Cytoarchitecture[edit]In humans the six cortical layers of area 10 have been described as having a "remarkably homogeneous appearance".[3] All of them are readily identified. Relative to each other, layer I is thin to medium in width making up 11% of the depth of area 10. Layer II is thin and contains small granular and pyramidal medium to dark staining cells (in terms of Nissl staining) which colors RNA and DNA. The widest layer is III. Its pyramidal neurons are smaller nearer the above layer II than the below layer IV. Like layer II its cells are medium to dark. Layers II and III make up 43% of the cortex depth. Layer IV has clear borders with layers III above and V below and it thin. Its cells are pale to medium in staining. Layer V is wide and contains two distinct sublayers, Va and Vb. The density of cells Va is greater than in Vb and have darker staining. Layers IV and V make up 40% of cortical thickness. Layer VI below layer V and above the white matter contains dark pyramidal and fusiform neurons. It contributes 6% of area 10 thickness.[3]
Area 10 differs from the adjacent Brodmann 9 in that the latter has a more distinct layer Vb and more prominent layer II. Neighbouring Brodmann area 11 compared to area 10 has a thinner layer IV with more prominent layers Va, Vb and II.[3]
Area 10 in humans has the lowest neuron density among primate brains.[3] It is also unusual in that its neurons have particularly extensive dendriticarborization and are highly dense with dendritic spines.[6] This situation has been suggested to enable integration of inputs from multiple areas.[2]
BA 10 is divided into three sub-areas, 10p, 10m and 10r. 10p occupies the frontal pole while the other two cover the ventromedial part of the prefrontal cortex.[7]
Function[edit]Although this region is extensive in humans, its function is poorly understood.[3] Koechlin & Hyafil have proposed that processing of 'cognitive branching' is the core function of the frontopolar cortex.[11] Cognitive branching enables a previously running task to be maintained in a pending state for subsequent retrieval and execution upon completion of the ongoing one. Many of our complex behaviors and mental activities require simultaneous engagement of multiple tasks, and they suggest the anterior prefrontal cortex may perform a domain-general function in these scheduling operations.
take into consideration the influence of the limbic system, to which the frontpolar cortex is connected through the ventromedial prefrontal cortex.
https://en.wikipedia.org/wiki/Brodmann_area_10
OCCIPITAL LOBE
The occipital lobe is the visual processing center of the mammalian brain containing most of the anatomical region of the visual cortex.[1] The primary visual cortex is Brodmann area 17, commonly called V1 (visual one). Human V1 is located on the medial side of the occipital lobe within the calcarine sulcus; the full extent of V1 often continues onto the posterior pole of the occipital lobe. V1 is often also called striate cortex because it can be identified by a large stripe of myelin, the Stria of Gennari. Visually driven regions outside V1 are called extrastriate cortex. There are many extrastriate regions, and these are specialized for different visual tasks, such as visuospatial processing, color differentiation, and motion perception. The name derives from the overlying occipital bone, which is named from the Latin ob, behind, and caput, the head. Bilateral lesions of the occipital lobe can lead to cortical blindness (See Anton's syndrome).
PARIETAL LOBE
The parietal lobe integrates sensory information among various modalities, including spatial sense and navigation (proprioception), the main sensory receptive area for the sense of touch (mechanoreception) in the somatosensory cortex which is just posterior to the central sulcus in the postcentral gyrus,[1] and the dorsal stream of the visual system. The major sensory inputs from the skin (touch, temperature, and pain receptors), relay through the thalamus to the parietal lobe.
http://www.sciencedirect.com/science/article/pii/S0092867414001378
The periaqueductal gray (PAG) (also known as the central gray) is the primary control center for descending pain modulation. It has enkephalin-producing cells that suppress pain.
The periaqueductal grey matter is the grey matter located around the cerebral aqueduct within the tegmentumof the midbrain. It projects to the nucleus raphe magnus, and also contains descending autonomic tracts. The ascending pain and temperature fibers of the spinothalamic tract send information to the PAG via the spinomesencephalic tract (so-named because the fibers originate in the spine and terminate in the PAG, in the mesencephalon or midbrain).
Role in analgesia[edit]Stimulation of the periaqueductal gray matter of the midbrain activates enkephalin-releasing neurons that project to the raphe nuclei in the brainstem. 5-HT (serotonin) released from the raphe nuclei descends to the dorsal horn of the spinal cord where it forms excitatory connections with the "inhibitory interneurons" located in Laminae II (aka the substantia gelatinosa). When activated, these interneurons release either enkephalin or dynorphin (endogenous opioid neurotransmitters), which bind to mu opioid receptors on the axons of incoming C and A-delta fibers carrying pain signals from nociceptors activated in the periphery. The activation of the mu-opioid receptor inhibits the release of substance P from these incoming first-order neurons and, in turn, inhibits the activation of the second-order neuron that is responsible for transmitting the pain signal up the spinothalamic tract to the ventroposteriolateral nucleus (VPL) of the thalamus. The nociceptive signal was inhibited before it was able to reach the cortical areas that interpret the signal as "pain" (such as the anterior cingulate). This is sometimes referred to as the Gate control theory of pain and is supported by the fact that electrical stimulation of the PAG results in immediate and profound analgesia.[1] The periaqueductal gray is also activated by viewing distressing images associated with pain.[2]
Three known kinds of opioid receptors have been identified: mu (μ), kappa (κ) and delta (δ). Synthetic opioid and opioid-derivative drugs activate these receptors (possibly by acting on the PAG directly, where these receptors are densely expressed) to produce analgesia. These drugs include morphine, heroin(diacetylmorphine), pethidine, hydrocodone, oxycodone, and similar pain-reducing compounds.
Area 10 differs from the adjacent Brodmann 9 in that the latter has a more distinct layer Vb and more prominent layer II. Neighbouring Brodmann area 11 compared to area 10 has a thinner layer IV with more prominent layers Va, Vb and II.[3]
Area 10 in humans has the lowest neuron density among primate brains.[3] It is also unusual in that its neurons have particularly extensive dendriticarborization and are highly dense with dendritic spines.[6] This situation has been suggested to enable integration of inputs from multiple areas.[2]
BA 10 is divided into three sub-areas, 10p, 10m and 10r. 10p occupies the frontal pole while the other two cover the ventromedial part of the prefrontal cortex.[7]
Function[edit]Although this region is extensive in humans, its function is poorly understood.[3] Koechlin & Hyafil have proposed that processing of 'cognitive branching' is the core function of the frontopolar cortex.[11] Cognitive branching enables a previously running task to be maintained in a pending state for subsequent retrieval and execution upon completion of the ongoing one. Many of our complex behaviors and mental activities require simultaneous engagement of multiple tasks, and they suggest the anterior prefrontal cortex may perform a domain-general function in these scheduling operations.
take into consideration the influence of the limbic system, to which the frontpolar cortex is connected through the ventromedial prefrontal cortex.
https://en.wikipedia.org/wiki/Brodmann_area_10
OCCIPITAL LOBE
The occipital lobe is the visual processing center of the mammalian brain containing most of the anatomical region of the visual cortex.[1] The primary visual cortex is Brodmann area 17, commonly called V1 (visual one). Human V1 is located on the medial side of the occipital lobe within the calcarine sulcus; the full extent of V1 often continues onto the posterior pole of the occipital lobe. V1 is often also called striate cortex because it can be identified by a large stripe of myelin, the Stria of Gennari. Visually driven regions outside V1 are called extrastriate cortex. There are many extrastriate regions, and these are specialized for different visual tasks, such as visuospatial processing, color differentiation, and motion perception. The name derives from the overlying occipital bone, which is named from the Latin ob, behind, and caput, the head. Bilateral lesions of the occipital lobe can lead to cortical blindness (See Anton's syndrome).
PARIETAL LOBE
The parietal lobe integrates sensory information among various modalities, including spatial sense and navigation (proprioception), the main sensory receptive area for the sense of touch (mechanoreception) in the somatosensory cortex which is just posterior to the central sulcus in the postcentral gyrus,[1] and the dorsal stream of the visual system. The major sensory inputs from the skin (touch, temperature, and pain receptors), relay through the thalamus to the parietal lobe.
http://www.sciencedirect.com/science/article/pii/S0092867414001378
The periaqueductal gray (PAG) (also known as the central gray) is the primary control center for descending pain modulation. It has enkephalin-producing cells that suppress pain.
The periaqueductal grey matter is the grey matter located around the cerebral aqueduct within the tegmentumof the midbrain. It projects to the nucleus raphe magnus, and also contains descending autonomic tracts. The ascending pain and temperature fibers of the spinothalamic tract send information to the PAG via the spinomesencephalic tract (so-named because the fibers originate in the spine and terminate in the PAG, in the mesencephalon or midbrain).
Role in analgesia[edit]Stimulation of the periaqueductal gray matter of the midbrain activates enkephalin-releasing neurons that project to the raphe nuclei in the brainstem. 5-HT (serotonin) released from the raphe nuclei descends to the dorsal horn of the spinal cord where it forms excitatory connections with the "inhibitory interneurons" located in Laminae II (aka the substantia gelatinosa). When activated, these interneurons release either enkephalin or dynorphin (endogenous opioid neurotransmitters), which bind to mu opioid receptors on the axons of incoming C and A-delta fibers carrying pain signals from nociceptors activated in the periphery. The activation of the mu-opioid receptor inhibits the release of substance P from these incoming first-order neurons and, in turn, inhibits the activation of the second-order neuron that is responsible for transmitting the pain signal up the spinothalamic tract to the ventroposteriolateral nucleus (VPL) of the thalamus. The nociceptive signal was inhibited before it was able to reach the cortical areas that interpret the signal as "pain" (such as the anterior cingulate). This is sometimes referred to as the Gate control theory of pain and is supported by the fact that electrical stimulation of the PAG results in immediate and profound analgesia.[1] The periaqueductal gray is also activated by viewing distressing images associated with pain.[2]
Three known kinds of opioid receptors have been identified: mu (μ), kappa (κ) and delta (δ). Synthetic opioid and opioid-derivative drugs activate these receptors (possibly by acting on the PAG directly, where these receptors are densely expressed) to produce analgesia. These drugs include morphine, heroin(diacetylmorphine), pethidine, hydrocodone, oxycodone, and similar pain-reducing compounds.