Interpersonal Neurobiology and Attachment

Author(s):  
Arlene Montgomery

The attachment phenomenon is increasingly the focus of many social work interventions. Biologically described, differentiated types of attachment relationships result from qualities of repetitive interpersonal brain-to-brain encounters with caregivers that affect variations in emotional/affective arousal regulation; this research takes place within the field of interpersonal neurobiology. The particular focus of this entry is implicit and explicit manifestations of certain structures and functions of the brain and nervous system critical to the bio-regulation of emotions. In-born emotional circuitry is sculpted by postnatal caregiving, resulting in a pattern of emotion regulation that leads to certain attachment types. Although there is no attachment circuit per se, emotional circuits in the low brain can work together with other parts of the brain to create various types of attachment. Neurobiological influences act on the development of attachment styles during childhood that may persist into adulthood are briefly reviewed. Attachment research and often subtle biological arousal considerations are also mentioned. Over the years since John Bowlby first began to contribute his work on attachment, research has highlighted, more and more, the various biological aspects. These include the profound biological significance of the circular relationship between separation, responses to separation, and resulting attachment templates. The roles in the attaching process of neuroception, mirror neurons, transfer of affect, and long-term potentiation are described. Selected treatment theories, primarily from the social work literature, are examined for their implicit focus on aspects of the neurobiology of attachment relationships.

2017 ◽  
Vol 23 (6) ◽  
pp. 587-604 ◽  
Author(s):  
Julien Gibon ◽  
Philip A. Barker

Neurotrophins have been intensively studied and have multiple roles in the brain. Neurotrophins are first synthetized as proneurotrophins and then cleaved intracellularly and extracellularly. Increasing evidences demonstrate that proneurotrophins and mature neurotrophins exerts opposing role in the central nervous system. In the present review, we explore the role of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT3), and neurotrophin 4 (NT4) and their respective proform in cellular processes related to learning and memory. We focused on their roles in synaptic activity and plasticity in the brain with an emphasis on long-term potentiation, long-term depression, and basal synaptic transmission in the hippocampus and the temporal lobe area. We also discuss new findings on the role of the Val66Met polymorphism on the BDNF propeptide on synaptic activity.


1999 ◽  
Vol 82 (4) ◽  
pp. 2024-2028 ◽  
Author(s):  
Hongyan Wang ◽  
John J. Wagner

The activity history of a given neuron has been suggested to influence its future responses to synaptic input in one prominent model of experience-dependent synaptic plasticity proposed by Bienenstock, Cooper, and Munro (BCM theory). Because plasticity of synaptic plasticity (i.e., metaplasticity) is similar in concept to aspects of the BCM proposal, we have tested the possibility that a form of metaplasticity induced by a priming stimulation protocol might exhibit BCM-like characteristics. CA1 field excitatory postsynaptic potentials (EPSPs) obtained from rat hippocampal slices were used to monitor synaptic responses before and after conditioning stimuli (3–100 Hz) of the Schaffer collateral inputs. A substantial rightward shift (>5-fold) in the frequency threshold between long-term depression (LTD) and long-term potentiation (LTP) was observed <1 h after priming. This change in the LTD/P crossover point occurred at both primed and unprimed synaptic pathways. These results provide new support for the existence of a rapid, heterosynaptic, experience-dependent mechanism that is capable of modifying the synaptic plasticity phenomena that are commonly proposed to be important for developmental and learning/memory processes in the brain.


2016 ◽  
Vol 23 (3) ◽  
pp. 221-231 ◽  
Author(s):  
Victor Briz ◽  
Michel Baudry

Although calpain was proposed to participate in synaptic plasticity and learning and memory more than 30 years ago, the mechanisms underlying its activation and the roles of different substrates have remained elusive. Recent findings have provided evidence that the two major calpain isoforms in the brain, calpain-1 and calpain-2, play opposite functions in synaptic plasticity. In particular, while calpain-1 activation is the initial trigger for certain forms of synaptic plasticity, that is, long-term potentiation, calpain-2 activation restricts the extent of plasticity. Moreover, while calpain-1 rapidly cleaves regulatory and cytoskeletal proteins, calpain-2-mediated stimulation of local protein synthesis reestablishes protein homeostasis. These findings have important implications for our understanding of learning and memory and disorders associated with impairment in these processes.


2010 ◽  
Vol 391 (4) ◽  
Author(s):  
Shigetaka Yoshida

Abstract Klk8 is a tryptic serine protease with limited substrate specificity. Klk8 mRNA is expressed in many developing organs, whereas its expression is confined to limited regions, including the hippocampus, in adults. In the hippocampus, Klk8 is involved in activity-dependent synaptic changes such as long-term potentiation, which was found to be suppressed in Klk8 knockout (KO) mice. Oligodendrocytes only expressed Klk8 mRNA after injury to the central nervous system. The epidermis of the skin is one of the tissues that exhibits a high level of KLK8 expression. Klk8 might be involved in desquamation through the degradation of adhesive molecules that connect layers of the epidermis. Klk8 might thus be involved in tissue development and rearrangement.


2020 ◽  
Author(s):  
Rachael L. Sumner ◽  
Meg J. Spriggs ◽  
Alexander D. Shaw

AbstractNeuroplasticity is essential to learning and memory in the brain; it has therefore also been implicated in numerous neurological and psychiatric disorders, making measuring the state of neuroplasticity of foremost importance to clinical neuroscience. Long-term potentiation (LTP) is a key mechanism of neuroplasticity and has been studied extensively, and invasively in non-human animals. Translation to human application largely relies on the validation of non-invasive measures of LTP. The current study provides validation for the use of a thalamocortical computational model of visual cortex for investigating and replicating interlaminar connectivity changes using non-invasive EEG recording of humans, and a commonly used visual sensory LTP paradigm. The model demonstrated remarkable accuracy recapitulating post-tetanus changes including increased excitatory connectivity from thalamus to layer IV and from layer IV to II/III. The findings also further validate visual sensory induced LTP and evoked potential modulation for measuring of the state of LTP in cortex.


2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Efrat Shavit-Stein ◽  
Amir Dori ◽  
Marina Ben Shimon ◽  
Shany Guly Gofrit ◽  
Nicola Maggio

The cholinergic system plays a fundamental role in learning and memory. Pharmacological activation of the muscarinic receptor M1R potentiates NMDA receptor activity and induces short-term potentiation at the synapses called muscarinic LTP, mLTP. Dysfunction of cholinergic transmission has been detected in the settings of cognitive impairment and dementia. Systemic inflammation as well as neuroinflammation has been shown to profoundly alter synaptic transmission and LTP. Indeed, intervention which is aimed at reducing neuroinflammatory changes in the brain has been associated with an improvement in cognitive functions. While cognitive impairment caused either by cholinergic dysfunction and/or by systemic inflammation suggests a possible connection between the two, so far whether systemic inflammation affects mLTP has not been extensively studied. In the present work, we explored whether an acute versus persistent systemic inflammation induced by LPS injections would differently affect the ability of hippocampal synapses to undergo mLTP. Interestingly, while a short exposure to LPS resulted in a transient deficit in mLTP expression, a longer exposure persistently impaired mLTP. We believe that these findings may be involved in cognitive dysfunctions following sepsis and possibly neuroinflammatory processes.


Author(s):  
Scott Giacomucci

AbstractThe rapidly emerging neuroscience research continues to validate the practice of social work, group therapy, and psychodrama. The centrality of human relationships is being supported by the field of interpersonal neurobiology. New technologies allow us to learn more about the brain and the ways it is impacted by adversity, healing, and action. The importance of safety, connection, integration, and a strength-s-based approach is supported in the neuroscience literature. The neurobiological mechanisms which promote change in psychodrama are becoming clearer. Furthermore, the words of contemporary neuroscientists appear to echo Moreno’s writings of sociometry and psychodrama nearly a decade earlier.


Author(s):  
Arianna Maffei

Synaptic connections in the brain can change their strength in response to patterned activity. This ability of synapses is defined as synaptic plasticity. Long lasting forms of synaptic plasticity, long-term potentiation (LTP), and long-term depression (LTD), are thought to mediate the storage of information about stimuli or features of stimuli in a neural circuit. Since its discovery in the early 1970s, synaptic plasticity became a central subject of neuroscience, and many studies centered on understanding its mechanisms, as well as its functional implications.


Author(s):  
Orlando B.C. Swayne ◽  
John C. Rothwell

Non-invasive brain stimulation methods such as transcranial magnetic stimulation and transcranial direct current stimulation allow us to interact directly with activity in neural circuits in the brain. Work has shown that these methods can also lead to changes in the effectiveness of synaptic connections, probably through mechanisms related to long-term potentiation/depression as described in animal preparations. Similar processes of synaptic plasticity are involved in many neurological rehabilitation techniques involve learning how to optimize performance in the face of neurological disease or injury. Thus combining non-invasive stimulation with rehabilitation may therefore be able to enhance plasticity and speed the response to therapy. We describe the techniques involved and summarize some of the recent clinical trials that have been conducted using this approach.


2002 ◽  
Vol 9 (4) ◽  
pp. 217-232 ◽  
Author(s):  
Jorge A. Bergado ◽  
William Almaguer

Aging affects all systems, but the brain seems to be particularly vulnerable to the action of negative, age-dependent factors. A gradual loss of memory functions is one of the earliest and most widespread consequences of brain aging. The causes for such impairment are still unclear. Long-term potentiation (LTP) is one form of neural plasticity, which has been proposed as the cellular correlate for memory. LTP is affected by aging, and such alteration might be causally related to memory dysfunction. In the present paper, we review the evidence sustaining the existence of a causal link between cognitive and LTP impairments, as well as the possible mechanisms involved. New results indicate a possible involvement of a deficient reinforcement of LTP by affective influences.


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