Biomedical subjects

T J Kornecook

Publications and source records attributed to T J Kornecook.

7 recordsLinked to original sources

PubMed2001

Application of in vivo microdialysis to the study of cholinergic systems.

The application of in vivo microdialysis to the study of acetylcholine (ACh) release has contributed greatly to our understanding of cholinergic brain systems. This article reviews standard experimental procedures for dialysis probe selection and implantation, perfusion parameters, neurochemical detection, and data analysis as they relate to microdialysis assessments of cholinergic function. Particular attention is focused on the unique methodological considerations that arise when in vivo microdialysis is dedicated expressly to the recovery and measurement of ACh as opposed to other neurotransmitters. Limitations of the microdialysis technique are discussed, as well as methodological adaptations that may prove useful in overcoming these limitations. This is followed by an overview of recent studies in which the application of in vivo microdialysis has been used to characterize the basic pharmacology and physiology of cholinergic neurons. Finally, the usefulness of the microdialysis approach for testing hypotheses regarding the cholinergic systems' involvement in cognitive processes is examined. It can be concluded that, in addition to being a versatile and practical method for studying the neurochemistry of cholinergic brain systems, in vivo microdialysis represents a valuable tool in our efforts to better comprehend ACh's underlying role in a variety of behavioral processes.

Acetylcholine↗

PubMed2000

Reversible lesions of the rhinal cortex produce delayed non-matching-to-sample deficits in rats.

Rats with cannulae guides implanted in the rhinal cortex were tested on a delayed non-matching-to-sample task, following either lidocaine or sham microinfusions. Bilateral lidocaine microinfusions to the rhinal cortex produced significant delayed non-matching-to-sample deficits. These results are consistent with the putative role of the rhinal cortex in object recognition but because the deficits were not shown to be time dependent, non-mnemonic interpretations cannot be ruled out. These results also illustrate the utility of reversible lidocaine lesions in the study of the neuroanatomical basis of delayed non-matching-to-sample.

Animals↗

PubMed1999

Rhinal cortex, but not medial thalamic, lesions cause retrograde amnesia for objects in rats.

Male Long-Evans rats were trained on five separate object discrimination problems at different times prior to surgery. Following surgery, retrograde amnesia was assessed by measuring retention of the preoperatively learned discrimination problems in lesioned rats and controls. Rats with rhinal cortex lesions displayed temporally graded retrograde amnesia; retention of object discriminations acquired in the recent past (i.e. 2 or 9 days prior to surgery) was significantly impaired, whereas retention of object discriminations acquired more remotely (i.e. 16, 37, or 58 days prior to surgery) was not. In contrast, rats with mediodorsal thalamic lesions exhibited normal savings of all discrimination problems. These results suggest that the rhinal cortex, but not the mediodorsal thalamus, plays a time-limited role in the consolidation of object memory.

Amnesia, Retrograde↗

PubMed1999

Basal forebrain damage and object-recognition in rats.

Damage to the basal forebrain (BF) produces permanent learning and memory impairments in humans. Most efforts to model these deficits in rats have focused on spatial memory dysfunction; this study was the first to assess the effects of BF damage in rats on the performance of a battery of object-memory tasks commonly employed to assess brain damage-produced amnesia in primates. The performance of rats with bilateral electrolytic lesions of the medial septum and diagonal band (MS/NDB) region of the BF was assessed on three object-memory tasks: nonrecurring items delayed nonmatching-to-sample (DNMS), simple object discrimination, and eight-pair concurrent object discrimination. Lesioned rats and sham-surgery controls were tested on the DNMS task at retention delays of 4, 15, 30, 60 and 120 s both before and after surgery. After surgery, the rats with MS/NDB lesions required significantly more trials than controls to relearn the nonmatching rule; and, once they relearned the rule, they were significantly and comparably impaired at all delays. This impairment did not diminish with either the passage of time or additional practice. In contrast, there were no significant differences between the MS/NDB-lesioned and control groups in the performance of either simple or concurrent object-discrimination tasks. The delay-independent nature of the DNMS deficit and the lack of deficits on the other two object-memory tasks suggest that the effect of the lesion is not the result of an impairment in retention.

Amygdala↗

PubMed1998

Noncontingent drug exposure facilitates the development of contingent tolerance to the anticonvulsant effects of ethanol and diazepam in kindled rats.

Tolerance to anticonvulsant drug effects on kindled convulsions can result from drug exposure alone, but convulsive activity during drug exposure has a substantial facilitatory effect on tolerance development. Tolerance produced by drug exposure in the absence of a criterion response (in this case convulsions) has been termed pharmacologic tolerance (10); tolerance produced by drug exposure with concomitant performance of the criterion response has been termed contingent tolerance (1). The present study examines whether noncontingent drug exposure facilitates the development of contingent tolerance to the anticonvulsant effects of ethanol and diazepam. Amygdala-kindled, Long-Evans rats were treated with either ethanol (5.0 g/kg once daily for 21 days) or diazepam (5.0 mg/kg three times daily for 10 days) in the absence of convulsive stimulation to produce pharmacologic tolerance--control rats received treatments of vehicle. Then, all of the rats were rendered contingently tolerant by a series of "bidaily" (once every 2 days) injections (ethanol 2.0 g/kg or diazepam 2.0 mg/kg), each 1 h prior to a kindled convulsion. The rats that had received noncontingent exposure to ethanol or diazepam developed contingent tolerance significantly faster than the control rats. These results suggest that the mechanisms underlying pharmacologic and contingent tolerance to anticonvulsant drug effects are additive.

Animals↗

PubMed1997

Object-recognition and spatial learning and memory in rats prenatally exposed to ethanol.

Prenatal ethanol exposure can produce cognitive and behavioral impairments. In the present study, rats from prenatal ethanol (E), pair-fed (PF), and ad libitum-fed control (C) treatment conditions were tested on the object-recognition delayed-nonmatching-to-sample (DNMS) task with nonrecurring items and on the spatial-navigation Morris water maze task. In Experiment 1, there were no significant differences among groups in object-recognition learning and memory, distractibility, or response perseveration on the DNMS task. In Experiment 2, the same rats were tested in the water maze; E rats took significantly longer to learn the task than did the PF or C rats. These data suggest that the mechanisms underlying spatial cognitive abilities are more vulnerable to the teratogenic effects of prenatal ethanol exposure than those underlying object-recognition abilities.

Animals↗

PubMed1996

Ischemia-induced object-recognition deficits in rats are attenuated by hippocampal ablation before or soon after ischemia.

The literature on the role of the hippocampus in object-recognition contains a paradox: Transient forebrain ischemia (ISC) produces hippocampal damage and severe deficits on the delayed nonmatching-to-sample (DNMS) task, yet hippocampal ablation (ABL) produces milder deficits. Experiment 1 confirmed that pretrained rats display severe DNMS deficits following ISC, but not ABL. Ischemia produced loss of CA1 neurons, but no obvious extrahippocampal damage. In Experiments 2 and 3, ISC rats from Experiment 1 received ABL, and ABL rats received ISC; neither treatment affected DNMS performance. In Experiment 4, rats that received ISC followed 1 hr later by ABL displayed only mild deficits. It is hypothesized that ISC-induced DNMS deficits are due to extrahippocampal damage produced by pathogenic processes that involve the hippocampus.

Animals↗