Differential investment in visual and olfactory brain regions is linked to the sensory needs of a wasp social parasite and its host

2021 ◽  
Author(s):  
Allison N. Rozanski ◽  
Alessandro Cini ◽  
Taylor E. Lopreto ◽  
Kristine M. Gandia ◽  
Mark E. Hauber ◽  
...  
Keyword(s):  
Brain Regions ◽  
Social Parasite

scholarly journals Differential investment in visual and olfactory brain regions mirrors the sensory needs of a paper wasp social parasite and its host

2021 ◽  
Author(s):  
Allison N. Rozanski ◽  
Alessandro Cini ◽  
Taylor E. Lopreto ◽  
Kristine M. Gandia ◽  
Mark E. Hauber ◽  
...  
Keyword(s):  
Brain Plasticity ◽  
Sensory Systems ◽  
Brain Regions ◽  
Paper Wasp ◽  
Social Parasite ◽  
Social Parasites ◽  
Antennal Lobes ◽  
Specific Investment ◽  
Host Colony ◽  
Sensory Adaptations

ABSTRACTObligate social parasites evolve traits to effectively locate and then exploit their hosts, whereas hosts have complex social behavioral repertoires, which include sensory recognition to reject potential conspecific intruders and heterospecific parasites. While social parasite and host behaviors have been studied extensively, less is known about how their sensory systems function to meet their specific selective pressures. Here, we compare investment in visual and olfactory brain regions in the paper wasp Polistes dominula, and its obligate social parasite P. sulcifer, to explore the link between sensory systems and brain plasticity. Our results show opposite and significant differences, consistent with their very different life-histories, in the sensory investments between these two closely-related species. Social parasites initially invest in the optic lobes to likely locate their hosts. After host colony usurpation, the parasite increases its brain volume, with specific investment in antennal lobes, which mirrors the behavioral switch from a usurping parasite to an integrated parasitic queen of the host colony. Contrastingly, hosts initially invest in the antennal lobes and sensory processing compared to social parasites, as predicted by their need to maintain social cohesion, allocate colony tasks, and recognize con- and heterospecific intruders. Host queens show a trend of higher investment in all sensory brain regions compared to workers, paralleling differences in task allocations. Our work provides novel insights into how intraspecific brain plasticity can facilitate the unique sensory adaptations needed to perform specific tasks by the host or to transition from searching to successful host exploitation by the social parasite.

Synaptic organization of the gustatory NST

1994 ◽  
Vol 52 ◽  
pp. 150-151
Author(s):  
M. C. Whitehead
Keyword(s):  
Central Nervous System ◽  
Dendritic Spines ◽  
Fundamental Problem ◽  
Cell Types ◽  
Brain Regions ◽  
Excitatory Synapses ◽  
Solitary Tract ◽  
Synaptic Organization ◽  
Synaptic Junctions ◽  
Afferent Terminals

A fundamental problem in taste research is to determine how gustatory signals are processed and disseminated in the mammalian central nervous system. An important first step toward understanding information processing is the identification of cell types in the nucleus of the solitary tract (NST) and their synaptic relationships with oral primary afferent terminals. Facial and glossopharyngeal (LIX) terminals in the hamster were labelled with HRP, examined with EM, and characterized as containing moderate concentrations of medium-sized round vesicles, and engaging in asymmetrical synaptic junctions. Ultrastructurally the endings resemble excitatory synapses in other brain regions.Labelled facial afferent endings in the RC subdivision synapse almost exclusively with distal dendrites and dendritic spines of NST cells. Most synaptic relationships between the facial synapses and the dendrites are simple. However, 40% of facial endings engage in complex synaptic relationships within glomeruli containing unlabelled axon endings particularly ones termed "SP" endings. SP endings are densely packed with small, pleomorphic vesicles and synapse with both the facial endings and their postsynaptic dendrites by means of nearly symmetrical junctions.

Musical Anhedonia

2020 ◽  
Vol 31 (2) ◽  
pp. 62-68
Author(s):  
Sara E. Holm ◽  
Alexander Schmidt ◽  
Christoph J. Ploner
Keyword(s):  
Quality Of Life ◽  
Nucleus Accumbens ◽  
Brain Damage ◽  
Parietal Cortex ◽  
Neurological Disorders ◽  
Brain Regions ◽  
Precise Information ◽  
Exact Localization ◽  
High Prevalence

Abstract. Some people, although they are perfectly healthy and happy, cannot enjoy music. These individuals have musical anhedonia, a condition which can be congenital or may occur after focal brain damage. To date, only a few cases of acquired musical anhedonia have been reported in the literature with lesions of the temporo-parietal cortex being particularly important. Even less literature exists on congenital musical anhedonia, in which impaired connectivity of temporal brain regions with the Nucleus accumbens is implicated. Nonetheless, there is no precise information on the prevalence, causes or exact localization of both congenital and acquired musical anhedonia. However, the frequent involvement of temporo-parietal brain regions in neurological disorders such as stroke suggest the possibility of a high prevalence of this disorder, which leads to a considerable reduction in the quality of life.

Serotonergic Genes and Suicidality

Crisis ◽  
2001 ◽  
Vol 22 (2) ◽  
pp. 54-60 ◽  
Author(s):  
Lisheng Du ◽  
Gabor Faludi ◽  
Miklos Palkovits ◽  
David Bakish ◽  
Pavel D. Hrdina
Keyword(s):  
Suicidal Ideation ◽  
Suicidal Behavior ◽  
Tryptophan Hydroxylase ◽  
Association Studies ◽  
Receptor Gene ◽  
Brain Regions ◽  
Depressive Illness ◽  
Control Group ◽  
Serotonergic Activity ◽  
Completed Suicide

Summary: Several lines of evidence indicate that abnormalities in the functioning of the central serotonergic system are involved in the pathogenesis of depressive illness and suicidal behavior. Studies have shown that the number of brain and platelet serotonin transporter binding sites are reduced in patients with depression and in suicide victims, and that the density of 5-HT2A receptors is increased in brain regions of depressed in suicide victims and in platelets of depressed suicidal patients. Genes that code for proteins, such as tryptophan hydroxylase, 5-HT transporter, and 5-HT2A receptor, involved in regulating serotonergic neurotransmission, have thus been major candidate genes for association studies of suicide and suicidal behavior. Recent studies by our group and by others have shown that genetic variations in the serotonin-system-related genes might be associated with suicidal ideation and completed suicide. We have shown that the 102 C allele in 5-HT2A receptor gene was significantly associated with suicidal ideation (χ2 = 8.5, p < .005) in depressed patients. Patients with a 102 C/C genotype had a significantly higher mean HAMD item #3 score (indication of suicidal ideation) than T/C or T/T genotype patients. Our results suggest that the 102T/C polymorphism in 5-HT2A receptor gene is primarily associated with suicidal ideation in patients with major depression and not with depression itself. We also found that the 5-HT transporter gene S/L polymorphism was significantly associated with completed suicide. The frequency of the L/L genotype in depressed suicide victims was almost double of that found in control group (48.6% vs. 26.2%). The odds ratio for the L allele was 2.1 (95% CI 1.2-3.7). The association between polymorphism in serotonergic genes and suicidality supports the hypothesis that genetic factors can modulate suicide risk by influencing serotonergic activity.

Inefficient Encoding as an Explanation for Age-Related Deficits in Recollection-Based Processing

2014 ◽  
Vol 28 (3) ◽  
pp. 148-161 ◽  
Author(s):  
David Friedman ◽  
Ray Johnson
Keyword(s):  
Older Adults ◽  
Young Adults ◽  
Cognitive Processes ◽  
Brain Activity ◽  
Memory Performance ◽  
Brain Regions ◽  
Semantic Retrieval ◽  
Age Related ◽  
The Face ◽  
Episodic Memories

A cardinal feature of aging is a decline in episodic memory (EM). Nevertheless, there is evidence that some older adults may be able to “compensate” for failures in recollection-based processing by recruiting brain regions and cognitive processes not normally recruited by the young. We review the evidence suggesting that age-related declines in EM performance and recollection-related brain activity (left-parietal EM effect; LPEM) are due to altered processing at encoding. We describe results from our laboratory on differences in encoding- and retrieval-related activity between young and older adults. We then show that, relative to the young, in older adults brain activity at encoding is reduced over a brain region believed to be crucial for successful semantic elaboration in a 400–1,400-ms interval (left inferior prefrontal cortex, LIPFC; Johnson, Nessler, & Friedman, 2013 ; Nessler, Friedman, Johnson, & Bersick, 2007 ; Nessler, Johnson, Bersick, & Friedman, 2006 ). This reduced brain activity is associated with diminished subsequent recognition-memory performance and the LPEM at retrieval. We provide evidence for this premise by demonstrating that disrupting encoding-related processes during this 400–1,400-ms interval in young adults affords causal support for the hypothesis that the reduction over LIPFC during encoding produces the hallmarks of an age-related EM deficit: normal semantic retrieval at encoding, reduced subsequent episodic recognition accuracy, free recall, and the LPEM. Finally, we show that the reduced LPEM in young adults is associated with “additional” brain activity over similar brain areas as those activated when older adults show deficient retrieval. Hence, rather than supporting the compensation hypothesis, these data are more consistent with the scaffolding hypothesis, in which the recruitment of additional cognitive processes is an adaptive response across the life span in the face of momentary increases in task demand due to poorly-encoded episodic memories.

Inflammational Animal Models for Schizophrenia

2015 ◽  
Vol 223 (3) ◽  
pp. 157-164 ◽  
Author(s):  
Georg Juckel
Keyword(s):  
Animal Model ◽  
Animal Models ◽  
Immune Activation ◽  
Microglial Activation ◽  
Treatment Options ◽  
Early Adulthood ◽  
Brain Regions ◽  
Synaptic Connections ◽  
Preventive Interventions ◽  
Immunological System

Abstract. Inflammational-immunological processes within the pathophysiology of schizophrenia seem to play an important role. Early signals of neurobiological changes in the embryonal phase of brain in later patients with schizophrenia might lead to activation of the immunological system, for example, of cytokines and microglial cells. Microglia then induces – via the neurotoxic activities of these cells as an overreaction – a rarification of synaptic connections in frontal and temporal brain regions, that is, reduction of the neuropil. Promising inflammational animal models for schizophrenia with high validity can be used today to mimic behavioral as well as neurobiological findings in patients, for example, the well-known neurochemical alterations of dopaminergic, glutamatergic, serotonergic, and other neurotransmitter systems. Also the microglial activation can be modeled well within one of this models, that is, the inflammational PolyI:C animal model of schizophrenia, showing a time peak in late adolescence/early adulthood. The exact mechanism, by which activated microglia cells then triggers further neurodegeneration, must now be investigated in broader detail. Thus, these animal models can be used to understand the pathophysiology of schizophrenia better especially concerning the interaction of immune activation, inflammation, and neurodegeneration. This could also lead to the development of anti-inflammational treatment options and of preventive interventions.

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