- 15th August
- 26th January
Asked by: aebl-deactivated20130619
Serotonin and prefrontal cortex function: neurons, networks, and circuits.
The Picower Institute for Learning and Memory and Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. email@example.com
Higher-order executive tasks such as learning, working memory, and behavioral flexibility depend on the prefrontal cortex (PFC), the brain region most elaborated in primates. The prominent innervation by serotonin neurons and the dense expression of serotonergic receptors in the PFC suggest that serotonin is a major modulator of its function. The most abundant serotonin receptors in the PFC, 5-HT1A, 5-HT2A and 5-HT3A receptors, are selectively expressed in distinct populations of pyramidal neurons and inhibitory interneurons, and play a critical role in modulating cortical activity and neural oscillations (brain waves). Serotonergic signaling is altered in many psychiatric disorders such as schizophrenia and depression, where parallel changes in receptor expression and brain waves have been observed. Furthermore, many psychiatric drug treatments target serotonergic receptors in the PFC. Thus, understanding the role of serotonergic neurotransmission in PFC function is of major clinical importance. Here, we review recent findings concerning the powerful influences of serotonin on single neurons, neural networks, and cortical circuits in the PFC of the rat, where the effects of serotonin have been most thoroughly studied.
Emotional enhancement of memory: how norepinephrine enables synaptic plasticity.
Department of Psychiatry, McLean Hospital, Harvard Medical School, 115 Mill Street, Belmont, Massachusetts 02478, USA. firstname.lastname@example.org
Changes in synaptic strength are believed to underlie learning and memory. We explore the idea that norepinephrine is an essential modulator of memory through its ability to regulate synaptic mechanisms. Emotional arousal leads to activation of the locus coeruleus with the subsequent release of norepineprine in the brain, resulting in the enhancement of memory. Norepinephrine activates both pre- and post-synaptic adrenergic receptors at central synapses with different functional outcomes, depending on the expression pattern of these receptors in specific neural circuitries underlying distinct behavioral processes. We review the evidence for noradrenergic modulation of synaptic plasticity with consideration of how this may contribute to the mechanisms of learning and memory.
Neurotransmitter roles in synaptic modulation, plasticity and learning in the dorsal striatum.
Laboratory for Integrative Neuroscience, NIAAA/NIH, 5625 Fishers Lane, Rockville, MD 20852, USA. email@example.com
The dorsal striatum is a large forebrain region involved in action initiation, timing, control, learning and memory. Learning and remembering skilled movement sequences requires the dorsal striatum, and striatal subregions participate in both goal-directed (action-outcome) and habitual (stimulus-response) learning. Modulation of synaptic transmission plays a large part in controlling input to as well as the output from striatal medium spiny projection neurons (MSNs). Synapses in this brain region are subject to short-term modulation, including allosteric alterations in ion channel function and prominent presynaptic inhibition. Two forms of long-term synaptic plasticity have also been observed in striatum, long-term potentiation (LTP) and long-term depression (LTD). LTP at glutamatergic synapses onto MSNs involves activation of NMDA-type glutamate receptors and D1 dopamine or A2A adenosine receptors. Expression of LTP appears to involve postsynaptic mechanisms. LTD at glutamatergic synapses involves retrograde endocannabinoid signaling stimulated by activation of metabotropic glutamate receptors (mGluRs) and D2 dopamine receptors. While postsynaptic mechanisms participate in LTD induction, maintained expression involves presynaptic mechanisms. A similar form of LTD has also been observed at GABAergic synapses onto MSNs. Studies have just begun to examine the roles of synaptic plasticity in striatal-based learning. Findings to date indicate that molecules implicated in induction of plasticity participate in these forms of learning. Neurotransmitter receptors involved in LTP induction are necessary for proper skill and goal-directed instrumental learning. Interestingly, receptors involved in LTP and LTD at glutamatergic synapses onto MSNs of the “indirect pathway” appear to have important roles in habit learning. More work is needed to reveal if and when synaptic plasticity occurs during learning and if so what molecules and cellular processes, both short- and long-term, contribute to this plasticity.
(c) 2009. Published by Elsevier Ltd.
Neuro-transmitters in the central nervous system & their implication in learning and memory processes.
This review article gives an overview of a number of central neuro-transmitters, which are essential for integrating many functions in the central nervous system (CNS), such as learning, memory, sleep cycle, body movement, hormone regulation and many others. Neurons use neuro-transmitters to communicate, and a great variety of molecules are known to fit the criteria to be classified as such. A process shared by all neuro-transmitters is their release by excocytosis, and we give an outline of the molecular events and protein complexes involved in this mechanism. Synthesis, transport, inactivation, and cellular signaling can be very diverse when different neuro-transmitters are compared, and these processes are described separately for each neuro-transmitter system. Here we focus on the most well known neuro-transmitters: acetyl-choline, catechol-amines (dopamine and nor-adrenalin), indole-amine (serotonin), glutamate, and gamma-amino-butyric acid (GABA). Glutamate is the major excitatory neuro-transmitter in the brain and its actions are counter-balanced by GABA, which is the major inhibitory substance in the CNS. A balance of neuronal transmission between these two neuro-transmitters is essential to normal brain function. Acetyl-choline, serotonin and catechol-amines have a more modulatory function in the brain, being involved in many neuronal circuits. Apart from summarizing the current knowledge about the synthesis, release and receptor signaling of these transmitters, some disease states due to alteration of their normal neuro-transmission are also described.
Serotonin/dopamine interaction in learning.
Laboratorio de Neurofisiología Experimental, Centro de Investigación Biomédica de Michoacán, Instituto Mexicano del Seguro Social, Morelia, México. firstname.lastname@example.org
Dopamine (DA)-serotonin interactions dealing with learning and memory functions have been apparent from experimental approaches over the past decade. However, since the former evidence showing that these cerebral neurotransmitter systems are involved in the regulation of the same cognitive processes, few experimental studies have been done to further clarify the nature of DA-serotonin interactions for cognitive processes sharing common brain structures. Nevertheless, a regulatory role of 5-HT/DA interactions in cognition and the prefrontal cortex (PFC) and the striatum as a neuroanatomical substrate for these DA/5-HT interactions, are now recognized. Experimental evidence indicates that pharmacological disruption of serotonin neurotransmission results in a facilitative effect on the processing of mnemonic information by cerebral regions under strong, functional DA modulation, such as the striatum and the PFC; on the other hand, increased serotonin neurotransmission appears to have a detrimental effect on cognitive functions integrated in these structures. These effects seem to occur through the interaction of different pre- and postsynaptic DA and serotonin receptor subtypes acting as opposite systems underlying cognitive abilities. Some studies, focused on DA-serotonin interactions underlying the pathophysiology of neurological and psychiatric diseases, which evolve with cognitive dysfunctions in human beings, have shown that drugs that are able to modify DA or serotonin neurotransmission may exert beneficial effects on cognitive functions, even though improvement of motor, mood and behavioural disturbances are the main objectives of pharmacological treatment of these diseases. The complete significance of DA-serotonin interactions in cognitive functions could be addressed by future experimental and clinical studies.
- 31st August
- 14th October
Learning is physical. Learning means the modification, growth, and pruning of our neurons, connections-called synapses- and neuronal networks, through experience…we are cultivating our own neuronal networks.Dr. James Zull, Biochem professor and author of The Art of Changing the Brain – Enriching Teaching by Exploring the Biology of Learning.
- 15th November
PKMZ activity promotes early life traumatic memory formation and retention. CREB (cAMP response element binding) is a protein that is also a transcription factor and is used as a neuronal marker to identify candidate brain areas involved in fear memory formation. It’s active form, phosphorylated CREB (pCREB) regulates protein synthesis necessary for synaptic strengthening during learning. PKMZ is a persistently active, memory-related protein kinase (transfers phosphate group) involved in late phase long-term potentiation (or synaptic strengthening). It has been demonstrated to be required for contextual fear memories in the amygdala but not in the hippocampus. Immediate increase in CREB activity in both the hippocampus and the amygdala, along with PKMZ activity in the amygdala after reconsolidation of fear memories play critical roles in fear learning and long-term memory maintenance. Recently, I’ve become more interested in PKMZ because of its multiple roles, including addiction and cue-related memories… Stopped by this poster at SfN and learned that it ties into my current research as well.
PKMZ activity promotes early life traumatic memory formation and retention.
CREB (cAMP response element binding) is a protein that is also a transcription factor and is used as a neuronal marker to identify candidate brain areas involved in fear memory formation. It’s active form, phosphorylated CREB (pCREB) regulates protein synthesis necessary for synaptic strengthening during learning.
PKMZ is a persistently active, memory-related protein kinase (transfers phosphate group) involved in late phase long-term potentiation (or synaptic strengthening). It has been demonstrated to be required for contextual fear memories in the amygdala but not in the hippocampus.
Immediate increase in CREB activity in both the hippocampus and the amygdala, along with PKMZ activity in the amygdala after reconsolidation of fear memories play critical roles in fear learning and long-term memory maintenance.
Recently, I’ve become more interested in PKMZ because of its multiple roles, including addiction and cue-related memories… Stopped by this poster at SfN and learned that it ties into my current research as well.