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This chapter examines the neuromolecular and plastic brain. Ideas about plasticity and the openness of brains to environment influences, from initial evidence about nerve development, through the recognition that synaptic plasticity was the very basis of learning and memory, to evidence about the influence of environment on gene expression and the persistence throughout life of the capacity to make new neurons—all this made the neuromolecular brain seem exquisitely open to its milieu, with changes at the molecular level occurring throughout the course of a human life and thus shaping the growth, organization, and regeneration of neurons and neuronal circuits at time scales from the millisecond to the decade. This was an opportunity to explore the myriad ways in which the milieu got “under the skin,” implying an openness of these molecular processes of the brain to biography, sociality, and culture, and hence perhaps even to history and politics.

VFO precedes electrographic seizures in vitro, as well as in vivo. The in vitro VFO is gap junction dependent, and is observed most readily in conditions when synaptic transmission is suppressed. One hypothesis as to seizure initiation is that synaptic excitation recovers prior to synaptic inhibition, so that classical synaptically mediated seizure discharges can arise. Epileptiform discharges in vivo can also be preceded by gamma oscillations, and there is an in vitro model in which gamma activity and bursting activity alternates. The alternating activity appears to arise because of use-dependent alterations in synaptic excitation and inhibition.

This chapter considers adaptive plasticity which allows experience-based cortical expansion within a modality if used as a model for the cross-modal plasticity accompanying the loss of a sense. This plasticity is shown through auditory and somatosensory activity in occipital cortex in blind subjects. Hebbian principles are thought to be the underlying mechanism of this reorganization.

Selection in complex and structured environments is likely to cause the divergence of differently adapted lines. This will lead to a diverse array of specialized types, or to one or a few broad generalists, or to some intermediate situation. The first section in this chapter is called GxE and details the ecogenetic landscape; the magnitude of GxE; inconsistency and responsiveness; the genetic correlation in relation to environmental variance; the outcome of selection in different environments; stability and responsiveness; and the evolution of stability and responsiveness. The second section is about specialization and generalization, and details niche separation; the cost of adaptation; divergent specialization; sources of antagonism: functional interference; sources of antagonism: mutational degradation; and the consequences of interference and degradation. It also gives an experimental adaptive radiation regarding pseudomonas and an historical adaptive radiation concerning anolis. The third section called Opportunities in space, obligations in time, explains simple environments; complex environments; the cost of adaptation in complex environments; structured environments; the outcome of selection in structured environments; fluctuating fitness; and the outcome of selection in variable environments. The final section is called Local adaptation and details the precision of local adaptation and gives reciprocal transplant experiments.

For ongoing coevolution of the grass-endophyte symbiosis through the agents of natural selection, there must be genetic variation within populations for both host and endophyte. The breeding systems of both symbiotic partners influence the distribution and level of genetic variation within populations. Traditional reaction norms and symbiotic interaction norms can be useful in depicting host genotype interactions with environment and infection. Examples are provided for both agronomic and native grass-endophyte symbioses. Endophytes can also modulate phenotypic plasticity of their grass hosts in relation to environmental variation. There is evidence that endophyte genotypes (haplotypes) can differ significantly in their impact on host growth and physiology. Genetic diversity of endophyte isolates has been quantified using isozymes and DNA markers. Host-endophyte compatibility can vary among endophytes and their host grasses as revealed by reciprocal inoculation experiments using fungal isolates from different host populations or species. Multistrain infections of single grass hosts and fungal hybridization within individual hosts have been determined for some symbioses. Genetic variation in both host and endophyte will expedite the continued coevolution of the symbiosis.

Understanding the ecology and evolution of morphological defences in animals and plants may help us to understand and protect biodiversity. Several species of dragonfly larvae express lateral and dorsal abdominal spines. In some species these spines seem to be fixed, and in others they are induced by the presence of predatory fish. Larger spines are adaptations to reduce predation risk by fish, but incur a cost because large spines are associated with a higher predation risk by invertebrate predators. The difference in vulnerability to different predators has the potential to affect temporal and spatial variation in the morphology of dragonfly larvae, and may ultimately result in speciation. Future focus on the joint evolution of correlated defensive traits such as morphology and behaviour and their plasticity might be fruitful for a better understanding of the development of animal diversity.

This chapter examines the hypothesis that attention aids memory formation by providing neuromodulatory input that turns transient, homosynaptic plasticity to long-lasting heterosynaptic plasticity. It addresses the following questions. Are the firing patterns of hippocampal neurons learned? Do they require plasticity like that seen in reduced hippocampal preparations? Are the firing properties of hippocampal neurons attentionally modulated? Evidence suggests that place fields require experience to be constructed, and that plasticity is involved in this process, thus, the first two questions can be answered positively even though the mechanistic details remain elusive. However, the role of attention in the firing patterns of hippocampal neurons, remains more problematic. This is not surprising because this part deals with cognitive rather than cellular mechanisms, and the mechanistic understanding of cognitive neuroscience is still in its infancy relative to that of cellular neuroscience.

Glutamate is an amino acid that your brain uses as a neurotransmitter and it is almost always is excitatory. GABA is also an amino acid that your brain uses as a neurotransmitter and it is almost always inhibitory. These two neurotransmitters are widespread in your brain and tend to compete for turning your neurons on or off. Glutamate makes and breaks connections between neurons; this action allows your brain to learn. For example, if you consume a chemical that blocks the actions of glutamate you become amnestic, unable to remember anything new. The street drugs PCP and ketamine block glutamate receptors and depress the activity of your brain. Your brain makes its own PCP-like neurotransmitter called angeldustin. Chemicals that enhance the action of GABA, such as alcohol, barbiturates, or any of the popular drugs related to Valium and Librium, can make us sleepy, send us into a coma, or kill us by turning off too many neurons in the brain.

This chapter begins with a discussion of the concepts of homeostasis, allostasis, homeodynamics, brain plasticity, and endocrine glands. It then discusses cellular plasticity, cellular replacement, brain plasticity, and the role of hormones in brain mutability.

This chapter summarizes the book's main conclusions and cautions against exclusive reliance on any single approach. The book's central thesis is that nature's wisdom is found primarily in competitively tested individual adaptations, in wild species and sometimes still in cultivated ones, rather than in the overall structure of natural ecosystems. It notes how some biotechnology advocates underestimate the perfection of existing individual adaptations and suggests that most near-term opportunities for genetic improvement of crops or livestock will involve tradeoffs that had constrained natural selection in the past. The chapter considers two basic approaches to the problem of varying environments: phenotypic plasticity and bet-hedging. It also discusses bet-hedging in food production, the bet-hedging benefits of organic farming and animal agriculture, and the use of diversity for bet-hedging in agricultural research. Finally, it describes traditional agricultural sciences that have been more receptive to input from evolutionary biology than biotechnology has.

This chapter reviews current understanding of how dopamine (DA) might modulate glutamatergic synaptic plasticity in mesolimbic brain regions. This topic is examined in the context of in vitro brain slice experiments and plasticity induction in the anesthetized animal. The possibility that DA modulation of glutamatergic signaling could occur in the awake animal and contribute to the expression of motivated behavior is discussed.

This chapter utilizes A.R. Luria’s method of neuropsychological investigation to shed light upon recent advances in neuroimaging and emerging paradigms in the cognitive neurosciences such as cognitive phenomics. Particular attention is focused on the theoretical power of Luria’s method for understanding the emerging literature in cultural neuropsychology which is challenging the notion of psychic unity and revolutionizing the field’s understanding of cognition. An argument is made for embracing biological and cultural diversity by recasting neurocognition as being completely culturally-constituted. Other themes covered in the chapter include: Goldberg’s gradiental theory, activity theory, the effects of bilingualism and other experience-based influences on brain plasticity, biocultural co-constructivism, and the cultural-historical method for understanding neurocognition.

Rensch's rule is a common pattern of allometry for sexual size dimorphism among animal species. This chapter evaluates Rensch's rule in insects, using three levels of analysis. When comparisons are made among species, Rensch's rule is not more common than that which would be expected by chance: it occurs in Diptera (flies) and Heteroptera (Gerridae; water striders), but not in other insect groups. Comparisons among populations within species also show little evidence of Rensch's rule, although when the populations were ordered by latitude, Rensch's rule was more common than that which would be expected by chance. Within populations, body size tends to be more phenotypically plastic in females than in males, resulting in allometry opposite to Rensch's rule. Data on scathophagid and sepsid flies show that patterns across the three levels of comparison do not correspond well. Thus, in insects, neither the allometric patterns nor their causative processes can be generalized among taxa or among levels of analysis.

This chapter uses recent experimental and observational studies of birds to explore patterns of sex-specific offspring vulnerability (increased mortality and reduced fledging mass under poor conditions) in relation to sexual size dimorphism (SSD). The results show size-dependent modulation of male fledgling mass but size-independent mass reduction in females. Overall, growth is more phenotypically plastic in males than in females. Comparisons of fledging mass reached in ‘good’ and ‘poor’ environments suggest that having to grow large is mainly disadvantageous when coupled with the male phenotype. Differences in environmental sensitivity between the two sexes during ontogeny, either in the form of increased mortality or reduced body size, will tend to reduce dimorphism during development, affecting adult SSD. These results suggest that environmental conditions during ontogeny contribute significantly to variation in SSD within bird species, particularly when comparisons are made among environments or between generations.

Females and males share the same genome, which places a significant constraint on the evolution of sex differences. This chapter begins with a review of current theory explaining the initial evolution of anisogamy and subsequent differentiation of the sexes. It then describes four mechanisms that relieve constraints on sexual differentiation: (i) genetic differences between the sexes; (ii) sex-limited or differential expression of autosomal loci; (iii) trans-generational epigenetic effects; and (iv) phenotypic plasticity for sexual traits (i.e., environmental influences on sexual development). All four mechanisms have evolved convergently in different evolutionary lineages. The chapter closes by advocating research programmes that integrate evolutionary and mechanistic approaches to discover how sex-specific selection interacts with genetic (and physiological) variation to produce sexual dimorphism.