- research article | New Research, Neuronal Excitability Metaplastic Regulation of CA1 Schaffer Collateral Pathway Plasticity by Hebbian MGluR1a-Mediated Plasticity at Excitatory Synapses onto Somatostatin-Expressing Interneurons
Published August 12, 2015
- research article | New Research, Neuronal Excitability Variability in State-Dependent Plasticity of Intrinsic Properties during Cell-Autonomous Self-Regulation of Calcium Homeostasis in Hippocampal Model Neurons
Published August 11, 2015
- research article | New Research, Neuronal Excitability Inhibitory Plasticity Permits the Recruitment of CA2 Pyramidal Neurons by CA3
Published July 15, 2015
- research article | New Research, Neuronal Excitability Leptin Induces a Novel Form of NMDA Receptor-Dependent LTP at Hippocampal Temporoammonic-CA1 Synapses
Hippocampal CA1 pyramidal neurons receive two anatomically distinct glutamatergic inputs that have distinct roles in learning and memory. The hormone leptin markedly influences excitatory synaptic transmission at the indirect Schaffer-collateral pathway to CA1 neurons.
Published May 26, 2015
- research article | New Research, Neuronal Excitability PKA and cAMP/CNG Channels Independently Regulate the Cholinergic Ca2+-Response of Drosophila Mushroom Body Neurons
The mushroom bodies (MBs) are the most prominent structures in adult Drosophila brain. They have been involved in several crucial functions, such as learning and memory, sleep, locomotor activity, and decision making.
Published April 17, 2015
- research article | New Research, Neuronal Excitability Role for Endogenous BDNF in Endocannabinoid-Mediated Long-Term Depression at Neocortical Inhibitory Synapses
Endocannabinoids and neurotrophins, particularly brain-derived neurotrophic factor (BDNF), are potent neuromodulators that play critical roles in many behavioral and physiological processes. Disruption of either BDNF or endocannabinoid signaling is associated with an overlapping set of neurologic and psychiatric diseases, and both systems are currently major targets for the development of novel therapeutics, particularly in relation to depression, anxiety, autism, and schizophrenia.
Published March 24, 2015
- research article | New Research, Neuronal Excitability What Elements of the Inflammatory System Are Necessary for Epileptogenesis In Vitro?
The inflammatory and central nervous systems share many signaling molecules, compromising the utility of traditional pharmacological and knockout approaches in defining the role of inflammation in CNS disorders such as epilepsy. In an in vitro model of post-traumatic epileptogenesis, the development of epilepsy proceeded in the absence of the systemic inflammatory system, and was unaffected by removal of cellular mediators of inflammation, including macrophages and T-lymphocytes.
Published March 3, 2015
- research article | New Research, Neuronal Excitability Presynaptic NR2A-Containing NMDARs Are Required for LTD between the Amygdala and the Perirhinal Cortex: A Potential Mechanism for the Emotional Modulation of Memory?
Emotional events are better remembered than emotionally neutral events. The ability of memory enhancement by emotion is dependent on amygdala-mediated alterations of synaptic activity.
Published February 25, 2015
- research article | New Research, Neuronal Excitability Acetylcholine Acts through Nicotinic Receptors to Enhance the Firing Rate of a Subset of Hypocretin Neurons in the Mouse Hypothalamus through Distinct Presynaptic and Postsynaptic Mechanisms
Neurons expressing the neuropeptide hypocretin regulate many behavioral functions, including sleep, motivation, and behaviors related to addiction. The ability of nicotine to stimulate nicotinic acetylcholine receptors (nAChRs) is essential for its addictive properties, but little is known about whether, and how, nicotine and the endogenous neurotransmitter acetylcholine affect hypocretin neurons.
Published February 18, 2015
- research article | New Research, Neuronal Excitability Dynamic Input Conductances Shape Neuronal Spiking
Reliable neuron activity is ensured by a tight regulation of the ion channels that resides in the neuron’s membrane. Understanding the causal mechanisms that relate this regulation to physiological and pathological neuronal activity is a necessary step for developing efficient therapies for neurological diseases associated with abnormal nervous system activity.
Published February 18, 2015