Retention Deficits Research Articles

Right inferior frontal gyrus structure and function predict smoking (re)lapse in real-world and laboratory contexts

It has been found that interference with neural activity after a consolidated memory is retrieved produces an amnestic state; this has been taken has indicative of destabilization of the memory trace that would have been produced by a process of reconsolidation (allowing for maintenance of the original trace). However, a growing body of evidence shows that this is not a reliable effect, and that it is dependent upon some experimental conditions, such as the age of the memory, memory reactivation procedures, the predictability of the reactivation stimulus, and strength of training. In some instances, where post-retrieval treatments induce a retention deficit (which would be suggestive of interference with reconsolidation), memory is rescued by simple passing of time or by repeated retention tests. We now report that post-training and post-retrieval inhibition of transcription and translation in dorsal striatum, a structure where both of these manipulations have not been studied, produce interference with consolidation and a transitory retention deficit, respectively. These results do not give support to the reconsolidation hypothesis and lead to the conclusion that the post-activation deficiencies are due to interference with retrieval of information.

Effects of practice and delays on learning and retention of skilled tool use in Parkinson's disease

Previous research has shown that individuals with Parkinson's disease (PD) show preserved learning of tool-related motor skills, while retention was impaired after a three-week delay, possibly as a result of striatal dysfunction. The goal of the current study was to identify if shorter delays and more extensive practice might reduce retention deficits related to complex tool use in PD. PD participants and healthy age and education-matched controls were trained to use novel tools across four sessions, spaced one-day, one-week, and three-weeks apart. Recall of tool attributes (e.g., function) and skilled motor performance using tools was investigated by examining patterns of learning and forgetting over time. Results showed that tool attribute recall was unimpaired in PD participants relative to controls. For motor skill performance, PD participants were unimpaired in motor skill learning within sessions, but they did not retain these skills across one-week and three-week delays between sessions. This dissociation suggests that the striatum plays a critical role in retention of motor skills needed in skilled tool use performance. Finally, in spite of forgetting, individuals with PD still demonstrated improvement across sessions with additional training, suggesting that people with PD may benefit from extensive practice when learning motor skills.

Ultraschallgesteuerte Nervenblockade des Nervus femoralis und ischiadicus im Vergleich zur Epiduralanästhesie bei orthopädischen Eingriffen am Hund

Comparison of ultrasound-guided femoral and sciatic nerve block versus epidural anaesthesia with bupivacaine and morphine for orthopaedic surgery of the pelvic limb in dogs with respect to analgesic effectiveness, clinical utility and side effects. The study included 22 dogs (American Society of Anesthesiologists, ASA grades I and II) undergoing orthopaedic surgery distal to the mid-femoral bone. The study was designed as a randomized, prospective, blinded clinical trial. All dogs were randomly assigned to receive 0.5mg/kg bupivacaine (0.5%) and 0.1mg/kg morphine sulphate (1%) either as epidural anaesthesia (group EPI) or by ultrasound-guided femoral and sciatic nerve block (group LA). During surgery, the heart rate, respiratory rate, mean arterial pressure (MAP), end-tidal isoflurane concentrations and dose of rescue analgesia (fentanyl boluses of 5µg/kg i.v.) were measured. Pain severity was scored (short form of the Glasgow Composite Measure Pain Scale, GCMPS) before surgery and postoperatively at 2, 4, 6, 12 and 24 hours after extubation. Post-operative rescue analgesia consisted of methadone (0.2mg/kg i.v.), and was applied when the GCMPS >6. For statistical analysis, the Chi-square, Fisher, and Wilcoxon tests and one- and two-way ANOVA were applied. Differences were considered statistically significant at p<0.05. Only the MAP was significantly different between the two treatment groups. Intra- and postoperative MAP of group LA (111.2±11.2mmHg and 119.3± 18.2mmHg, respectively) was higher than in group EPI (86.6± 8.7mmHg and 95.2±13.1mmHg, respectively). None of the dogs developed urinary retention or ambulatory deficits when completely recovered from anaesthesia. No other side effects were noted. In conclusion, femoral and sciatic nerve blocks and epidural anaesthesia ensure comparable analgesic effects in canine patients undergoing orthopaedic surgery of the pelvic limb. The lower mean arterial blood pressure of group EPI was not of clinical relevance.

Inhibition of transcription and translation in the striatum after memory reactivation: Lack of evidence of reconsolidation

It has been found that interference with neural activity after a consolidated memory is retrieved produces an amnestic state; this has been taken has indicative of destabilization of the memory trace that would have been produced by a process of reconsolidation (allowing for maintenance of the original trace). However, a growing body of evidence shows that this is not a reliable effect, and that it is dependent upon some experimental conditions, such as the age of the memory, memory reactivation procedures, the predictability of the reactivation stimulus, and strength of training. In some instances, where post-retrieval treatments induce a retention deficit (which would be suggestive of interference with reconsolidation), memory is rescued by simple passing of time or by repeated retention tests. We now report that post-training and post-retrieval inhibition of transcription and translation in dorsal striatum, a structure where both of these manipulations have not been studied, produce interference with consolidation and a transitory retention deficit, respectively. These results do not give support to the reconsolidation hypothesis and lead to the conclusion that the post-activation deficiencies are due to interference with retrieval of information.

Mechanisms of Memory Dysfunction during High Altitude Hypoxia Training in Military Aircrew.

Cognitive dysfunction from high altitude exposure is a major cause of civilian and military air disasters. Pilot training improves recognition of the early symptoms of altitude exposure so that countermeasures may be taken before loss of consciousness. Little is known regarding the nature of cognitive impairments manifesting within this critical window when life-saving measures may still be taken. Prior studies evaluating cognition during high altitude simulation have predominantly focused on measures of reaction time and other basic attention or motor processes. Memory encoding, retention, and retrieval represent critical cognitive functions that may be vulnerable to acute hypoxic/ischemic events and could play a major role in survival of air emergencies, yet these processes have not been studied in the context of high altitude simulation training. In a series of experiments, military aircrew underwent neuropsychological testing before, during, and after brief (15 min) exposure to high altitude simulation (20,000 ft) in a pressure-controlled chamber. Acute exposure to high altitude simulation caused rapid impairment in learning and memory with relative preservation of basic visual and auditory attention. Memory dysfunction was predominantly characterized by deficiencies in memory encoding, as memory for information learned during high altitude exposure did not improve after washout at sea level. Retrieval and retention of memories learned shortly before altitude exposure were also impaired, suggesting further impairment in memory retention. Deficits in memory encoding and retention are rapidly induced upon exposure to high altitude, an effect that could impact life-saving situational awareness and response. (JINS, 2017, 23, 1-10).

Neural circuits via which single prolonged stress exposure leads to fear extinction retention deficits.

Single prolonged stress (SPS) has been used to examine mechanisms via which stress exposure leads to post-traumatic stress disorder symptoms. SPS induces fear extinction retention deficits, but neural circuits critical for mediating these deficits are unknown. To address this gap, we examined the effect of SPS on neural activity in brain regions critical for extinction retention (i.e., fear extinction circuit). These were the ventral hippocampus (vHipp), dorsal hippocampus (dHipp), basolateral amygdala (BLA), prelimbic cortex (PL), and infralimbic cortex (IL). SPS or control rats were fear conditioned then subjected to extinction training and testing. Subsets of rats were euthanized after extinction training, extinction testing, or immediate removal from the housing colony (baseline condition) to assay c-Fos levels (measure of neural activity) in respective brain region. SPS induced extinction retention deficits. During extinction training SPS disrupted enhanced IL neural activity and inhibited BLA neural activity. SPS also disrupted inhibited BLA and vHipp neural activity during extinction testing. Statistical analyses suggested that SPS disrupted functional connectivity within the dHipp during extinction training and increased functional connectivity between the BLA and vHipp during extinction testing. Our findings suggest that SPS induces extinction retention deficits by disrupting both excitatory and inhibitory changes in neural activity within the fear extinction circuit and inducing changes in functional connectivity within the Hipp and BLA.

Effect of creatine supplementation on cognitive performance and apoptosis in a rat model of amyloid-beta-induced Alzheimer's disease.

Neuroprotective effect of creatine (Cr) against β-amyloid (Aβ) is reported in an in vitro study. This study investigated the effect of Cr supplementation on β-amyloid toxicity in vivo. Thirty two, male Wistar rats were divided into 4 groups. During ten weeks of study, control group went through no surgical or dietary intervention. At the 4th week of study Sham group had a hippocampal normal saline injection, while Aβ and AβCr groups had an β-amyloid injection in the hippocampus. AβCr group were fed by Cr diet during the study. After 10 weeks, Morris water maze (MWM) test was administered to measure learning ability and memory retrieval. Animals were sacrificed for TUNEL anti apoptotic assay and staining of amyloid plaques by Thioflavin-T. There was a significant retention deficit among AβCr and Aβ group while the escape latency and the distance traveled to the platform were significantly higher in AβCr group compared to Aβ group. AβCr group had same percent of TUNEL positive neurons compared to Aβ group. Cr supplementation before and after β-amyloid injection into the CA1 area of hippocampus deteriorates the learning and memory impairment of rats and it does not protect neuronal apoptosis caused by β-amyloid.

Transcriptional Coactivator and Chromatin Protein PC4 Is Involved in Hippocampal Neurogenesis and Spatial Memory Extinction

Although the elaborate combination of histone and non-histone protein complexes defines chromatin organization and hence regulates numerous nuclear processes, the role of chromatin organizing proteins remains unexplored at the organismal level. The highly abundant, multifunctional, chromatin-associated protein and transcriptional coactivator positive coactivator 4 (PC4/Sub1) is absolutely critical for life, because its absence leads to embryonic lethality. Here, we report results obtained with conditional PC4 knock-out (PC4(f/f) Nestin-Cre) mice where PC4 is knocked out specifically in the brain. Compared with the control (PC4(+/+) Nestin-Cre) mice, PC4(f/f) Nestin-Cre mice are smaller with decreased nocturnal activity but are fertile and show no motor dysfunction. Neurons in different areas of the brains of these mice show sensitivity to hypoxia/anoxia, and decreased adult neurogenesis was observed in the dentate gyrus. Interestingly, PC4(f/f) Nestin-Cre mice exhibit a severe deficit in spatial memory extinction, whereas acquisition and long term retention were unaffected. Gene expression analysis of the dorsal hippocampus of PC4(f/f) Nestin-Cre mice revealed dysregulated expression of several neural function-associated genes, and PC4 was consistently found to localize on the promoters of these genes, indicating that PC4 regulates their expression. These observations indicate that non-histone chromatin-associated proteins like PC4 play a significant role in neuronal plasticity.

Neuropathologic Associations of Learning and Memory in Primary Progressive Aphasia.

The dementia syndrome of primary progressive aphasia (PPA) can be caused by 1 of several neuropathologic entities, including forms of frontotemporal lobar degeneration (FTLD) or Alzheimer disease (AD). Although episodic memory is initially spared in this syndrome, the subtle learning and memory features of PPA and their neuropathologic associations have not been characterized. To detect subtle memory differences on the basis of autopsy-confirmed neuropathologic diagnoses in PPA. Retrospective analysis was conducted at the Northwestern Cognitive Neurology and Alzheimer's Disease Center in August 2015 using clinical and postmortem autopsy data that had been collected between August 1983 and June 2012. Thirteen patients who had the primary clinical diagnosis of PPA and an autopsy-confirmed diagnosis of either AD (PPA-AD) or a tau variant of FTLD (PPA-FTLD) and 6 patients who had the clinical diagnosis of amnestic dementia and autopsy-confirmed AD (AMN-AD) were included. Scores on the effortless learning, delayed retrieval, and retention conditions of the Three Words Three Shapes test, a specialized measure of verbal and nonverbal episodic memory. The PPA-FTLD (n = 6), PPA-AD (n = 7), and AMN-AD (n = 6) groups did not differ by demographic composition (all P > .05). The sample mean (SD) age was 64.1 (10.3) years at symptom onset and 67.9 (9.9) years at Three Words Three Shapes test administration. The PPA-FTLD group had normal (ie, near-ceiling) scores on all verbal and nonverbal test conditions. Both the PPA-AD and AMN-AD groups had deficits in verbal effortless learning (mean [SD] number of errors, 9.9 [4.6] and 14.2 [2.0], respectively) and verbal delayed retrieval (mean [SD] number of errors, 6.1 [5.9] and 12.0 [4.4], respectively). The AMN-AD group had additional deficits in nonverbal effortless learning (mean [SD] number of errors, 10.3 [4.0]) and verbal retention (mean [SD] number of errors, 8.33 [5.2]), which were not observed in the PPA-FTLD or PPA-AD groups (all P < .005). This study identified neuropathologic associations of learning and memory in autopsy-confirmed cases of PPA. Among patients with clinical PPA syndrome, AD neuropathology appeared to interfere with effortless learning and delayed retrieval of verbal information, whereas FTLD-tau pathology did not. The results provide directions for future research on the interactions between limbic and language networks.

The effect of CA1 α2 adrenergic receptors on memory retention deficit induced by total sleep deprivation and the reversal of circadian rhythm in a rat model

The α2 adrenergic receptors which abundantly express in the CA1 region of the hippocampus play an important role in the regulation of sleep and memory retention processes. Based on the available evidence, the aim of our study was to investigate consequences of the activation and deactivation of CA1 α2 adrenergic receptors (by clonidine and yohimbine, respectively) on the impairment of memory retention induced by total sleep deprivation (TSD) and the reversal of circadian rhythm (RCR) in a rat model. To this end, the water box apparatus and passive avoidance task were in turn used to induce sleep deprivation and assess memory retention. Our findings suggested that TSD (for 24 and 36, but not 12h) and RCR (12h/day for 3 consecutive days) impair memory function. The post-training intra-CA1 administration of yohimbine (α2 adrenergic receptor antagonist) on its own, at the dose of 0.1μg/rat, decreased the step-through latency and locomotor activity in the TSD- sham treated but not undisturbed sleep rats. Unlike yohimbine, clonidine (α2 adrenergic receptor agonist), in all applied doses (0.001, 0.01 and 0.1μg/rat), failed to induce such an effect. While the subthreshold dose of yohimbine (0.001μg/rat) abrogated the impairment of memory retention induced by the 24-h TSD, it could potentiate the impairment of memory retention induced by 36-h TSD, suggesting the modulatory effect of yohimbine. Moreover, the subthreshold dose of clonidine (0.1μg/rat) restored the memory retention deficit in TSD rats (24 and 36h). On the other hand, the subthreshold dose of clonidine (0.1μg/rat), but not yohimbine (0.001μg/rat) restored the memory retention deficit in RCR rats. Such interventions however did not alter the locomotor activity. The above observations proposed that CA1 α2 adrenergic receptors play a potential role in memory retention deficits induced by TSD and RCR.

Deletion of novel protein TMEM35 alters stress-related functions and impairs long-term memory in mice.

The mounting of appropriate emotional and neuroendocrine responses to environmental stressors critically depends on the hypothalamic-pituitary-adrenal (HPA) axis and associated limbic circuitry. Although its function is currently unknown, the highly evolutionarily conserved transmembrane protein 35 (TMEM35) is prominently expressed in HPA circuitry and limbic areas, including the hippocampus and amygdala. To investigate the possible involvement of this protein in neuroendocrine function, we generated tmem35 knockout (KO) mice to characterize the endocrine, behavioral, electrophysiological, and proteomic alterations caused by deletion of the tmem35 gene. While capable of mounting a normal corticosterone response to restraint stress, KO mice showed elevated basal corticosterone accompanied by increased anxiety-like behavior. The KO mice also displayed impairment of hippocampus-dependent fear and spatial memories. Given the intact memory acquisition but a deficit in memory retention in the KO mice, TMEM35 is likely required for long-term memory consolidation. This conclusion is further supported by a loss of long-term potentiation in the Schaffer collateral-CA1 pathway in the KO mice. To identify putative molecular pathways underlying alterations in plasticity, proteomic analysis of synaptosomal proteins revealed lower levels of postsynaptic molecules important for synaptic plasticity in the KO hippocampus, including PSD95 and N-methyl-d-aspartate receptors. Pathway analysis (Ingenuity Pathway Analysis) of differentially expressed synaptic proteins in tmem35 KO hippocampus implicated molecular networks associated with specific cellular and behavioral functions, including decreased long-term potentiation, and increased startle reactivity and locomotion. Collectively, these data suggest that TMEM35 is a novel factor required for normal activity of the HPA axis and limbic circuitry.

Evolution of Wechsler’s Memory Scales: Content and structural analysis

ABSTRACTThe Wechsler Memory Scale-1 was introduced to the professional community 70 years ago and has been the most widely used standardized memory battery for over 50 years. Since its introduction, the test has been revised three times, with the last revision occurring in 2009. Few clinicians are aware that Wechsler developed a prior memory battery in 1917, which was used to assess retention deficits in persons with Korsakoff psychosis. The purpose of the present article is to describe the development of Wechsler’s memory scales from 1917 through 2009. Suggestions for the next revision are offered.

Deletion of the γ-secretase subunits Aph1B/C impairs memory and worsens the deficits of knock-in mice modeling the Alzheimer-like familial Danish dementia.

Mutations in BRI2/ITM2b genes cause Familial British and Danish Dementias (FBD and FDD), which are pathogenically similar to Familial Alzheimer Disease (FAD). BRI2 inhibits processing of Amyloid precursor protein (APP), a protein involved in FAD pathogenesis. Accumulation of a carboxyl-terminal APP metabolite –β-CTF- causes memory deficits in a knock-in mouse model of FDD, called FDDKI. We have investigated further the pathogenic function of β-CTF studying the effect of Aph1B/C deletion on FDDKI mice. This strategy is based on the evidence that deletion of Aph1B/C proteins, which are components of the γ-secretase that cleaves β-CTF, results in stabilization of β-CTF and a reduction of Aβ. We found that both the FDD mutation and the Aph1B/C deficiency mildly interfered with spatial long term memory, spatial working/short-term memory and long-term contextual fear memory. In addition, the Aph1BC deficiency induced deficits in long-term cued fear memory. Moreover, the two mutations have additive adverse effects as they compromise the accuracy of spatial long-term memory and induce spatial memory retention deficits in young mice. Overall, the data are consistent with a role for β-CTF in the genesis of memory deficits.

Forgetting in temporal lobe epilepsy: When does it become accelerated?

The notion of ‘accelerated long-term forgetting’ has often been attributed to disrupted ‘late’ memory consolidation. Nevertheless, methodological issues in the literature have left this theory unproven, leading some to suggest such findings may be reflective of subtle acquisition or early retention deficits. This study attempts to address such issues, and also to explore which pathophysiological variables are associated with forgetting rates. Eighteen participants with temporal lobe epilepsy (TLE) and eighteen matched controls completed background neuropsychological measurement of immediate and short-delay memory that showed comparable performance, both on verbal and visual tests. Using two novel experimental tasks to measure long-term forgetting, cued recall of verbal and visuospatial material was tested 30 sec, 10 min, one day, and one week after learning. Forgetting of verbal material was found to be progressively faster during the course of a week in the TLE group. For visuospatial memory, participants in the TLE group exhibited faster early forgetting in the first 10 min after learning, as indicated by planned comparisons, with comparable forgetting rates thereafter. Our findings provide evidence for two patterns of disruption to ‘early’ memory consolidation in this population, occurring either at the initial delay only or continuing progressively through time. Differences in how soon after learning accelerated forgetting was detectable were related to factors associated with greater severity of epilepsy, such as presence of medial temporal lobe sclerosis (MTS) on magnetic resonance imaging (MRI) and use of multiple anti-epileptic agents.

Additive effect of BLA GABAA receptor mechanism and (+)-MK-801 on memory retention deficit, an isobologram analysis

There is a near correlation between N-methyl-d-aspartate (NMDA) and γ-aminobutyric acid (GABA) receptors in the modulation of learning and memory in the basolateral amygdala (BLA). In this study, we investigated the involvement of GABAA receptors in the BLA in amnesia induced by (+)-MK-801, a noncompetitive antagonist of NMDA receptors, in male Wistar rats. After guide cannulae were bilaterally placed in the BLA, animals were trained in a step-through type passive avoidance task and then tested 24h after training to measure memory retrieval and locomotor activity. Post-training intra-BLA microinjection of (+)-MK-801 (0.5μg/rat) and GABAA receptor agonists (muscimol at doses 0.05 and 0.1μg/rat) or antagonist (bicuculline at doses 0.05 and 0.1μg/rat) decreased step-through latency during retrieval but did not alter locomotor activity. Results also showed that a subthreshold dose of muscimol (0.025μg/rat) potentiated impairment induced by (+)-MK-801, whereas bicuculline (0.025μg/rat) restored it. Furthermore, the highest dose of muscimol (0.5μg/rat) increased locomotor activity induced by (+)-MK-801. Isobologram analysis showed that there was an additive but not synergistic effect between muscimol and (+)-MK-801 on memory retention deficits in the BLA. In conclusion, muscimol and bicuculline decreased retention of memory formation in the BLA, and GABAA receptors in the BLA may be involved in the additive effect on (+)-MK-801-induced memory retention deficits.

Pain Induced during Both the Acquisition and Retention Phases of Locomotor Adaptation Does Not Interfere with Improvements in Motor Performance.

Cutaneous pain experienced during locomotor training was previously reported to interfere with retention assessed in pain-free conditions. To determine whether this interference reflects consolidation deficits or a difficulty to transfer motor skills acquired in the presence of pain to a pain-free context, this study evaluated the effect of pain induced during both the acquisition and retention phases of locomotor learning. Healthy participants performed a locomotor adaptation task (robotized orthosis perturbing ankle movements during swing) on two consecutive days. Capsaicin cream was applied around participants' ankle on both days for the Pain group, while the Control group was always pain-free. Changes in movement errors caused by the perturbation were measured to assess global motor performance; temporal distribution of errors and electromyographic activity were used to characterize motor strategies. Pain did not interfere with global performance during the acquisition or the retention phases but was associated with a shift in movement error center of gravity to later in the swing phase, suggesting a reduction in anticipatory strategy. Therefore, previously reported retention deficits could be explained by contextual changes between acquisition and retention tests. This difficulty in transferring skills from one context to another could be due to pain-related changes in motor strategy.

Jumping Stand Apparatus Reveals Rapidly Specific Age-Related Cognitive Impairments in Mouse Lemur Primates.

The mouse lemur (Microcebus murinus) is a promising primate model for investigating normal and pathological cerebral aging. The locomotor behavior of this arboreal primate is characterized by jumps to and from trunks and branches. Many reports indicate insufficient adaptation of the mouse lemur to experimental devices used to evaluate its cognition, which is an impediment to the efficient use of this animal in research. In order to develop cognitive testing methods appropriate to the behavioral and biological traits of this species, we adapted the Lashley jumping stand apparatus, initially designed for rats, to the mouse lemur. We used this jumping stand apparatus to compare performances of young (n = 12) and aged (n = 8) adults in acquisition and long-term retention of visual discriminations. All mouse lemurs completed the tasks and only 25 trials, on average, were needed to master the first discrimination problem with no age-related differences. A month later, all mouse lemurs made progress for acquiring the second discrimination problem but only the young group reached immediately the criterion in the retention test of the first discrimination problem. This study shows that the jumping stand apparatus allows rapid and efficient evaluation of cognition in mouse lemurs and demonstrates that about half of the old mouse lemurs display a specific deficit in long-term retention but not in acquisition of visual discrimination.

Curricular response to increase recall and transfer of anatomical knowledge into the obstetrics/gynecology clerkship.

Deficits in retention of anatomy knowledge from the preclinical years to clinical application on the wards have been well documented in the medical education literature. We developed and evaluated a web and laboratory-based curriculum to address deficits in anatomy knowledge retention and to increase anatomy knowledge recall through repetition and application of clinical concepts during the obstetrics and gynecology (Ob/Gyn) core clinical clerkship. Using principles of adult learning and instructional design, a curriculum was designed consisting of (1) interactive, case-based e-modules reviewing clinically relevant anatomical topics and (2) a hands-on laboratory session reinforcing the content of the e-modules, with the practice of clinical techniques using anatomical cadaveric dissections. The curriculum's effectiveness was evaluated by using multiple choice testing and comparing baseline and final test scores. For questions testing content directly covered in this curriculum, mean final scores increased by 14.3% (P < 0.001). In contrast, for questions not directly addressed in this curriculum, mean final scores did not increase significantly, only by 6.0% (P = 0.31). Questions related to the uterus showed the greatest gains in final scores (30.3% improvement, P = 0.002). A curriculum with web-based preparatory material and a hands-on gross anatomy laboratory session effectively addresses deficits in anatomy retention and improves anatomical knowledge recall for medical students on a clinical clerkship. In the future, the authors plan to conduct a multicenter study to further evaluate the ability of this curriculum to improve clinically relevant anatomical knowledge. Anat Sci Educ 9: 337-343. © 2015 American Association of Anatomists.

Improving Anatomical Knowledge Through Nested Interactive Modules on the Obstetrics and Gynecology Clinical Clerkship

BACKGROUND: Deficits in retention of anatomy knowledge from the preclinical years to clinical application on the wards have been well-documented in medical education literature. OBJECTIVE: This study aims to determine if interactive clinically-oriented basic anatomy modules nested longitudinally in the curriculum increase anatomy knowledge in medical students on the obstetrics and gynecology clinical clerkship. METHODS: A 20-question multiple-choice examination was administered to 143 consenting third-year medical students at the beginning and end of each obstetrics and gynecology rotation at a large, urban medical school. Students participated in a 2-hour hands-on skills laboratory with preparatory e-modules linking basic anatomy to clinical application during each rotation. Topics included perineal muscle anatomy (obstetric laceration repair), anterior abdominal wall anatomy (cesarean delivery), vulvovaginal and uterine anatomy (intrauterine device insertion), and pelvic organ, vasculature, and neural anatomy (hysterectomy). Data were analyzed using a univariate analysis of variance with post-hoc t tests. RESULTS: Mean anatomy knowledge scores improved significantly after nesting of interactive modules, increasing from 57% to 69% (P<.001). Knowledge retention was the lowest in the topics of embryology (45%), uterine anatomy (47%), pelvic vasculature (46%), and fallopian tube anatomy (54%). Mean postrotation scores for uterine, vasculature, and fallopian tube anatomy increased significantly to 78% (P<.001), 72% (P<.001) and 71% (P<.001) respectively. CONCLUSIONS: Medical students' baseline anatomical knowledge before entering the obstetrics and gynecology clerkship is poor. Nesting anatomical science into the clinical curriculum through preparatory e-modules and hands-on anatomy laboratory sessions may improve pelvic anatomy knowledge. These data may be used to increase longitudinal integration of the various disciplines across the undergraduate medical curriculum.

Auraptene consolidates memory, reverses scopolamine-disrupted memory in passive avoidance task, and ameliorates retention deficits in mice.

Auraptene (7-geranyloxycoumarin) (AUR), from Citrus species has shown anti-inflammatory, neuroprotective, and acetylcholinesterase (AChE) and beta-secretase inhibitory effects. Scopolamine is a nonselective muscarinic receptor antagonist which causes short-term memory impairments and is used for inducing animal model of Alzheimer's disease (AD). This research aimed to investigate the effect of AUR on scopolamine-induced avoidance memory retention deficits in step-through task in mice. The effect of four-day pre-training injections of AUR (50, 75, and 100 mg/kg, subcutaneous (SC)) and scopolamine (1 mg/kg, IP), and their co-administration on avoidance memory retention in step-through passive avoidance task, was investigated by measuring the latency to enter to the dark chamber. Pre-training administration of AUR caused significant increase in step-through latency in comparison with control group, 48, 96, and 168 hr after training trial. The findings of this study showed that scopolamine (1 mg/kg, IP, for four consecutive days) impaired passive avoidance memory retention compared to saline-treated animals. Step-through passive avoidance task results showed that AUR markedly reversed scopolamine-induced avoidance memory retention impairments, 24 and 168 hr after training trial in step-through task. Results from co-administration of AUR and scopolamine showed that AUR reversed scopolamine-induced passive avoidance memory retention impairments.