From a functional stand-point, the brain and its two hemispheric constituents may be divided into
Four Major Components:
SENSORY INPUT ENTERS THE PRIMARY SENSORY ZONES, is elaborated in the Secondary Zones, and is then integrated in the Tertiary Zones of the sensory (or Posterior) unit of the brain. For an action to be executed, activity from the posterior tertiary sensory zones is sent to the tertiary zone of the motor, or Frontal Unit of the brain, to the secondary zone, and then to the primary motor zone, where execution is initiated.
Secondary Sensory Zones (higher zones of the Neocortex), process the more abstract features from the sensory projections of the primary zones. In the case of vision, for example, the secondary cortex encompasses Brodmann's areas 18, 19, 20, 21, and 37. For audition, Brodmann's areas 22, and 42. The secondary zones retain the modality (i.e., vision, or audition) of the information, but have a less fixed topographic organization (i.e., for vision, the remapping of the retinal field).
Habituation -
at the molecular level,
is the result of progressive closure of the calcium channels in the terminal neural membrane. In the process, much smaller than normal amounts of calcium diffuse into this terminal when action potentials occur, and much less transmitter is therefore released because it is the calcium entry that is the stimulus for transmitter release from the primary input sensory terminal.
Conversely, noxious stimuli excite the
Facilitator Terminal at the same time that the sensory terminal is stimulated. Instead of the transmitted signal becoming progressively weaker, the ease of transmission becomes stronger and will remain strong for hours, days or even weeks without any further stimulation on the facilitator terminal. Therefore noxious stimuli cause the memory pathway to become Facilitated for days to weeks thereafter. Once habituation has occured, the synapses can become facilitated very rapidly with only a few noxious stimuli!
The biochemical mechanism for
Facilitation is
as follows:
Stimulation of the facilitator neuron along with the sensory neuron causes release of serotonin from the facilitator cell onto the sensory presynaptic terminal.
Serotonin activates the
Serotonin Receptor site (a specialized protein on the post-synaptic membrane of the sensory neuron), which in turn actives intracellular adenylate cyclase, causing the production of
cyclic-Adenosyn Mono Phosphate (cAMP) inside of the sensory neuron. cAMP activates a protein kinase which blocks the release of potassium ions from inside of the cell. This subsiquently prolongs the normal mechanism for recovery of the cell from the action potential. The prolonged action potential causes prolonged activation of the calcium ion channels, allowing larger amounts of calcium ions to enter the sensory cell. The greatly increased concentration of calcium ions within the cell causes a greatly increased amount of transmitter to be release, thereby, greatly facilitating synaptic transmission.
The state of Deep Trance effects the Sympathetic Nervous System, by its stimulation of the Beta-2 (ß-2) adrenergic receptors, while inhibiting the effects of sympathetic Alpha receptor stimulation! This causes a reduction in blood pressure, a decrease in bleeding and reduction in awareness of pain.
The Sympathomimetic Effects of Deep Trance Cause:
- Vasodilitation
- Intestinal relaxation
- Uterine relaxation
- Bronchodilitation
- Calorigenesis
- Glycogenolysis
- Bladder relaxation
- Coronary artery dilation, and
- Arteriole dilation in skeletal muscles.