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Michael Davis

Publications and source records attributed to Michael Davis.

83 records · Page 5Linked to original sources
PubMed2001

Light-enhanced startle: further pharmacological and behavioral characterization.

RATIONALE: Previous findings indicate that the acoustic startle response is elevated when rats are tested in bright light. The phenomenon is disrupted by the 5HT1A partial agonist and the D2 receptor antagonist buspirone, a compound that also blocks the effect on startle of conditioned fear, and it was suggested that light-enhanced startle reflects an anxious state produced by bright light. It was also suggested that pre-test handling may be necessary for light-enhanced startle. To characterize this phenomenon further, we evaluate here the sensitivity of light-enhanced startle to the anxiolytic compound chlordiazepoxide, to the noradrenergic beta-receptor antagonist propranolol, and to pre-test handling. METHODS: Startle was measured for 20 min in the dark (phase I), followed 5 min later by a second test (phase II) either in the dark or the light. Immediately prior to testing, rats received IP injections of chlordiazepoxide (5, 10, or 20 mg/kg; experiment 1), propranolol (10 or 20 mg/kg; experiment 2) or saline. Using the minimally effective doses from the light-enhanced startle experiments, conditioned fear to a shock-paired cue was also evaluated. In a third experiment, rats were (a) removed from the test cages and briefly handled between phases I and II, (b) were not handled during this interval, or (c) were tested without the interposed delay. RESULTS: Propranolol (10 and 20 mg/kg) and chlordiazepoxide (10 mg/kg) disrupted light-enhanced startle at doses comparable to those required to disrupt fear-potentiated startle to a shock-paired cue. There was no effect of handling. CONCLUSION: These results further characterize the pharmacology of light-enhanced startle, provide additional support for the view that the effects of light on startle reflect an influence of anxiety, and offer additional information concerning the procedural variables that influence this behavior.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Different mechanisms of fear extinction dependent on length of time since fear acquisition.

Fear extinction is defined as a decline in conditioned fear responses (CRs) following nonreinforced exposure to a feared conditioned stimulus (CS). Behavioral evidence indicates that extinction is a form of inhibitory learning: Extinguished fear responses reappear with the passage of time (spontaneous recovery), a shift of context (renewal), and unsignaled presentations of the unconditioned stimulus (reinstatement). However, there also is evidence to suggest that extinction is an "unlearning" process corresponding to depotentiation of potentiated synapses within the amygdala. Because depotentiation is induced more readily at short intervals following LTP induction and is not inducible at all at a sufficient delay, it may be that extinction initiated shortly following fear acquisition preferentially engages depotentiation/"unlearning," whereas extinction initiated at longer delays recruits a different mechanism. We investigated this possibility through a series of behavioral experiments examining the recoverability of conditioned fear following extinction. Consistent with an inhibitory learning mechanism of extinction, rats extinguished 24-72 h following acquisition exhibited moderate to strong reinstatement, renewal, and spontaneous recovery. In contrast, and consistent with an erasure mechanism, rats extinguished 10 min to 1 h after acquisition exhibited little or no reinstatement, renewal, or spontaneous recovery. These data support a model in which different neural mechanisms are recruited depending on the temporal delay of fear extinction.

Animals↗
PubMedDate not supplied

Conditioned fear extinction and reinstatement in a human fear-potentiated startle paradigm.

The purpose of this study was to analyze fear extinction and reinstatement in humans using fear-potentiated startle. Participants were fear conditioned using a simple discrimination procedure with colored lights as the conditioned stimuli (CSs) and an airblast to the throat as the unconditioned stimulus (US). Participants were extinguished 24 h after fear conditioning. Upon presentation of unsignaled USs after extinction, participants displayed significant fear reinstatement. In summary, these procedures produced robust fear-potentiated startle, significant CS+/CS- discrimination, within-session extinction, and significant reinstatement. This is the first demonstration of fear extinction and reinstatement in humans using startle measures.

Conditioning, Classical↗
PubMedDate not supplied

Second-order olfactory-mediated fear-potentiated startle.

Recently, we reported that discrete (4-sec) olfactory cues paired with footshock serve as effective conditioned stimuli (CSs) for potentiating the acoustic startle response in rats using the fear-potentiated startle paradigm. Because odors are such salient cues for the rat, and because of the robust olfactory conditioning observed previously, the current studies investigated second-order fear conditioning using olfactory and visual cues. In Experiments 1 and 2, we used a small number of first-order and second-order training trials on separate days to investigate second-order fear-potentiated startle. Significant potentiated startle was observed in animals receiving Paired/Paired training in both studies, but surprisingly, control animals in the Unpaired/Paired group (Exp. 1) also showed significant potentiated startle to a light S2 at testing. These findings are addressed in the Discussion. Overall, the results of both experiments suggest that olfactory cues serve as efficient S1 and S2 stimuli in second-order fear-potentiated startle paradigms when only a small number of first and second-order training trials are presented.

Animals↗
PubMedDate not supplied

Temporal relationship between gastrointestinal protein loss, gastric ulceration or erosion, and strenuous exercise in racing Alaskan sled dogs.

BACKGROUND: Alterations in the appearance and function of gastrointestinal mucosa are common after strenuous exercise. However, the duration of exercise required to alter the gastrointestinal mucosa has not been reported. HYPOTHESIS: We used 42 sled dogs to test the hypothesis that the magnitude of exercise-induced gastrointestinal mucosal dysfunction is related to exercise duration. ANIMALS: Six dogs served as conditioned controls, and the remaining dogs were randomly chosen for examination after 1-5 consecutive days of running at 100 miles/d. METHODS: Gastroduodenoscopy and measurement of gastric permeability were performed 24 hours after cessation of exercise. Intestinal protein loss (represented by fecal alpha-1 protease inhibitor concentration) was measured within 6 hours of cessation of exercise. Twelve of the 42 dogs were examined again after 5 months of detraining to determine the effect of training on gastrointestinal mucosal function. RESULTS: Exercise increased gastric permeability (P = .04) and endoscopic severity of gastric lesions (P < .0001), but neither variable was significantly affected by distance traveled. Acute exercise had no effect on intestinal protein loss. Untrained dogs had significantly lower fecal alpha-1 protease inhibitor concentrations compared with trained, unexercised dogs. Training had no effect on gastric permeability to sucrose or the endoscopic appearance of the stomach. CONCLUSIONS AND CLINICAL IMPORTANCE: These data suggest that relatively modest exercise is required to increase intestinal protein loss, but more substantial exercise is required to cause alterations in the proximal gastrointestinal tract. However, none of these alterations appear to progress with increasing exercise duration.

Alaska↗