Deciphering the molecular components of the quorum sensing system in the fungus Ophiostoma piceae.

IMPORTANCE: This manuscript presents a comprehensive study on the molecular mechanisms triggered by the quorum sensing (QS) molecule farnesol in the biotechnologically relevant fungus Ophiostoma piceae. We present for the first time, using a multiomics approach, an in-depth analysis of the QS response in a saprotroph fungus, detailing the molecular components involved in the response and their possible mechanisms of action. We think that these results are particularly relevant in the knowledge of the functioning of the QS in eukaryotes, as well as for the exploitation of these mechanisms.

Efficacy of the myofascial approach as a manual therapy technique in patients with clinical anxiety: A randomized controlled clinical trial.

BACKGROUND: To analyze the efficacy of the myofascial approach in patients with clinical anxiety and to study its relationship with associated symptoms. METHODS: Randomized placebo-controlled clinical trial. Thirty-six adult patients with clinical anxiety were randomized to receive the myofascial treatment (n = 18) or placebo (n = 18). The patients and the evaluators were blinded to this assignation. The treatment consisted of four myofascial sessions of 40 min each for four weeks. The placebo intervention consisted of four sessions of simulated myofascial intervention of the same duration and frequency as the treatment. Follow-up was at one, three and six months. The primary outcome was clinical anxiety measured using the STAI (State-Trait Anxiety Inventory). Secondary outcomes were central sensitization, general health, somatization, depression, and pain. RESULTS: There were significant differences in the behavior of the groups over time for clinical anxiety (STAI Trait-Anxiety) (p < 0.001), central sensitization (p = 0.005) and somatization (p = 0.008) in favor of the myofascial group, with a large effect size for anxiety and a medium effect size for central sensitization and somatization. Regarding clinical anxiety, after the intervention a mean difference was observed with respect to the baseline of 19.98 points in the myofascial group (p < 0.001) and 5.95 in the placebo group (p = 0.22). The intention-to-treat principle was used. There were no adverse events or side effects in either group. CONCLUSIONS: The myofascial approach is effective in improving anxiety levels and associated central sensitization processes in patients with clinical anxiety and this improvement is maintained over time. CLINICAL TRIAL REGISTRATION: NCT04826302.

What Concept of Manual Therapy Is More Effective to Improve Health Status in Women with Fibromyalgia Syndrome? A Study Protocol with Preliminary Results.

BACKGROUND: Fibromyalgia (FM) is defined as a chronic syndrome characterized by diffuse musculoskeletal pain, associated with characteristic signs and symptoms such as fatigue and/or sleep and mood disorders, and whose etiology, pathogenesis and prognosis may or may not be known. There is growing evidence of manual therapy as a treatment for pain in the short and medium term, also in patients affected by FM. However, the heterogeneity of the manual therapy treatments administered are a very common clinical practice, as they are based more on the judgment or tendency of the physiotherapist, rather than on clear scientific evidence. Therefore, the aim of the present study protocol will be to determine which manual therapy approach is more effective in addressing health status by improving symptoms (sensory, cognitive, emotional and social) in patients with FM. METHODS: a randomized controlled clinical trial with a 3-month follow-up will be carried out with 52 female patients affected by rheumatologist-diagnosed FM will be recruited and evaluated at the Asociación de Fibromialgia y Síndrome de Fatiga Crónica (AFINSYFACRO) in Móstoles, Madrid, Spain. For more details on the protocol, a pilot study was carried out using a non-probability method of judgmental or purposive sampling. Thirteen patients were also evaluated, treated and reevaluated; eight patients were assigned to the myofascial techniques approach (MTA) group and five to the Maitland's mobilization approach (MMA) group. RESULTS: the preliminary results presented here are intended to show how the planned randomized controlled clinical trial will develop. Patients who received MTA had significantly improved pain and health status outcomes after treatment and at 1-month follow-up, with no significant change in those who received MMA. CONCLUSIONS: the exact details of the study protocol on which the manual therapy approach is more effective in addressing health status by improving symptoms (sensory, cognitive, emotional, and social) in patients with FM are presented. Preliminary results show that manual therapy is effective in improving pain and health status in patients with fibromyalgia at short and medium term, with significant results in those who received MTA.

Environmental enrichment reverses cerebellar impairments caused by prenatal exposure to a synthetic glucocorticoid.

During prenatal life, exposure to synthetic glucocorticoids (SGCs) can alter normal foetal development, resulting in disease later in life. Previously, we have shown alterations in the dendritic cytoarchitecture of Purkinje cells in adolescent rat progeny prenatally exposed to glucocorticoids. However, the molecular mechanisms underlying these alterations remain unclear. A possible molecular candidate whose deregulation may underlie these changes is the glucocorticoid receptor (GR) and neurotrophin 3/ tropomyosin receptor kinase C, neurotrophic complex (NT-3/TrkC), which specifically modulates the development of the neuronal connections in the cerebellar vermis. To date, no evidence has shown that the cerebellar expression levels of this neurotrophic complex are affected by exposure to a synthetic glucocorticoid in utero. Therefore, the first objective of this investigation was to evaluate the expression of GR, NT-3 and TrkC in the cerebellar vermis using immunohistochemistry and western blot techniques by evaluating the progeny during the postnatal stage equivalent to adolescence (postnatal Day 52). Additionally, we evaluated anxiety-like behaviours in progeny using the elevated plus maze and the marble burying test. In addition, an environmental enrichment (EE) can increase the expression of some neurotrophins and has anxiolytic power. Therefore, we wanted to assess whether an EE reversed the long-term alterations induced by prenatal betamethasone exposure. The major findings of this study were as follows: i) prenatal betamethasone (BET) administration decreases GR, NT-3 and TrkC expression in the cerebellar vermis ii) prenatal BET administration decreases GR expression in the cerebellar hemispheres and iii) enhances the anxiety-like behaviours in the same progeny, and iv) exposure to an EE reverses the reduced expression of GR, NT-3 and TrkC in the cerebellar vermis and v) decreases anxiety-like behaviours. In conclusion, an enriched environment applied 18 days post-weaning was able to restabilize GR, NT-3 and TrkC expression levels and reverse anxious behaviours observed in adolescent rats prenatally exposed to betamethasone.

Environmental enrichment restores the reduced expression of cerebellar synaptophysin and the motor coordination impairment in rats prenatally treated with betamethasone.

Preterm babies treated with synthetic glucocorticoids in utero exhibit behavioural alterations and disturbances in brain maturation during postnatal life. Accordingly, it has been shown in preclinical studies that SGC exposure at a clinical dose alters the presynaptic and postsynaptic structures and results in synaptic impairments. However, the precise mechanism by which SGC exposure impairs synaptic protein expression and its implications are not fully elucidated. Therefore, the purpose of this study was to investigate the effect of prenatal exposure to a clinical dose of betamethasone on the pre- and postsynaptic proteins expression in the developing rat cerebellum and prefrontal cortex, whose synchronized synaptic activity is crucial for motor control and learning. Consequently, the first objective of the present study was to determine whether prenatal betamethasone -equivalent to the clinically used dose- alters cerebellar vermal and cortical expression of synaptophysin, synaptotagmin I, post-synaptic density protein 95 and gephyrin - four important pre- and post-synaptic proteins, respectively- at a relevant adolescent stage. In addition, our second objective was to assess whether prenatal betamethasone administration induced coordination impairment using a rotarod test. On the other hand, it has been shown that the environmental enrichment is capable of improving synaptic transmission and recovering various behavioural impairments. Nevertheless, there is not enough information about the effect of this non-pharmacological preclinical approach on the regulation of this cerebellar and cortical synaptic proteins. Therefore, the third objective of this study was to examine whether environmental enrichment exposure could recover the possible molecular and behavioural impairments in the offspring at the same developmental stage. The principal data showed that adolescent rats prenatally treated with betamethasone exhibited underexpression of synaptophysin in the vermal cerebellum, but not change in levels of synaptotagmin I, post-synaptic density protein 95 and gephyrin. Analysis of the same pre- and post-synaptic proteins no showed differences in the frontal cortex of the same rats. These results were accompanied by an increase in the number of falls in the rotarod test, when the speed of rotation was fixed and when it was in acceleration, which means motor coordination impairments. Importantly, we found that environmental enrichment restores the betamethasone-induced reduction in the cerebellar synaptophysin together with a recover in the motor coordination impairments in prenatally betamethasone-exposed adolescent rats.

Prenatal glucocorticoid administration persistently increased the immunohistochemical expression of type-1 metabotropic glutamate receptor and Purkinje cell dendritic growth in the cerebellar cortex of the rat.

Several studies have indicated that abnormal prenatal changes in the circulating glucocorticoids (GCs), induced by either maternal stress or exogenous GC administration, significantly alter the development of Purkinje cells (PCs). Among the suggested mechanisms that could mediate this GC-dependent PC susceptibility are changes in the expression of type-1 metabotropic glutamate receptors (mGluR1). In the current study, we analyzed whether a single course of prenatally administered betamethasone phosphate (BET) in pregnant rats increased the immunohistochemical expression of mGluR1 in PCs and decreased PC dendritic growth. The data obtained showed that in utero BET exposure resulted in a significant immunohistochemical overexpression of mGluR1 and a significant reduction in Purkinje cell dendritic outgrowth during postnatal life.

Influence of antenatal synthetic glucocorticoid administration on pyramidal cell morphology and microtubule-associated protein type 2 (MAP2) in rat cerebrocortical neurons.

Previous animal studies have indicated that excessive prenatal circulating glucocorticoid (GC) levels induced by the antenatal administration of synthetic GC (sGC) significantly alter neuronal development in the cerebellar and hippocampal neurons of the offspring. However, it is unknown whether antenatal sGC administration results in long-term neocortical pyramidal cell impairment. In the current study, we examined whether an equivalent therapeutic dose of antenatal betamethasone phosphate (BET) in pregnant rats alters the Golgi-stained basilar dendritic length and histochemical expression of dendritic microtubule-associated protein 2 (MAP2) of neocortical pyramidal cells in infant, adolescent, and young adult offspring. The results obtained showed that in utero BET exposure resulted in a significant reduction in the basilar dendritic length per neuron and a transient reduction in histochemical MAP2 immunoreactivity. Consistent with previous hippocampal and cerebellar data, the present findings suggest that prenatal BET administration alters the dendritic growth of cerebrocortical pyramidal cells.

Effect of functional electrical stimulation on the proprioception, motor function of the paretic upper limb, and patient quality of life: A case report.

Functional electrical stimulation (FES) has shown to improve motor function of the affected side in stroke patients; however, the effects of FES on proprioception, the functional recovery of the paretic upper limb, and the patient quality of life (QoL) are not clear. The aim of the current case report was to determine whether FES can improve joint position sense and the scores on measurements of upper limb function and a QoL survey. The participant was assessed before and after 10 consecutive intervention sessions; in addition, the patient performed the training tasks in the workstation assisted by the FES device. Improvements in angles and time only in the affected wrist and enhancement in the Action Research Arm Test scores for both upper limbs were found after FES intervention. In addition, the patient's health-related QoL measurements improved. FES could ameliorate the proprioceptive deficit and the activity limitations of a stroke survivor. OXFORD LEVEL OF EVIDENCE: 3b; individual case control study.

Antenatal betamethasone produces protracted changes in anxiety-like behaviors and in the expression of microtubule-associated protein 2, brain-derived neurotrophic factor and the tyrosine kinase B receptor in the rat cerebellar cortex.

Using classic Golgi staining methods, we previously showed that the administration of synthetic glucocorticoid betamethasone in equivalent doses to those given in cases of human premature birth generates long-term alterations in Purkinje cell dendritic development in the cerebellar cortex. In the present study, we evaluated whether betamethasone alters the immunohistochemical expression of proteins that participate in cerebellar Purkinje cell dendritic development and maintenance, including microtubule-associated protein 2 (MAP2), brain-derived neurotrophic factor (BDNF) and the tyrosine kinase B receptor (TrkB), which are located predominantly in the cerebellar molecular layer where Purkinje cell dendritogenesis occurs. Consistent with our previous Golgi stain studies, we observed that animals prenatally exposed to a single course of betamethasone showed long-term alterations in the expression of MAP2, BDNF and TrkB. Additionally, these protracted molecular changes were accompanied by anxiety-like behaviors in the elevated plus maze and marble burying tests.

Purkinje cell dendritic atrophy induced by prenatal stress is mitigated by early environmental enrichment.

BACKGROUND: Prenatal stress (PS) in experimental animals causes long-lasting changes in Purkinje cell dendritic morphology. Furthermore, these structural changes are associated with an increase in anxiogenic behaviors in the elevated plus maze (EPM) and open-field (OF) test. OBJECTIVES: As environmental enrichment (EE) has significant restorative effects on brain neurons and behavior, the aim of this study was to evaluate if postweaning EE mitigates the decrease in Purkinje cell dendritic expansion and exploratory behavior induced by PS in mice. MATERIALS AND METHODS: Restraint stress was induced from gestational day 14 (G14) to G21. Approximately 50% of the PS animals were submitted to the EE paradigm between postnatal days 22 (P22) and P52. At P52 and P82, male animals were behaviorally evaluated, and then the morphology of the cerebellar vermal Purkinje cells was analyzed. RESULTS: We found that EE significantly ameliorates the Purkinje cell dendritic atrophy and anxiety-like behavior in the EPM. CONCLUSION: Our data show that long-lasting Purkinje cell dendritic impairments and anxiety-like behavior can be mitigated by postweaning EE.

Effects of a single course of prenatal betamethasone on dendritic development in dentate gyrus granular neurons and on spatial memory in rat offspring.

BACKGROUND: Preterm babies treated with synthetic glucocorticoids (sGC) in utero exhibit behavioral alterations and disturbances in brain maturation during infancy. However, the effects on dentate granule cell morphology and spatial memory in rats that were given clinically equivalent doses of antenatal betamethasone remain unclear. METHODS: Pregnant rats were randomly divided into the following two experimental groups: control (CON) and betamethasone-treated (BET) groups. At gestational day 20 (G20), BET dams were subcutaneously injected with a 0.17 mg/kg betamethasone solution, and CON animals received a similar volume of saline. At postnatal days 22 (P22) and P52, BET and CON offsprings were behaviorally evaluated in the Y-Maze test, and the dentate gyrus granular neurons were histologically analyzed. RESULTS: Animals prenatally treated with a single course of betamethasone exhibit a significant decrement in the dendritic outgrowth of dentate granule cells along with impaired spatial memory when evaluated at P52. Moreover, the body and brain weight of the BET group was significantly lower than the CON group at P0, P22, and P52. CONCLUSION: The current results indicate that a single course of betamethasone in pregnant rats produces significant neuronal and behavioral impairments of the offspring at adolescence along with a decrement in somatic and brain weights at each of the three ages evaluated.

Single course of antenatal betamethasone produces delayed changes in morphology and calbindin-D28k expression in a rat's cerebellar Purkinje cells.

In the current study, we analyzed the impact of antenatal betamethasone on macroscopic cerebellar development, Purkinje cell morphology and the expression of the neuroprotective protein calbindin-D28k. Pregnant rats (Sprague-Dawley) were randomly divided into two experimental groups: control (CONT) and betamethasone-treated (BET). At gestational day 20 (G20), BET dams were subcutaneously injected with a solution of 0.17 mg kg⁻¹ of betamethasone, while CONT animals received a similar volume of saline. At postnatal days 22 (P22) and P52, BET and CONT offspring were behaviorally evaluated, and the cerebella were histologically and immunohistochemically processed. Animals that were prenatally treated with a single course of betamethasone exhibited long-lasting behavioral changes consistent with anxiety-like behavior in the open-field test, together with (1) reduced cerebellar weight and volume, (2) Purkinje cell dendritic atrophy, and (3) an overexpression of calbindin-D28k. The current results indicate that an experimental single course of betamethasone in pregnant rats produces long-lasting anxiety-like behaviors, together with macroscopic and microscopic cerebellar alterations.

Early postweaning social isolation but not environmental enrichment modifies vermal Purkinje cell dendritic outgrowth in rats.

In the present study, we analyzed the effects of enriched, social and isolated experiences on vermal Purkinje cell of the rat, together with anxiety-like behavior in the elevated-plus maze. Sprague-Dawley male rats were randomly submitted to either enriched, social, or isolated environments during the early postweaning period (postnatal days 22-32) and were then behaviorally evaluated in the elevated-plus maze and euthanized for histological analysis. Vermal Purkinje cells (sub-lobules VIa and VIb) were sampled, drawn under camera lucida and morphometrically assessed using the Sholl's concentric ring method. Data obtained indicate that environmental enrichment did not significantly modify the Purkinje cell dendritic branching. On the contrary, Purkinje cell of animals reared in social isolation exhibited a significant reduction in dendritic arborization, which was closely associated with anxiety-like behaviors. The data obtained indicate that, although environmental stimulation in normal animals does not produce significant changes in vermal Purkinje cell dendritic arborization, these cells are vulnerable to early stressful experiences, which is in close association with anxiety-like behaviors.

Prenatal stress alters the behavior and dendritic morphology of the medial orbitofrontal cortex in mouse offspring during lactation.

Several preclinical and clinical studies have shown that prenatal stress alters neuronal dendritic development in the prefrontal cortex, together with behavioral disturbances (anxiety). Nevertheless, neither whether these alterations are present during the lactation period, nor whether such findings may reflect the onset of anxiety disorders observed in childhood and adulthood has been studied. The central aim of the present study was to determine the effects of prenatal stress on the neuronal development and behavior of mice offspring during lactation (postnatal days 14 and 21). We studied 24 CF-1 male mice, grouped as follows: (i) control P14 (n=6), (ii) stressed P14 (n=6), (iii) control P21 (n=6) and (iv) stressed P21 (n=6). On the corresponding days, animals were evaluated with the open field test and sacrificed. Their brains were then stained in Golgi-Cox solution for 30 days. The morphological analysis dealt with the study of 96 pyramidal neurons. The results showed, first, that prenatal stress resulted in a significant (i) decrease in the apical dendritic length of pyramidal neurons in the orbitofrontal cortex at postnatal day 14, (ii) increase in the apical dendritic length of pyramidal neurons in the orbitofrontal cortex at postnatal day 21, and (iii) reduction in exploratory behavior at postnatal day 14 and 21.

Maternal exercise during pregnancy ameliorates the postnatal neuronal impairments induced by prenatal restraint stress in mice.

Clinical and preclinical studies have demonstrated that prenatal stress (PS) induces neuronal and behavioral disturbances in the offspring. In the present study, we determined whether maternal voluntary wheel running (VWR) during pregnancy could reverse the putative deleterious effects of PS on the neurodevelopment and behavior of the offspring. Pregnant CF-1 mice were randomly assigned to control, restraint stressed or restraint stressed+VWR groups. Dams of the stressed group were subjected to restraint stress between gestational days 14 and delivery, while control pregnant dams remained undisturbed in their home cages. Dams of the restraint stressed+VWR group were subjected to exercise between gestational days 1 and 17. On postnatal day 23 (P23), male pups were assigned to one of the following experimental groups: mice born from control dams, stressed dams or stressed+VWR dams. Locomotor behavior and pyramidal neuronal morphology were evaluated at P23. Animals were then sacrificed, and Golgi-impregnated pyramidal neurons of the parietal cortex were morphometrically analyzed. Here, we present two major findings: first, PS produced significantly diminished dendritic growth of parietal neurons without altered locomotor behavior of the offspring; and second, maternal VWR significantly offset morphological impairments.

Selegiline (deprenyl) decreases calbindin-D28k expression in cortical neurons of rats socially deprived during the post-weaning period.

Preclinical studies indicate that selegiline (deprenyl), frequently used in some neurodegenerative diseases, exert protective effects on central nervous system neurons of individuals exposed to social isolation (SI). Furthermore, it has been suggested that SI produces neuronal dysfunction due in part to an excessive intracellular Ca(2+) overload. Since the main intracellular Ca(2+) buffering mechanism involves changes in the calcium-binding protein calbindin-D28k (CB), and that CB neuronal expression can increase in response to Ca(2+) transients, we hypothesized that chronic selegiline administration in early socially isolated animals could minimize cell CB expression as an indirect indicator of protective mechanism against Ca(2+) overload. In the present study male rats were weaned at postnatal day 21 (P21) and randomly assigned to social deprivation (SI) or control (SC) environments for 30 days (P21-51). SI animals were further subdivided in two experimental groups: socially deprived-saline (SI-SAL) and socially isolated-selegiline (SI-SEL) for additional 30 days (P52-82). Medial frontal CB immunoreactivity (CB-ir) neurons were quantitatively and qualitatively analyzed. The results obtained indicate that neocortical cells of adult rats submitted to early SI show a significant increase in the number of CB-ir neurons per cortical field, while selegiline treatment significantly reduces this parameter.

Melatonin ameliorates neocortical neuronal dendritic impairment induced by toluene inhalation in the rat.

The present study investigated the effects of toluene inhalation and the restorative effects of melatonin on branching and basal dendritic outgrowth of superficial pyramidal neurons in rat's frontal, parietal, and occipital cortices. At postnatal day 21 (P21), Sprague-Dawley male rats were randomly assigned to either an air-only group or a toluene group. From P22 to P32 the animals were exposed to either clean air or toluene vapors (5000-6000 ppm) for 10 min/day. This strategy simulated common toluene abuse in humans, which consists of 15-20 rapid inhalations of highly concentrated solvent. Once the inhalation period was over (P32), toluene exposed animals were randomly reassigned to one of following experimental groups: (i) air-control/saline; (ii) toluene/saline; (iii) toluene/melatonin 0.5mg/kg; (iv) toluene/melatonin 1.0mg/kg; (v) toluene/melatonin 5.0mg/kg; and (vi) toluene/melatonin 10mg/kg. Seven days after the last inhalation (P39), all the animals were sacrificed under deep anesthesia; brains were dissected out and stained according to the Golgi-Cox-Sholl procedure. Layer II/III pyramidal neurons were morphologically analyzed by measuring their basilar dendritic length and the number of branches. The results obtained revealed that (i) toluene inhalation significantly reduced dendritic outgrowth and branching in all cortical areas studied, and (ii) intraperitoneal administration of melatonin (0.5-10mg/kg) was able to restore the dendritic impairment induced by toluene exposure.

Structural neuroplasticity induced by melatonin in entorhinal neurons of rats exposed to toluene inhalation.

Several clinical studies have shown that abusing volatile solvents, mainly toluene, produces neurological, neuropathological and neuropsychiatric disorders. Symptoms of these disorders include loss in impulse control, distractibility and memory deficits, which are associated with mild brain atrophy. The entorhinal cortex is critically involved in mnemonic processes, and memory disorders are the major symptom detected in chronic solvent abusers. Therefore, in the present study, we evaluated (1) whether the entorhinal neuronal morphology was impaired by subchronic toluene exposure and (2) if melatonin protected the neuronal cytoarchitecture, as has been demonstrated in neocortical neurons. Consistent with our previous findings, the present study indicates that the entorhinal cell dendritic arborization was significantly reduced in toluene exposed animals, and melatonin administration significantly rescued the reduced dendritic branching induced by toluene neurotoxicity.

Melatonin promotes distal dendritic ramifications in layer II/III cortical pyramidal cells of rats exposed to toluene vapors.

We have previously shown that toluene inhalation produces significant impairments in the basilar dendritic outgrowth of pyramidal cortical cells. This neurotoxic effect was markedly inhibited by melatonin administration at a dose of 5mg kg(-1). The present study was designed to determine whether toluene and melatonin equally affect all basilar dendritic segments or if a differential response exists between the segments. Twenty-eight male mice were weaned at postnatal day 21 (P21) and randomly assigned to either the control (C; n=10,) or toluene (T; n=18) group. Between P22-P32, male rats were placed into a glass chamber and exposed to either toluene vapors (5-000-6000 ppm) or clean air for 10 min a day. When toluene exposure ended (P32), animals were further assigned to the following experimental groups: (a) control/saline (C/S; n=10), (b) toluene/saline (T/S; n=10), or (c) toluene/melatonin 5mg kg(-1) (T/M; n=8). Melatonin or vehicle solutions were administered daily between P32 and P38. Forty-eight hours after the final toluene exposure, the animals were sacrificed, and the pyramidal cortical cells were stained using the Golgi-Cox-Sholl procedure. The number of basilar dendritic branches/order was counted using the centrifugal ordering method. The results indicate that (i) toluene inhalation significantly impairs both proximal and distal basilar dendritic ramifications (in the parietal and frontal/occipital cortices, respectively) and (ii) melatonin both protects neurons from toluene neurotoxicity in all cortical areas studied and increases the complexity of the dendritic tree above control values.

Maternal stress induces long-lasting Purkinje cell developmental impairments in mouse offspring.

A number of clinical studies suggest that prenatal stress can be a risk factor in the development of various psychopathologies, including schizophrenia, depression, anxiety, and autism. The cerebellar vermis has been shown to be involved in most of these disorders. In the present study, therefore, we evaluate the effect of maternal stress on long-term alterations in vermal Purkinje cell morphology. Furthermore, to discern whether these structural changes are associated with anxious behavior, the exploratory drive in the elevated plus maze was evaluated. Pregnant CF-1 mice were randomly assigned to control (n = 14) or stressed (n = 16) groups. Dams of the stressed group were subjected to restraint stress between gestational days 14 and 20, while control pregnant dams remained undisturbed in their home cages. Anxious behavior and Purkinje cell morphology were evaluated in three ontogenetic stages: postweaning, adolescence, and adulthood. Although exploratory behavior in the elevated plus maze was unaffected by prenatal stress, the Purkinje cell morphology showed a transient period of abnormal growth (at postweaning and juvenile stages) followed by dramatic dendritic atrophy in adulthood. In conclusion, prenatal stress induced significant long-lasting bimodal changes in the morphology of vermal Purkinje cells. These structural alterations, however, were not accompanied by anxious behaviors in the elevated plus maze.