Note: MACD can be pronounced as either "MAC-DEE" or "M-A-C-D."
Here is an example chart with the MACD indicator in the lower panel:
ABSTRACT The postsynaptic actions of acetylcholine,
adenosine, yaminobutyric acid, histamine, norepinephrine,
and serotonin were analyzed in human cortical pyramidal cells
maintained in vitro. The actions of these six putative neurotransmitters
converged onto three distinct potassium currents.
Application of acetylcholine, histamine, norepinephrine, or
serotonin all increased spiking by reducing spike-frequency
adaptation, in part by reducing the current that underlies the
slow afterhyperpolarization. In addition, application of muscarinic
receptor agonists to all neurons or of serotonin to
middle-layer cells substantially reduced or blocked the Mcurrent
(a K+ current that is voltage and time dependent).
Inhibition of neuronal firing was elicited by adenosine, baclofen
(a yaminobutyric acid type B receptor agonist), or serotonin
and appeared to be due to an increase in the same potassium
current by all three agents. These data reveal that individual
neuronal currents in the human cerebral cortex are under the
control of several putative neurotransmitters and that each
neurotransmitter may exhibit more than one postsynaptic
action. The specific anatomical connections of these various
neurotransmitter systems, as well as their heterogeneous distribution
of postsynaptic receptors and responses, allows each
to make a specific contribution to the modulation of cortical
activity.
Human cerebral cortical activity may be under the influence
of a large number of neuroactive substances, including acetylcholine
(ACh), adenosine, 'y-aminobutyric acid (GABA),
histamine, norepinephrine, and serotonin (5-HT) (1-8). The
postsynaptic actions of these putative neurotransmitters in
human neocortical neurons are largely unknown, although
the demonstration of muscarinic receptor-mediated block of
the voltage- and time-dependent K+ current known as Mcurrent
(IM) is a notable exception (2). Investigations of
neurotransmitter actions in nonhuman subcortical neurons
have revealed a wide variety of postsynaptic responses as
well as a remarkable convergence and divergence of neurotransmitter
action (9-22). For example, individual neurons in
the rodent hippocampus, thalamus, and substantia nigra
respond to more than one putative neurotransmitter with the
same ionic response (12, 17, 20-22). Conversely, a single
neurotransmitter, such as acetylcholine, can elicit markedly
different ionic responses in separate brain regions and even
in distinct morphological cell classes in the same nucleus
(e.g., refs. 15 and 19).
Convergence and divergence of neurotransmitter action
has important implications for understanding functional systems
in the brain. Not only do the neuronal systems underlying
behavior consist of a number of transmitter pathways,
but each pathway is involved in more than one functional
system (e.g., ref. 22). In addition, many neurological disorders
กิจกรรม ของมนุษย์ที่ เยื่อหุ้มสมอง สมอง อาจ จะอยู่ภายใต้ อิทธิพลของ
ของจำนวนมาก ของสาร neuroactive รวมทั้ง acetylcholine
( ACh ) adenosine , กรด y- aminobutyric ( GABA )
กระ norepinephrine และ serotonin ( 5 -HT ) ( 1-8 )
การกระทำ ของสารสื่อประสาท postsynaptic สมมุติ เหล่านี้ใน
เซลล์ประสาท neocortical มนุษย์ เป็นที่รู้จัก ส่วนใหญ่ แม้ว่า
release ofACh, norepinephrine, 5-HT, and/or histamine may
also lead to an increase in baseline firing rate, although this
excitation will be much less than the enhancement of phasic
barrages of EPSPs because of the marked activation voltage
dependence of IAHp and IM. Furthermore, reduction of these
two currents will have much less effect on inhibitory postsynaptic
potentials or unitary EPSPs because neither of these
results in substantial activation of IAHP or IMP
Convergence and divergence of transmitter actions in the
human cerebral cortex complicates our understanding of the
control and modulation of neuronal activity. It is likely that
in the natural state cortical pyramidal cells are under the
constant influence of a dynamically changing array of neuroactive
substances. Additive and nonadditive interactions
among these substances may allow for subtleties in neuromodulation
that could not otherwise occur. Understanding
these actions and interactions may facilitate the development
of more specific pharmacological therapies for neurological
disorders, such as epilepsy, Alzheimer disease, and agerelated
cognitive decline.
We thank Dr. Dennis Spencer for his collaboration in this project
and the patients for their informed consent to the use of the tissue.
This work was supported by a grant from the National Institute of
Neurological and Communicative Disorders and Stroke, fellowships
from the Klingenstein Foundation (D.A.M.), and the American
Epilepsy Foundation (A.W.), and by the Jacob Javits Center in
Neuroscience.
1. Palacios, J. M., Probst, A. & Cortes, R. (1986) Trends Neurosci. 9,
284-289.
2. Halliwell, J. V. (1986) Neurosci. Lett. 67, 1-6.
3. Pazos, A., Probst, A. & Palacois, J. M. (1987) Neuroscience 21,
97-122.
4. Fastbom, J., Pazos, A., Probst, A. &