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The goal of the Bain's lab is to understand how physiological and behavioural challenges lead to long-term changes in neural circuitry. They focus on neurons that coordinate an organism's response to stress, with a particular interest in clarifying how the molecules released at the onset of a stressful stimulus leave a lasting imprint on how ‘stress-relevant' ciruitry functions. Within this context, they conduct experiments that will allow them to understand the fundamental rules that govern cell to cell communication within the hypothalamus and elucidate the molecular machinery that contributes to changes in synaptic function which, in turn, may be critical for changing network output.
They currently explore three lines of investigation:
• They have demonstrated that glial cells can permanently increase the strength of excitatory, glutamatergic synapses in the paraventricular nucleus of the hypothalamus. They are now focused on elucidating the extent of this novel interaction between glial cells and neurons and will examine the role of this interaction during physiological challenges.
• Based on new observations that homeostatic set points in vivo are defended by metaplastic synaptic changes, they are now exploring additional mechanisms through which the activity-dependent release of retrograde signals impacts synaptic transmission.
• The inhibitory synapses onto neuroendocrine parvocellular neurons, the "command" neurons of the stress axis, exhibit remarkable state-dependent plasticity. They have shown that the onset of stress is accompanied by a loss of GABA inhibition due to a collapse of transmembrane chloride gradients. They are now pursuing the cellular and molecular mechanisms that underline this remarkable switch. Furthermore, we are exploring the impact of repetitive stress on synaptic function/plasticity in this system.
They use a number of experimental techiques to answer the above questions. These include, but are not limited to: patch clamp recordings from neurons in brain slices for the measurement of excitatory and inhibitory synaptic currents; UV laser uncaging of bioactive molecules; immunohistochemistry for the labeling of receptors and neuronal subpopulations.
Stress and the synapse [electronic resource] / Jaideep Bains.
Series:
Neuroscience seminar series
Author:
Bains, Jaideep. National Institutes of Health (U.S.)
Publisher:
[Bethesda, Md. : National Institutes of Health, 2012]
Other Title(s):
Neuroscience seminar series
Abstract:
(CIT): Neuroscience Seminar Series The goal of the Bain's lab is to understand how physiological and behavioural challenges lead to long-term changes in neural circuitry. They focus on neurons that coordinate an organism's response to stress, with a particular interest in clarifying how the molecules released at the onset of a stressful stimulus leave a lasting imprint on how "stress-relevant' ciruitry functions. Within this context, they conduct experiments that will allow them to understand the fundamental rules that govern cell to cell communication within the hypothalamus and elucidate the molecular machinery that contributes to changes in synaptic function which, in turn, may be critical for changing network output. They currently explore three lines of investigation: .They have demonstrated that glial cells can permanently increase the strength of excitatory, glutamatergic synapses in the paraventricular nucleus of the hypothalamus. They are now focused on elucidating the extent of this novel interaction between glial cells and neurons and will examine the role of this interaction during physiological challenges. .Based on new observations that homeostatic set points in vivo are defended by metaplastic synaptic changes, they are now exploring additional mechanisms through which the activity-dependent release of retrograde signals impacts synaptic transmission. .The inhibitory synapses onto neuroendocrine parvocellular neurons, the "command" neurons of the stress axis, exhibit remarkable state-dependent plasticity. They have shown that the onset of stress is accompanied by a loss of GABA inhibition due to a collapse of transmembrane chloride gradients. They are now pursuing the cellular and molecular mechanisms that underline this remarkable switch. Furthermore, we are exploring the impact of repetitive stress on synaptic function/plasticity in this system. They use a number of experimental techiques to answer the above questions. These include, but are not limited to: patch clamp recordings from neurons in brain slices for the measurement of excitatory and inhibitory synaptic currents; UV laser uncaging of bioactive molecules; immunohistochemistry for the labeling of receptors and neuronal subpopulations. For more information go to http://neuroseries.info.nih.gov.
