Biomedical subjects

B G Lyeth

Publications and source records attributed to B G Lyeth.

At least 19 recordsLinked to original sources

PubMed1999

Combined therapy affects outcomes differentially after mild traumatic brain injury and secondary forebrain ischemia in rats.

Muscarinic and NMDA receptors contribute to post-traumatic hypersensitivity to secondary ischemia. However, the effect of these receptor antagonists on behavior and CA1 neuronal death after traumatic brain injury (TBI) with acute (1 h after TBI) forebrain ischemia has not been systematically assessed. We examined cognitive and motor dysfunction and the relationship of behavior deficits to neuronal death in this model using muscarinic and NMDA antagonists. Three behavioral groups (n=10/group) of Wistar rats were subjected to mild TBI and 6 min of forebrain ischemia imposed 1 h after TBI with 45 days survival. Motor and spatial memory performance were assessed using the rotarod task and Morris water maze. Seven additional groups (n=6/group) were evaluated only for CA1 death after 7 days survival following sham, individual or combined injury with and without drug treatments. Rats were given 0.3 mg/kg MK-801 (M) and 1.0 mg/kg scopolamine (S) alone or combined (M-S) before or 45 min after TBI. Rotarod performance was tested at days 1-5 and maze performance on days 11-15 and 40-44 after M-S treatment. The 7-day studies showed M-S treatment (p<0.01) reduced CA1 neuronal death better than either S or M alone. Behavioral groups had inadvertent post-ischemic hypothermia that decreased CA1 death and likely influenced behavioral morbidity. M-S given before TBI (p<0.01) decreased memory deficits on day 15, while M-S treatment given after TBI was ineffective. Unexpectedly, M-S treatment before or after TBI produced transient motor deficits (p<0. 01). Memory improvement occurred independent of CA1 death.

Animals↗

PubMed1998

Glutamate antagonism during secondary deafferentation enhances cognition and axo-dendritic integrity after traumatic brain injury.

The combination of central fluid percussion traumatic brain injury (TBI) followed 24 h later by a bilateral entorhinal cortical deafferentation (BEC) produces profound cognitive morbidity. We recently showed that MK-801 given prior to TBI in this insult improved spatial memory for up to 15 days. In the present study we examine whether MK-801 treatment of the BEC component in the combined insult model affects cognitive recovery. Two strategies for drug treatment were tested. Fifteen minutes prior to the BEC lesion in the combined insult, rats were given i.p. doses of either 3 mg/kg (acute group) or 1 mg/kg (chronic group) MK-801. The acute group received no further injections, whereas the chronic group received 1 mg/kg MK-801 i.p. twice a day for 2 days post-BEC lesion. Two additional groups of animals received BEC lesion alone and either acute or chronic MK-801 treatment identical with the combined insult cases. Each group was then assessed for spatial memory deficits with the Morris water maze at days 11-15 and 60-64 postinjury. Both acute and chronic MK-801 treatment in the combined insult group significantly reduced spatial memory deficits at 15 days postinjury relative to untreated injured cases (P < .01). This reduction appeared more robust at 15 days and persisted for up to 64 days in the chronically treated group (P < .05). By contrast, neither acute nor chronic MK-801 treatment affected memory performance with the BEC insult alone. Immunocytochemical localization of parvalbumin showed that chronic administration of MK-801 in the combined insult cases attenuated the injury-induced dendritic atrophy of inhibitory neurons in the dentate gyrus and area CA1. Synaptophysin immunobinding revealed that chronic MK-801 treatment of the BEC component of the combined insult normalized the distribution of presynaptic terminals within the dentate gyrus. These results suggest that cognitive deficits produced by head trauma involving both neuroexcitation and deafferentation can be attenuated with chronic application of glutamatergic antagonists during the period of deafferentation injury and that this attenuation is correlated with axo-dendritic integrity.

Afferent Pathways↗

PubMed1998

Status epilepticus causes long-term NMDA receptor-dependent behavioral changes and cognitive deficits.

PURPOSE: The role of N-methyl-D-aspartate (NMDA)-receptor activation on behavioral and cognitive changes after status epilepticus (SE) is unknown. In this study, behavioral and cognitive changes after SE were evaluated in the short and long term and in rats in which the NMDA receptor was inactivated during SE. METHODS: Pilocarpine (350 mg/kg) was injected to induce SE. Inhibition of the NMDA receptor during SE was achieved with MK-801 (4 mg/kg). Seizure intensity during SE was monitored by electroencephalography (EEG). After SE, behavioral studies were performed to identify abnormal behavior by using behavioral tests adapted from Moser's functional observational battery. Cognitive changes were assessed by using the Morris Water Maze (MWM). RESULTS: Pilocarpine-treated animals scored significantly higher on two of the behavioral tests: the Touch test and the Pick-Up test. These behavioral changes occurred very soon after SE, with the earliest changes observed 2 days after SE and persisting for the life of the animal. Inhibition of the NMDA receptor with MK-801 completely inhibited these behavioral changes under conditions that did not alter the duration of SE. In addition, pilocarpine-treated animals exhibited cognitive deficits as determined by using the MWM. Six weeks after SE, the animals displayed significantly longer latencies to locate the hidden platform on this test. The impaired performance on the MWM also occurred as early as 5 days after SE. These cognitive deficits were prevented in animals treated with MK-801 during SE. CONCLUSIONS: The results indicate that behavioral and cognitive changes occur soon after SE, are permanent, and are dependent on NMDA-receptor activation during SE. NMDA-receptor activation may play an important role in causing cognitive and behavioral morbidity after recovery from SE.

Animals↗

PubMed1997

Effect of prior receptor antagonism on behavioral morbidity produced by combined fluid percussion injury and entorhinal cortical lesion.

We have used an animal model of traumatic brain injury (TBI) that incorporates both the neurotransmitter toxicity of fluid percussion TBI and deafferentation of bilateral entorhinal cortical (BEC) lesion to explore whether administration of muscarinic cholinergic or N-methyl-D-aspartate glutamatergic antagonists prior to injury ameliorates cognitive morbidity. Fifteen minutes prior to moderate central fluid percussion TBI, rats were given intraperitoneal injections of either scopolamine (1.0 mg/kg) or MK-801 (0.3 mg/kg) and 24 hr later underwent BEC lesion. Body weight was followed for 5 days postinjury, as was beam balance and beam walk performance to assure motor recovery prior to spatial memory testing. Each group was assessed for spatial memory deficits with the Morris water maze at short term (days 11-15) and long-term (60-64 days) postinjury intervals and then compared with untreated combined insult and sham-injured controls. Results showed that each drug significantly elevated body weight relative to untreated injured cases. Both scopolamine and MK-801 reduced beam balance deficits, whereas neither drug had a significant effect on beam walk deficits. Interestingly, short-term cognitive deficits assessed on days 11-15 were differentially affected by the two drugs: MK-801 pretreatment enhanced the recovery of spatial memory performance, whereas scopolamine pretreatment did not. Long-term (days 60-64) deficits in spatial memory were not altered by pretreatment with either drug. Our results suggest that, unlike fluid percussion TBI alone, behavioral impairment may require more select intervention when deafferentation is part of the head trauma pathology.

Animals↗

PubMed1997

The effects of traumatic brain injury on inhibition in the hippocampus and dentate gyrus.

Changes in inhibitory neuronal functioning may contribute to morbidity following traumatic brain injury (TBI). Evoked responses to orthodromic paired-pulse stimulation were examined in the hippocampus and dentate gyrus at 2 and 15 days following lateral fluid percussion TBI in adult rats. The relative strength of inhibition was estimated by measuring evoked paired pulses in three afferent systems: the CA3 commissural input to the CA1 region of the hippocampus; the entorhinal cortical input to the ipsilateral CA1 area (temporoammonic system); and the entorhinal input to the ipsilateral dentate gyrus (perforant path). In addition to quantitative electrophysiological estimates of inhibitory efficacy, levels of gamma-aminobutyric acid (GABA) were qualitatively examined with immunohistochemical techniques. Effects of TBI on paired-pulse responses were pathway-specific, and dependent on time postinjury. At 2 days following TBI, inhibition of population spikes was significantly reduced in the CA3 commissural input to CA1, which contrasted with injury-induced increases in inhibition in the dentate gyrus seen at both 2 and 15 days postinjury. Low-level stimulation, subthreshold for population spikes, also revealed changes in paired-pulse facilitation of field extracellular postsynaptic potentials (fEPSPs), which depended on fiber pathway and time postinjury. Significant injury-induced electrophysiological changes were almost entirely confined to the hemisphere ipsilateral to injury. Intensity of GABA immunobinding exhibited a regional association with electrophysiological indices of inhibition, with the most pronounced increases in GABA levels and inhibition found in the dentate gyrus. TBI-induced effects showed a regional pattern within the hippocampus which corresponds closely to inhibitory changes reported to follow ischemia and kindling. This degree of similarity in outcome following dissimilar injuries may indicate common mechanisms in the nervous system response to injury.

Animals↗

PubMed1997

Effect of tetrahydroaminoacridine, a cholinesterase inhibitor, on cognitive performance following experimental brain injury.

An emerging literature exists in support of deficits in cholinergic neurotransmission days to weeks following experimental traumatic brain injury (TBI). In addition, novel cholinomimetic therapeutics have been demonstrated to improve cognitive outcome following TBI in rats. We examined the effects of repeated postinjury administration of a cholinesterase inhibitor, tetrahydroaminoacridine (THA), on cognitive performance following experimental TBI. Rats were either injured at a moderate level of central fluid percussion TBI (2.1+/-0.1 atm) or were surgically prepared but not delivered a fluid pulse (sham injury). Beginning 24 h after TBI or sham injury, rats were injected (IP) daily for 15 days with an equal volume (1.0 ml/kg) of either 0.0, 1.0, 3.0, or 9.0 mg/kg THA (TBI: n = 8, 8, 10, and 7, respectively, and Sham: n = 5, 7, 8, 7, respectively). Cognitive performance was assessed on Days 11-15 after injury in a Morris water maze (MWM). Analysis of maze latencies over days indicated that chronic administration of THA produced a dose-related impairment in MWM performance in both the injured and sham groups, with the 9.0 mg/kg dose producing the largest deficit. The 1.0 and 3.0 mg/kg doses of THA impaired MWM performance without affecting swimming speeds. Thus, the results of this investigation do not support the use of THA as a cholinomimetic therapeutic for the treatment of cognitive deficits following TBI.

Animals↗

PubMed1996

Effects of muscarinic receptor antagonism on the phosphatidylinositol bisphosphate signal transduction pathway after experimental brain injury.

Hippocampal levels of fatty acids extracted from phosphatidylinositol 4,5-bisphosphate (PIP2), free fatty acids (FFA), and lactate were measured after central fluid percussion traumatic brain injury (TBI) in rats. At 5 min after injury, there was a decrease in fatty acids extracted from PIP2 suggesting a decrease in PIP2. At the same time point, total FFA increased in saline-treated TBI rats. Levels of arachidonic acid were significantly decreased in PIP2, while at the same time arachidonic and stearic acids increased in FFA in saline-treated TBI rats. No significant alterations in PIP2-derived fatty acids or FFA were observed at 20 min after TBI. Hippocampal concentrations of lactate were significantly elevated at 5 and 20 min after injury in saline-treated rats. In general, these alterations were blunted by preinjury administration of the muscarinic antagonist, scopolamine. These results suggest that the PIP2 signal transduction pathway is activated in the hippocampus at the onset of central fluid percussion TBI and that the enhanced phospholipase C-catalyzed phosphodiestric breakdown of PIP2 is a major mechanism of liberation of FFA in these sites immediately after such injury. The blunting of PIP2 and FFA alterations in animals treated with scopolamine suggests that activation of muscarinic receptors significantly contributes to the phospholipase C (PLC) signal transduction pathophysiology in TBI. The attenuation of lactate accumulation in scopolamine-treated rats suggests that TBI-induced muscarinic receptor activation also contributes to increased glycolytic metabolism and/or ionic imbalances.

Animals↗

PubMed1996

Brain injury-induced enhanced limbic epileptogenesis: anatomical and physiological parallels to an animal model of temporal lobe epilepsy.

Traumatic brain injury (TBI) is a leading cause of symptomatic epilepsy in young adults. This study examined physiological and anatomical epileptogenic consequences of a prior incident of TBI in rats. Rats were subjected to a fluid percussion brain injury one week prior to experimentation, and in vitro electrophysiological recording studies were conducted using combined hippocampal-entorhinal cortical slices (HEC slices). Results were compared to sham operated controls and rats in which a condition of chronic temporal lobe epilepsy was induced by a 2 h bout of pilocarpine-induced status epilepticus 2 months prior to recording (PILO). In field potential recording, PILO HEC slices evidenced a greater degree of disinhibition in Ca1 than did TBI or control slices. TBI slices showed greater disinhibition in the dentate gyrus than did PILO or control rats. In in vitro kindling experiments, 86% of TBI HEC slices generated self-sustaining epileptic activity within 9 stimulus trains. This type of activity was never triggered in control slices. HEC slices prepared from PILO animals generated self-sustaining epileptic activity with fewer stimulus trains than did TBI slices. In anatomical studies, both TBI and PILO hippocampi evidenced significant loss of neurons within the hilar region. TBI induces a series of changes within the limbic system of rats, which are qualitatively similar in many aspects but quantitatively less severe than changes seen in rats with chronic temporal lobe epilepsy. These physiological and anatomical TBI-associated alterations in the limbic system may contribute to the development of epilepsy following head trauma.

Adult↗

PubMed1996

Working memory deficits following traumatic brain injury in the rat.

This study was designed to examine working memory following fluid-percussion traumatic brain injury (TBI) using the Morris water maze (MWM). Rats were injured (n = 9) at a moderate level of central fluid percussion injury (2.1 atm) or were prepared for injury but did not receive a fluid pulse (sham injury) (n = 10). On days 11-15 postinjury, working memory was assessed using the MWM. Each animal received 8 pairs of trials per day. For each pair of trials, animals were randomly assigned to one of four possible starting points and one of four possible escape platform positions. On the first trial of each pair, rats were placed in the maze facing the wall and were given 120 sec to locate the hidden escape platform. After remaining on the goal platform for 10 sec, they were placed back into the maze for the second trial of the pair. The platform position and the start position remained unchanged on this trial. After the second trial, the animal was given a 4 min intertrial rest. Between pairs of trials, both the start position and the goal location were changed. Analyses of the latency to reach the goal platform indicated that sham-injured animals performed significantly better on the second trial than on the first trial of each pair. However, injured animals did not significantly differ between first and second trial goal latencies on any day. These results indicate that injured animals have a profound and enduring deficit in spatial working memory function on days 11-15 after TBI.

Animals↗

PubMed1996

Exposure to environmental complexity promotes recovery of cognitive function after traumatic brain injury.

This study was designed to determine whether exposure to a complex environment after traumatic brain injury (TBI) would promote the recovery of cognitive function. Rats were injured at a moderate level of fluid percussion injury (2.1 atm) or were prepared for injury but were not injured (sham injury). Immediately after the injury or sham injury, the injured/complex (n = 8) and the sham/complex (n = 7) groups were placed into a complex environment. The complex environment was a 89 x 89-cm enclosure with different types of bedding and objects that provided motor, olfactory, tactile, and visual stimulation. The injured/standard (n = 8) and the sham/standard (n = 8) groups were returned to the animal vivarium where they were housed individually in standard wire mesh cages (24 x 20 x 18 cm). On days 11-15 (postinjury), performance in the Morris water maze was assessed. Analysis of the latency to reach the goal platform indicated that injured animals recuperating in the complex environment performed significantly better than injured animals recovering in the standard environment (p < 0.01). In fact, injured animals in the complex environment performed as well as both sham-injured groups. The improved performance of injured rats recovering in the enriched environment occurred in the absence of environmentally induced alterations in brain weight. These results indicate that exposure to environmental complexity enhances recovery of cognitive function after TBI.

Animals↗

PubMed1996

Voltage-dependent Na+/K+ ion channel blockade fails to ameliorate behavioral deficits after traumatic brain injury in the rat.

Traumatic brain injury (TBI) induces massive, transient ion flux, after impact. This may be via agonist gated channels, such as the muscarinic, cholinergic or NMDA receptor, or via voltage-dependent channels. Pharmacological blockade of the former, is neuroprotective in most TBI models, but the role of voltage-dependent Na+/K+ channels has not been tested. We have therefore tested the hypothesis that intraventricular tetrodotoxin (TTX) (20 microliters, 5 mM) induced blockade of post-TBI ion flux will prevent cytotoxic cell swelling, Na+ and K+ flux, and behavioral deficit. Microdialysis demonstrated blockade of [K+]d flux in the TTX group compared to controls. Behavioral evaluation of motor (days 1-5) and memory function (days 11-15) after TBI revealed no beneficial effect in the TTX group compared to controls. Thus, although evidence of reduced ionic flux was demonstrated in the TTX group, memory and behavior were unaffected, suggesting that agonist-operated channel-mediated ion flux is more important after TBI.

Animals↗

PubMed1995

Metabotropic glutamate antagonist, MCPG, treatment of traumatic brain injury in rats.

The metabotropic glutamate receptor (mGluR) antagonist, alpha-methyl-4-carboxyphenylglycine (MCPG) was administered into the left lateral ventricle 5 min prior to fluid percussion traumatic brain injury (TBI) in the rat. A single 5.0 microliters ventricular infusion of the active isomer. (+)-MCPG (0.2 mumol), significantly reduced beam walking motor deficits on days 1-5 after injury and learning/memory deficits measured on days 11-15 after injury. Neither a lower dose of (+)-MCPG (0.2 mumol) affected behavioral outcome. (+)-MCPG (0.2 mumol) did not affect systemic hemodynamic responses to injury. These results suggest that TBI induced activation of mGluRs contributes to behavioral morbidity and that blockade of certain mGluR subtypes (mGluR1, mGluR5 and/or mGluR2) may reduce these pathophysiological responses.

Analysis of Variance↗

PubMed1995

The effect of postinjury kindled seizures on cognitive performance of traumatically brain-injured rats.

The purpose of this experiment was to examine the consequences of postinjury seizures on cognitive performance after experimental traumatic brain injury (TBI). Rats either were injured at a moderate (2.1 atm) level of central fluid percussion TBI (n = 16) or were surgically prepared but did not receive a fluid pulse (sham-injured control, n = 16). Beginning 24 h after TBI, injured animals were injected (ip) once daily (Days 1-24 postinjury) with either saline (n = 8) or 25 mg/kg pentylenetetrazol (PTZ) (n = 8). Sham-injured rats were injected with an equal volume of saline (n = 8) or PTZ (n = 8). In both injured and sham-injured animals, daily injections of PTZ resulted in an increase in the severity of behavioral seizures over days. On Days 25-29 after injury or sham injury, all animals were tested in the Morris water maze (MWM). Analysis of maze performance indicated that in sham-injured animals PTZ-produced seizures had a detrimental effect on performance. In injured animals, however, PTZ-treated animals exhibited significantly faster acquisition and better terminal performance in the MWM than did untreated injured animals. These results show that posttraumatic kindled seizures do not exacerbate behavioral deficits after TBI and may, in fact, improve recovery following injury. The findings of this experiment are consistent with the hypothesis that post-TBI neuronal depression may contribute to behavioral morbidity following injury.

Animals↗

PubMed1995

Long-term potentiation deficits and excitability changes following traumatic brain injury.

The effects of traumatic brain injury (TBI) on hippocampal long-term potentiation (LTP) and cellular excitability were assessed at postinjury days 2, 7, and 15. TBI was induced using a well-characterized central fluid-percussion model. LTP of the Schaffer collateral/commissural system was assessed in vivo in urethane-anesthetized rats. Significant LTP of the population excitatory postsynaptic potential (EPSP) slope was found only in controls, and no recovery to control levels was observed for any postinjury time point. Four measurement parameters reflecting pyramidal cell discharges (population spike) indicated that TBI significantly increased cellular excitability at postinjury day 2: (1) pretetanus baseline recording showed that TBI reduced population spike threshold and latency; (2) tetanic stimulation (400 Hz) increased population spike amplitudes to a greater degree in injured animals than in control animals; (3) tetanus-induced population spike latency shifts were greater in injured cases; and (4) tetanic stimulation elevated EPSP to spike ratios (E-S potentiation) to a greater degree in injured animals. These parameters returned to control levels, as measured on postinjury days 7 and 15. These results suggest that TBI-induced excitability changes persist at least through 2 days postinjury and involve a differential impairment of mechanisms subserving LTP of synaptic efficacy and mechanisms related to action potential generation.

Action Potentials↗

PubMed1995

Differential modulation of carbachol and trans-ACPD-stimulated phosphoinositide turnover following traumatic brain injury.

In the fluid percussion model of traumatic brain injury (TBI), we examined muscarinic and metabotropic glutamate receptor-stimulated polyphosphoinositide (PPI) turnover in rat hippocampus. Moderate injury was obtained by displacement and deformation of the brain within the closed cranial cavity using a fluid percussion device. Carbachol and (+/-)-1-Aminocyclopentane-trans-1,3-dicarboxylic acid (trans-ACPD)-stimulated PPI hydrolysis was assayed in hippocampus from injured and sham-injured controls at both 1 hour and 15 days following injury. At 1 hour after TBI, the response to carbachol was enhanced in injured rats by up to 200% but the response to trans-ACPD was diminished by as much as 28%. By contrast, at 15 days after TBI, the response to carbachol was enhanced by 25% and the response to trans-ACPD was enhanced by 73%. The ionotropic glutamate agonists N-methyl-D-aspartate (NMDA), and alpha-amino-3 hydroxy-5-methyl-4-isoxazolepropionate (AMPA), did not increase PPI hydrolysis in either sham or injured rats and injury did not alter basal hydrolysis. Thus, hippocampal muscarinic and metabotropic receptors linked to phospholipase C are differentially altered by TBI.

Animals↗

PubMed1995

Effects of mu opioid agonist and antagonist on neurological outcome following traumatic brain injury in the rat.

We examined the effects of an exogenous mu opioid agonist and antagonist on systemic physiology and neurological outcome following TBI in the rat. Experiment I: [D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin (DAMGO) (0.1 nMol or 0.3 nMol in 5 microliters) (n = 10) or artificial CSF (n = 10) was administered 5 min prior to fluid-percussion brain injury (2.1 atmospheres). Motor performance was assessed on days 1-5 after TBI. The mu receptor agonist, DAMGO significantly reduced both beam-walking latency and body weight loss after injury (p < 0.05). DAMGO-treated rats (n = 5) did not differ from CSF-treated rats (n = 5) on either systemic arterial blood pressure or heart rate responses to injury. Experiment II: Beta-funaltrexamine (beta-FNA) (20.0 nMol in 5.0 microliters) (n = 10) or artificial CSF (n = 10) was administered (icv) to rats 5 min prior to fluid-percussion brain injury (1.8 atmospheres). Motor performance was assessed on days 1-5 after TBI. The mu receptor antagonist, beta-FNA, significantly increased beam-walking latency after injury (p < 0.05). beta-FNA-treated rats (n = 5) did not differ from CSF-treated rats (n = 5) on either systemic arterial blood pressure or heart rate responses to injury. Experiment III: Neither beta-FNA nor DAMGO affected motor performance in uninjured rats. These results suggest that activation of mu opioid receptors by exogenous agonists may provide protection against deficits in motor performance produced by fluid percussion brain injury.

Animals↗

PubMed1995

Differential consequences of lateral and central fluid percussion brain injury on receptor coupling in rat hippocampus.

We have identified alterations in the responses of muscarinic and metabotropic receptors in rat hippocampus that persist for at least 15 days after central fluid percussion injury. This study compares the effect of lateral fluid percussion and central fluid percussion on these responses. Moderate injury was obtained by displacement and deformation of the brain within the closed cranial cavity using a fluid percussion device positioned either centrally or laterally. Carbachol and (+/-)-1-aminocyclopentane-trans-1,3-dicarboxylic acid (trans-ACPD)-stimulated polyphosphoinositide (PPI) hydrolysis was assayed in hippocampus from injured and sham-injured controls at 15 days following injury. At 15 days after central fluid percussion traumatic brain injury (TBI), the response to carbachol was enhanced by 30% and the response to trans-ACPD was enhanced by 75% compared to sham-injured animals. At 15 days after lateral fluid percussion TBI the response to trans-ACPD was enhanced by 40% both ipsilateral and contralateral to the side of injury. In contrast, the response to carbachol was enhanced by 29% contralateral to the side of injury but was diminished by 12% ipsilateral to the side of injury. Cresyl violet staining shows no hippocampal cell death after central fluid percussion injury or on the side contralateral to lateral fluid percussion injury but on the ipsilateral side cell death was identified in hippocampal area CA3. Thus, abnormal hippocampal cell signaling through the phosphoinositide pathway occurs in the absence of cell death and may contribute to cognitive impairment.

Animals↗

PubMed1995

Impaired gustatory neophobia following traumatic brain injury in rats.

To investigate the function of the amygdala following traumatic brain injury (TBI), rats were tested on a gustatory neophobia task that is sensitive to amygdala and hippocampal damage. Rats were either injured at a moderate level of fluid percussion injury (2.1 atm) or surgically prepared but not injured (sham-injury). Seven days after injury (n = 8) or sham injury (n = 9), rats were habituated to the testing chamber without food items present for 30 min. All rats were then food deprived. Twenty-four hours later, rats were placed in the testing chamber for 30 min and allowed to eat freely from four dishes of different foods: rat chow, raisins, potatoes, and cookies. Results showed that injured and sham-injured rats did not differ in their ability to find hidden food, suggesting that TBI does not produce an enduring impairment of olfaction. There was also no difference in the total amount of food eaten between injured and sham groups (p > 0.05). The percentage of each type of food consumed did differ between the two groups with sham controls consuming more familiar food (rat chow) compared to the unfamiliar foods (p < 0.01). The injured animals distributed their eating evenly among the four foods with no particular preference for any one food (p < 0.05). This pattern of eating behavior in injured animals is similar to animals that have lesions to both the hippocampus and amygdala (Sutherland and McDonald, 1990). Therefore, the results of this experiment suggest that, in addition to the hippocampus, the amygdala may also contribute to the behavioral changes observed following TBI.

Amygdala↗