New Approaches to the Founding of the Sierra Leone Colony, 1786–1808

This special issue of the Journal of Colonialism and Colonial History consists of a forum of innovative ways to consider and reappraise the founding of Britain’s Sierra Leone colony. It originated with a conversation among the two of us and Pamela Scully – all having research interests touching on Sierra Leone in that period – noting that the recent historical inquiry into the origins of this colony had begun to reach an important critical mass. Having long been dominated by a few seminal works, it has begun to attract interest from a number of scholars, both young and established, from around the globe.1 Accordingly, we set out to collect new, exemplary pieces that, taken together, present a variety of innovative theoretical, methodological, and topical approaches to Sierra Leone. We expect that these articles will be of great interest to those invested in the history of that particular time and place. But we also believe that the wider readership of this journal will find that the following articles raise provocative questions, both in method and in interpretation, that hold significant implications for the study of colonialism in its broadest historical context. After all, the establishment of the first British settlement colony in Africa illuminates numerous themes recurring often in our studies of empires before and after: early plans reflecting a mix of colonizing experience and untested metropolitan assumptions; colonization as a physical, cultural, economic, racialized and gendered project; complex relations not only between colonizers and colonized but also the formation of new political, diplomatic, and economic patterns beyond the colony’s borders; and the ambiguous status and culture of settlers as colonizers and clients, to name a few

Continent, Interrupted: Insularity and Adjacency in William Daniell’s Voyage Round Great Britain

Philip Allott has written: “Britain’s oddness is Britain’s oldest tradition.” Britain’s status as an island has often been equated with the oddness, or deployed to explain it, as if that were an unproblematic truism. In his essay “Insular Outsider,” the historian Keith Robbins remarked that “insularity is such a fundamental determinant of British history that it is surprising how little attention historians have paid to it. In century after century, we can find expressions of pride in the mere fact of belonging to a ‘sea-girt’ country.” The now uncommon English word “girt,” meaning surrounded or enclosed by, is closely related to the word “gird,” a verb associated with gripping, supporting, or fastening, and “girth,” a noun referring to the circumference of an object. All of these words connote stoutness, heft, or strength; it is not surprising that a “girder” refers to a supporting beam, made of wood or metal, sturdy enough to hold up a building

Double Dissociation of Spike Timing–Dependent Potentiation and Depression by Subunit-Preferring NMDA Receptor Antagonists in Mouse Barrel Cortex

Spike timing–dependent plasticity (STDP) is a strong candidate for an N-methyl-D-aspartate (NMDA) receptor-dependent form of synaptic plasticity that could underlie the development of receptive field properties in sensory neocortices. Whilst induction of timing-dependent long-term potentiation (t-LTP) requires postsynaptic NMDA receptors, timing-dependent long-term depression (t-LTD) requires the activation of presynaptic NMDA receptors at layer 4-to-layer 2/3 synapses in barrel cortex. Here we investigated the developmental profile of t-LTD at layer 4-to-layer 2/3 synapses of mouse barrel cortex and studied their NMDA receptor subunit dependence. Timing-dependent LTD emerged in the first postnatal week, was present during the second week and disappeared in the adult, whereas t-LTP persisted in adulthood. An antagonist at GluN2C/D subunit–containing NMDA receptors blocked t-LTD but not t-LTP. Conversely, a GluN2A subunit–preferring antagonist blocked t-LTP but not t-LTD. The GluN2C/D subunit requirement for t-LTD appears to be synapse specific, as GluN2C/D antagonists did not block t-LTD at horizontal cross-columnar layer 2/3-to-layer 2/3 synapses, which was blocked by a GluN2B antagonist instead. These data demonstrate an NMDA receptor subunit-dependent double dissociation of t-LTD and t-LTP mechanisms at layer 4-to-layer 2/3 synapses, and suggest that t-LTD is mediated by distinct molecular mechanisms at different synapses on the same postsynaptic neuron

Ubiquitous molecular substrates for associative learning and activity-dependent neuronal facilitation.

Recent evidence suggests that many of the molecular cascades and substrates that contribute to learning-related forms of neuronal plasticity may be conserved across ostensibly disparate model systems. Notably, the facilitation of neuronal excitability and synaptic transmission that contribute to associative learning in Aplysia and Hermissenda, as well as associative LTP in hippocampal CA1 cells, all require (or are enhanced by) the convergence of a transient elevation in intracellular Ca2+ with transmitter binding to metabotropic cell-surface receptors. This temporal convergence of Ca2+ and G-protein-stimulated second-messenger cascades synergistically stimulates several classes of serine/threonine protein kinases, which in turn modulate receptor function or cell excitability through the phosphorylation of ion channels. We present a summary of the biophysical and molecular constituents of neuronal and synaptic facilitation in each of these three model systems. Although specific components of the underlying molecular cascades differ across these three systems, fundamental aspects of these cascades are widely conserved, leading to the conclusion that the conceptual semblance of these superficially disparate systems is far greater than is generally acknowledged. We suggest that the elucidation of mechanistic similarities between different systems will ultimately fulfill the goal of the model systems approach, that is, the description of critical and ubiquitous features of neuronal and synaptic events that contribute to memory induction

Critical Period Plasticity Is Disrupted in the Barrel Cortex of Fmr1 Knockout Mice

SummaryAlterations in sensory processing constitute prominent symptoms of fragile X syndrome; however, little is known about how disrupted synaptic and circuit development in sensory cortex contributes to these deficits. To investigate how the loss of fragile X mental retardation protein (FMRP) impacts the development of cortical synapses, we examined excitatory thalamocortical synapses in somatosensory cortex during the perinatal critical period in Fmr1 knockout mice. FMRP ablation resulted in dysregulation of glutamatergic signaling maturation. The fraction of silent synapses persisting to later developmental times was increased; there was a temporal delay in the window for synaptic plasticity, while other forms of developmental plasticity were not altered in Fmr1 knockout mice. Our results indicate that FMRP is required for the normal developmental progression of synaptic maturation, and loss of this important RNA binding protein impacts the timing of the critical period for layer IV synaptic plasticity