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Efrain C Azmitia

Publications and source records attributed to Efrain C Azmitia.

7 recordsLinked to original sources
PubMed2005

Gender-specific 5-HT1A receptor changes in BrdU nuclear labeling patterns in neonatal dentate gyrus.

The actions of 5-HT1A receptors on cell proliferation in the rat neonatal dentate gyrus are unknown. We injected a 5-HT1A receptor agonist (ipsapirone) or antagonist (Way 100635) 1 h before injections of BrdU in neonates of both genders between days 2-4, a peak time of dentate gyrus granule cell proliferation. The BrdU immunoreactive (IR) nuclei in the granule cell layer and subgranular zone were examined after 2 weeks. The BrdU-IR nuclear staining patterns were classified as being either diffuse (homogenous dark BrdU-staining throughout the nucleus) or punctate (multiple distinct small stained spots within the nucleus). Most BrdU-labeled nuclei with a diffuse pattern were seen in the subgranular zone while the punctate pattern nuclei were seen within the granular cell layer of the dentate gyrus. 5-HT1A antagonist showed no overall change in absolute number or pattern of labeled nuclei compared to control animals. After a 5-HT1A agonist, there was also no differences in the total number of BrdU-IR nuclei (punctate and diffuse pattern). However, in both genders, the proportion of the BrdU-labeled nuclei showing a punctate compared to diffuse pattern increased: 33% in females and 18% in males. In females, the 5-HT1A receptor agonist increased the number of nuclei showing a punctate pattern by 41%, while in males the 5-HT1A receptor agonist decreased the number of nuclei showing a diffuse pattern by 29%. These results indicate gender-specific 5-HT1A receptor action on the state of nuclear DNA in the cells of the dentate gyrus, without increasing the total number of BrdU-labeled nuclei.

Analysis of Variance↗
PubMed2005

Chronic gliosis induced by loss of S-100B: knockout mice have enhanced GFAP-immunoreactivity but blunted response to a serotonin challenge.

Serotonin (5-HT) can induce a release of intraglial S-100B and produce a change in glial morphology. Because S-100B can inhibit polymerization of glial fibrillary acidic protein (GFAP), we hypothesize that glial reactivity may reflect the loss of intraglial S-100B. Adult male transgenic S-100B homozygous knockout (-/-) mice (KO) and wild-type CD-1 (WT) mice were studied. S-100B-immunoreactivity (IR) was seen in the brain tissue of WT (CD-1) but not S-100B KO (-/-) mice. GFAP-IR was seen in both WT (CD-1) and S-100B KO (-/-) glia cells, but S-100B KO (-/-) GFAP-IR cells appeared larger, darker, and more branched than in WT (CD-1). To compare the response of GFAP-IR cells to 5-HT in S-100B KO (-/-) and WT (CD-1) mice, we injected animals with para-chloroamphetamine (PCA) over 2 days (5 and 10 mg/ml). PCA is a potent 5-HT releaser which can induce gliosis in the rodent brain. In WT (CD-1) mice, the size, branching, and density of GFAP-IR cells were significantly increased after PCA injections. No increase in GFAP-IR activation was seen in the S-100B KO (-/-) after PCA injections. Cell-specific densitometry (set at a threshold of 0-150 based on a scale of 255) in these animals statistically showed an increase in GFAP-IR after PCA injections in WT (CD-1) but not S-100B KO (-/-) mice. These results are consistent with the hypothesis that 5-HT may modulate glial morphology by inducing a release of intracellular S-100B, and this pathway is inoperable in the S-100B KO (-/-).

Animals↗
PubMed2004

Differential effects on somatic and reflex development by chronic clomipramine treatment.

The developmental effect of altered 5-HT and NE levels is a subject that requires more attention, especially when considering the increased demand for antidepressive dual reuptake inhibitors. Serotonin and norepinephrine are bioamines that differentially influence the nervous tissue growth. This study investigated the somatic maturation and the ontogeny of reflexes in neonate rats treated from the 1st to the 21st postnatal day (PND) with clomipramine (20 mg/kg sc, daily), a potent monoamine reuptake inhibitor. Indicators of both general body growth (body weight, axis of the head and body lengths) and physical maturation (ear unfolding, auditory conduit opening, eruption of the lower incisors and eye opening) were appraised. Ontogeny of motor and sensory reflexes (righting, free-fall righting--acceleration, negative geotaxis, cliff avoidance, auditory startle response and vibrissa placing) was also observed. The results demonstrated that chronic neonatal treatment with clomipramine alters the somatic growth. However, it did not interfere with the onset time of many physical features and reflexes. These results provide insights into the consequences of dual transmitter during early development.

Age Factors↗
PubMed2004

Serotonin1A receptors at the axon initial segment of prefrontal pyramidal neurons in schizophrenia.

OBJECTIVE: Inhibition mediated by gamma-aminobutyric acid at the axon initial segment of pyramidal neurons appears to be altered in the prefrontal cortex in schizophrenia. This study examined the densities and laminar distribution of axon initial segments labeled with an antibody against the serotonin(1A) (5-HT(1A)) receptor, which also mediates inhibitory regulation of pyramidal neurons, in subjects with schizophrenia. METHOD: The densities and laminar distribution of axon initial segments with 5-HT(1A)-like immunoreactivity were assessed in postmortem tissue from the prefrontal cortex (Brodmann's area 46) of 14 matched triads of subjects with schizophrenia, subjects with major depressive disorder, and comparison subjects with no psychiatric disorder. RESULTS: The relative densities of the labeled axon initial segment in both the superficial and the deep cortical layers did not differ across the three subject groups. CONCLUSIONS: The findings do not support a role for altered serotonin transmission by means of the 5-HT(1A) receptor in dysfunction of prefrontal cortex pyramidal neurons in schizophrenia.

Axons↗
PubMed2002

Cajal's hypotheses on neurobiones and neurotropic factor match properties of microtubules and S-100 beta.

Cajal described both the morphology and plasticity of neurons. He summarized the structure of neurons as composed of membrane, protoplasm, Golgi apparatus, nucleus, spongioplasm and neurofibrils (cytoskeleton). He initially considered the cytoskeleton as absorbing excitation energy and forming a "conductive pathway in the protoplasm" within the neuron. Later, he viewed the neurofibrillary threads as independent, living entities and called them neurobiones. Cajal recognized neuroplasticity in development, memory, sleep, injury and dementia, as well as after exposure to cold and starvation. He noted cytoskeletal changes during these events. However, he did not causatively connect the plastic changes in neurons with the changes in cytoskeleton. Finally, Cajal proposed a theory of chemoaffinity in 1892, and modified his neurotropic theory over the next 40 years. Today we accept that changes in the cytoskeleton produce changes in neuronal morphology. The properties of the cytoskeleton and neurobione as described by Cajal are similar to those of microtubules. These long intraneuronal neurofibrils are polymers of the protein tubulin and, whilst not being living entities, are highly dynamic, sensitive to environmental stimuli, and stabilized by microtubule associated proteins (MAPs). Furthermore, Cajal was very specific in his characterization of the neurotropic factor derived from Schwann cells. Initially, he thought the chemicals attracted the axonal fibers, but later he wrote that the factor was not attractant but rather was involved in assimilation, growth and ramifications. The neurotropic hypothesis described by Cajal in Degeneration and Regeneration in the Nervous System is more similar to a neurite extension factor (NEF) than to a neurotrophic growth factor or specific chemoaffinity (attractant) molecule. S-100 beta is the major NEF found in PNS Schwann cells and CNS astroglial cells. In summary, the views of Cajal on neuroplasticity, its frequency and function, agree with the modern hypothesis of neuronal instability. This concept states that MAPs regulate microtubule stability by a S-100 beta sensitive phosphorylation processes. Serotonin, by acting on the astroglial 5-HT1A receptor, releases S-100 beta and regulates neuronal morphology and apoptosis. This neuronal-glial connection provides a fresh view for linking neuroplasticity, mental illness, and memory with changes in the cytoskeleton.

Animals↗
PubMed2002

Deviations in brain early serotonergic development as a result of fetal alcohol exposure.

Serotonin (5-HT) has specific roles not only as a transmitter but also as a signal for differentiation. We recently found that alcohol drinking during pregnancy resulted in incomplete-neural-tube-fusion which hindered the development of midline cells such as 5-HT neurons in mice. We now report that, at the birth of 5-HT neurons (E11), the 5-HT immunoreative (5-HT-im) neurons are often found missing medial projecting fibers towards ventricle in the Alcohol treated group (ALC) as compared with pair-fed (PF) and Chow-fed groups (Chow) in mice. At E13, there are fewer 5-HT-im neurons in either dorsal or median raphe of ALC as compared with PF or Chow; furthermore, neurite outgrowth and migration of the 5-HT neurons are also compromised with alcohol exposure. We, thus, demonstrated that fetal alcohol exposure compromised 5-HT development as early as at the 5-HT neuron birth. Since 5-HT is a signal for development of many forebrain neurons, the deviation of 5-HT in early life may have consequences on brain development that extend beyond those seen in the 5-HT system.

Journal Article↗