesioned animals, whereas CeA-lesioned animals exhibited

148 tions of muscimol was markedly attenuated in lesioned animals, whereas the inhibition by VTA injectio

149 ase was similar to control in unlesioned and lesioned animals with chronic oral nicotine.

150 nition or motor function in symptomatic MPTP-lesioned animals with deficits in both of these areas.

151 When both non-lesioned and lesioned animals with different ages were pooled for lin

152 Lesioned animals with ectopic grafts or sham surgery as

153 ditioned response (CR) more slowly than sham-lesioned animals with either the 1.5-s ISI or with the 2

154 R and D3R binding in the ventral striatum of lesioned animals with lentiviral over-expression of both

155 irole generated only modest motor effects in lesioned animals with sole over-expression of D2R or D3R

156 imb and produced robust circling behavior in lesioned animals with striatal over-expression of both D

157 in expression was significantly increased in lesioned animals within proximal and distal regions of p

158 ute and transient working memory deficits in lesioned animals without effect in unlesioned controls.

159 Lesioned animals without transplants maintained higher t

160 ar reduction of trkC probed hybridization in lesioned animals without transplants.