Is humanlike cytoarchitectural asymmetry present in another species with complex social vocalization? A stereologic analysis of mustached bat auditory cortex
asymmetry; cerebral-cortex; combination-sensitive neurons; DSCF; hemispheric-specialization; human-brain; japanese macaques; lateralization; mustached bat; neural; Neurosciences & Neurology; planum temporale; pteronotus-parnellii; rhesus-monkeys; social vocalization; stereology; temporal speech region; V1
Considerable evidence suggests that left hemispheric lateralization for language comprehension in humans is associated with cortical microstructural asymmetries. However, despite the fact that left hemispheric dominance for the analysis of species-specific social vocalizations has been reported in several other species, little is known concerning microstructural asymmetries in auditory cortex of nonhumans. To test whether such neuroanatomical lateralization characterizes another species with complex social vocalizations, we performed stereologic analyses of Nissl-stained cells in layer III of area DSCF in mustached bats (Pteronotus parnellii). Area DSCF was selected because it contains neurons which are sensitive to several temporal features of conspecific vocalizations. Primary visual cortex (V I) was also studied as a comparative reference. We measured neuron densities, glial densities, and neuronal volumes in both hemispheres of 10 adult male bats. Results indicate that these variables are not significantly lateralized in area DSCF or V I. Additionally, magnopyramidal cells (i.e., the largest 10% of neurons from both hemispheres) were not asymmetric in their frequency of distribution at the population level. Although several individual bats had asymmetric neuron distributions, consistent hemispheric bias was not evident. Absence of population-level microstructural asymmetry in area DSCF of mustached bats suggests alternative evolutionary scenarios including: (1) microstructural lateralization of auditory cortical circuitry may be a unique adaptation for human language, and (2) the specialized biosonar function of mustached bat auditory cortex may require symmetrical cytoarchitectural structure. Resolution of these alternatives will require further data on the microstructure of auditory cortex in species with lateralized perception of acoustic social communication. (C) 2005 Elsevier B.V. All rights reserved.
Sherwood C C; Raghanti M A; Wenstrup J J
Brain Research
2005
2005-05
Journal Article
<a href="http://doi.org/10.1016/j.brainres.2005.03.023" target="_blank" rel="noreferrer noopener">10.1016/j.brainres.2005.03.023</a>
Astrocytic changes with aging and Alzheimer's disease-type pathology in chimpanzees
Aging; Alzheimer's disease; astrocytes; cerebral cortex; chimpanzees; hippocampus; prefrontal cortex; RRID: AB2109645; RRID: AB223647; RRID: AB2313952; RRID: AB2314223; stereology
Astrocytes are the main homeostatic cell of the central nervous system. In addition, astrocytes mediate an inflammatory response when reactive to injury or disease known as astrogliosis. Astrogliosis is marked by an increased expression of glial fibrillary acidic protein (GFAP) and cellular hypertrophy. Some degree of astrogliosis is associated with normal aging and degenerative conditions such as Alzheimer's disease (AD) and other dementing illnesses in humans. The recent observation of pathological markers of AD (amyloid plaques and neurofibrillary tangles) in aged chimpanzee brains provided an opportunity to examine the relationships among aging, AD-type pathology, and astrocyte activation in our closest living relatives. Stereologic methods were used to quantify GFAP-immunoreactive astrocyte density and soma volume in layers I, III, and V of the prefrontal and middle temporal cortex, as well as in hippocampal fields CA1 and CA3. We found that the patterns of astrocyte activation in the aged chimpanzee brain are distinct from humans. GFAP expression does not increase with age in chimpanzees, possibly indicative of lower oxidative stress loads. Similar to humans, chimpanzee layer I astrocytes in the prefrontal cortex are susceptible to AD-like changes. Both prefrontal cortex layer I and hippocampal astrocytes exhibit a high degree of astrogliosis that is positively correlated with accumulation of amyloid beta and tau proteins. However, unlike humans, chimpanzees do not display astrogliosis in other cortical layers. These results demonstrate a unique pattern of cortical aging in chimpanzees and suggest that inflammatory processes may differ between humans and chimpanzees in response to pathology.
Munger Emily L; Edler Melissa K; Hopkins William D; Ely John J; Erwin Joseph M; Perl Daniel P; Mufson Elliott J; Hof Patrick R; Sherwood Chet C; Raghanti Mary Ann
The Journal of Comparative Neurology
2019
2019-05
<a href="http://doi.org/10.1002/cne.24610" target="_blank" rel="noreferrer noopener">10.1002/cne.24610</a>
Single low doses of MPTP decrease tyrosine hydroxylase expression in the absence of overt neuron loss.
1-Methyl-4-phenyl-1; 2; 3; 6-tetrahydropyridine/*administration & dosage; Animals; Catecholamines/metabolism; Cell Count; Corpus Striatum/*drug effects/metabolism; Dopamine; Dopamine transporter; Dopaminergic Neurons/*drug effects/metabolism; Inbred C57BL; Male; Mice; MPTP; MPTP Poisoning; Parkinsonian Disorders/*metabolism/*pathology; Stereology; Substantia Nigra/*drug effects/metabolism; Tyrosine 3-Monooxygenase/*metabolism; Tyrosine hydroxylase; Vesicular monoamine transporter
Parkinson's disease (PD) is the second most common age-related neurodegenerative disease. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a prototypical neurotoxicant used in mice to mimic primary features of PD pathology including striatal dopamine depletion and dopamine neuron loss in the substantia nigra pars compacta (SNc). In the literature, there are several experimental paradigms involving multiple doses of MPTP that are used to elicit dopamine neuron loss. However, a recent study reported that a single low dose caused significant loss of dopamine neurons. Here, we determined the effect of a single intraperitoneal injection of one of three doses of MPTP (0.1, 2 and 20mg/kg) on dopamine neurons, labeled by tyrosine hydroxylase (TH(+)), and total neuron number (Nissl(+)) in the SNc using unbiased stereological counting. Data reveal a significant loss of neurons in the SNc (TH(+) and Nissl(+)) only in the group treated with 20mg/kg MPTP. Groups treated with lower dose of MPTP (0.1 and 2mg/kg) only showed significant loss of TH(+) neurons rather than TH(+) and Nissl(+) neurons. Striatal dopamine levels were decreased in the groups treated with 2 and 20mg/kg MPTP and striatal terminal markers including, TH and the dopamine transporter (DAT), were only decreased in the groups treated with 20mg/kg MPTP. These data demonstrate that lower doses of MPTP likely result in loss of TH expression rather than actual dopamine neuron loss in the SN. This finding reinforces the need to measure both total neuron number along with TH(+) cells in determining dopamine neuron loss.
Alam Gelareh; Edler Melissa; Burchfield Shelbie L; Richardson Jason R
Neurotoxicology
2017
2017-05
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/j.neuro.2017.03.008" target="_blank" rel="noreferrer noopener">10.1016/j.neuro.2017.03.008</a>
Astrocytic changes with aging and Alzheimer's disease-type pathology in chimpanzees.
aging; Alzheimer's disease; astrocytes; cerebral cortex; chimpanzees; hippocampus; prefrontal cortex; RRID: AB2109645; RRID: AB223647; RRID: AB2313952; RRID: AB2314223; stereology
Astrocytes are the main homeostatic cell of the central nervous system. In addition, astrocytes mediate an inflammatory response when reactive to injury or disease known as astrogliosis. Astrogliosis is marked by an increased expression of glial fibrillary acidic protein (GFAP) and cellular hypertrophy. Some degree of astrogliosis is associated with normal aging and degenerative conditions such as Alzheimer's disease (AD) and other dementing illnesses in humans. The recent observation of pathological markers of AD (amyloid plaques and neurofibrillary tangles) in aged chimpanzee brains provided an opportunity to examine the relationships among aging, AD-type pathology, and astrocyte activation in our closest living relatives. Stereologic methods were used to quantify
Munger Emily L; Edler Melissa K; Hopkins William D; Ely John J; Erwin Joseph M; Perl Daniel P; Mufson Elliott J; Hof Patrick R; Sherwood Chet C; Raghanti Mary Ann
The Journal of comparative neurology
2018
2018-12
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1002/cne.24610" target="_blank" rel="noreferrer noopener">10.1002/cne.24610</a>