Stress Impairs Prefrontal Cortex Function: Why Stress Can Produce an ADHD-Like Profile
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1 Stress Impairs Prefrontal Cortex Function: Why Stress Can Produce an ADHD-Like Profile Amy F.T. Arnsten, Ph.D. Professor of Neurobiology Yale University School of Medicine
2 SOME IMAGES HAVE BEEN REMOVED TO REDUCE THE MEMORY REQUIREMENTS FOR THIS PRESENTATION
3 Disclosures Dr. Arnsten and Yale University have license agreements with: Shire Pharmaceuticals for the development of guanfacine for the treatment of ADHD, and Marinus Pharmaceuticals for the development of chelerythrine for the treatment of bipolar disorder, schizophrenia, PTSD and related illnesses
4 Goals of Talk Learn about the prefrontal cortex, and why dysfunction of the prefrontal cortex produces symptoms of Attention Deficit Hyperactivity Disorder (ADHD). Learn about how brain cells (neurons) in prefrontal cortex communicate with each other, and how they form networks that allow high order regulation of behavior and thought. Learn about how sensitive prefrontal networks are to chemicals released according to our state of arousal, and how either too little (fatigue, boredom) or too much (stress) of these chemicals impairs prefrontal abilities. Understand how chemical changes in the prefrontal cortex produced by genetic and/or environmental insults associated with ADHD, bipolar disorder, schizophrenia and lead poisoning lead to weakened prefrontal function, and how optimal use of medications may be able to correct some of these insults.
5 Prefrontal Cortex
6 Prefrontal Cortex The most highly evolved brain region
7 Prefrontal Cortex Our Mental Sketchpad Our Central Executive
8 Prefrontal Cortex The ability to represent information that is not currently in the environment, and use that information to thoughtfully guide attention, actions and emotions.
9 Prefrontal Cortex Inhibits inappropriate behaviors, thoughts, and emotions Inhibits interference from external and internal distractions
10 Prefrontal Cortex Allows us to make decisions, and have insight and judgment Allows us to organize and plan for the future
11 Prefrontal Cortex Understands what others are thinking (Theory of Mind) Monitors errors, knows what is real vs. imagined
12 Prefrontal Cortex Allows us to delay gratification Allows us to multi-task and sort through high levels of information
13 Prefrontal Cortex Increasingly needed for success in the Information Age and in school
14 Functional Organization of Prefrontal Cortex
15 Functional Organization of Prefrontal Cortex Regulates attention and thoughts
16 Functional Organization of Prefrontal Cortex Regulates attention and thoughts Regulates motor behavior
17 Functional Organization of Prefrontal Cortex Regulates attention and thoughts Regulates motor behavior Regulates emotions, social behavior
18 Functional Organization of Prefrontal Cortex projections to motor cortices projections to sensory cortices Regulates attention and thoughts Regulates motor behavior projections lower brain systems that create motor patterns projections to primitive brain regions that generate emotion Regulates emotions, social behavior
19 Functional Organization of Prefrontal Cortex In humans, also organized by hemisphere Regulates attention and thoughts Regulates motor behavior Regulates emotions, social behavior
20 Functional Organization of Prefrontal Cortex Regulates attention and thoughts LEFT: GENERATION Regulates motor behavior Regulates emotions, social behavior
21 Functional Organization of Prefrontal Cortex language Regulates attention and thoughts LEFT: GENERATION Regulates motor behavior Regulates emotions, social behavior
22 Functional Organization of Prefrontal Cortex Regulates attention and thoughts RIGHT: INHIBITION Regulates motor behavior Regulates emotions, social behavior
23 Lesions to Right PFC Produce Symptoms of Disinhibition RIGHT: INHIBITION
24 Lesions to Right PFC Produce Symptoms of Disinhibition distractibility, poor sustained attention, disorganized, poor planning RIGHT: INHIBITION
25 Lesions to Right PFC Produce Symptoms of Disinhibition distractibility, poor sustained attention, disorganized, poor planning RIGHT: INHIBITION poor impulse control, locomotor hyperactivity
26 Lesions to Right PFC Produce Symptoms of Disinhibition distractibility, poor sustained attention, disorganized, poor planning RIGHT: INHIBITION poor impulse control, locomotor hyperactivity oppositionality, aggression
27 Lesions to Right PFC Produce Symptoms of Disinhibition Symptoms of ADHD distractibility, poor sustained attention, disorganized, poor planning RIGHT: INHIBITION poor impulse control, locomotor hyperactivity oppositionality, aggression
28 Lesions to Right PFC Produce Symptoms of Disinhibition Symptoms of ADHD distractibility, poor sustained attention, disorganized, poor planning RIGHT: INHIBITION poor impulse control, locomotor hyperactivity Symptoms of conduct disorder oppositionality, aggression
29 ALTERED PFC FUNCTION IN ADHD Rubia et al, 1999 Reduced activityespecially in right hemisphere Schulz et al, 2004
30 ALTERED PFC STRUCTURE IN ADHD Mostofsky et al, 2002 Reduced volume Makris et al, 2007 Disorganized white matter pathways
31 Lesions to Right PFC Produce Symptoms of Disinhibition Severe distractibility, and inability to sustain attention, fractionated thought, disorganized, loss of insight, delusions poor impulse control, locomotor hyperactivity RIGHT: INHIBITION The manic phase of bipolar disorder is also associated with severe right prefrontal cortical dysfunction Poor reality testing, error monitoring disinhibited emotions
32 ALTERED PFC ACTIVITY AND STRUCTURE IN MANIA Blumberg et al, 1999
33 Prefrontal cortex regulates behavior, thought and feelings through networks of interconnected neurons
34 Networks of prefrontal pyramidal cells represent stimuli (e.g. I left my math book 90º from the TV), and represent goals and rules (I will finish my homework, I must sit in my seat). Network activity is used to guide correct choices, and to inhibit inappropriate responses. Networks maintain their activity through recurrent excitation ; i.e. the cells excite each other in the absence of environmental stimulation.
35 Irrelevant information 265º 270º 275º Neurons also receive inputs from nonpreferred neurons, i.e. noise
36 How neurons communicate
37 PARTS OF THE NEURON
38 PARTS OF THE NEURON Cell body
39 PARTS OF THE NEURON Dendrites- Receive messages Cell body
40 PARTS OF THE NEURON Dendritic spines- Specialized for receiving messages, can readily change size/shape, spines can be lost or added Dendrites- Receive messages Cell body
41 PARTS OF THE NEURON Dendritic spines- Specialized for receiving messages, can readily change size/shape, spines can be lost or added Dendrites- Receive messages Cell body Axon- Sends messages Cell fires off an action potential
42 PARTS OF THE NEURON Dendritic spines- Specialized for receiving messages, can readily change size/shape, spines can be lost or added Dendrites- Receive messages Cell body Axon- Sends messages Cell fires off an action potential Axon terminal- Communicates with next cell Full of packets of chemical messages
43 PARTS OF THE NEURON A single neuron in the human prefrontal cortex often receives hundreds of thousands of connections
44 TYPES OF NEURONS
45 TYPES OF NEURONS excitatory cell
46 TYPES OF NEURONS Inhibitory cell excitatory cell
47 A NETWORK OF EXCITATORY NEURONS
48 A NETWORK OF EXCITATORY NEURONS
49 A NETWORK OF EXCITATORY NEURONS
50 A NETWORK OF EXCITATORY NEURONS
51 A NETWORK OF EXCITATORY NEURONS
52 A NETWORK OF EXCITATORY NEURONS
53 A NETWORK OF EXCITATORY NEURONS
54 A NETWORK OF EXCITATORY NEURONS
55 A NETWORK OF EXCITATORY NEURONS
56 A NETWORK OF EXCITATORY NEURONS
57 A NETWORK OF EXCITATORY NEURONS
58 A NETWORK OF EXCITATORY NEURONS
59 A NETWORK OF EXCITATORY NEURONS
60 A NETWORK OF EXCITATORY NEURONS
61 A NETWORK OF EXCITATORY NEURONS
62 A NETWORK OF EXCITATORY NEURONS
63 A NETWORK OF EXCITATORY NEURONS
64 Neurons Communicate Using Chemical Signals axon terminal spine synapse
65 Neurons Communicate Using Chemical Signals PFC dendrite Axon from excitatory neuron packets of neurotransmitter receptors spine
66 Neurons Communicate Using Chemical Signals PFC dendrite Axon from excitatory neuron spine
67 Neurons Communicate Using Chemical Signals PFC dendrite Axon from excitatory neuron spine
68 Neurons Communicate Using Chemical Signals PFC dendrite Axon from excitatory neuron spine
69 Neurons Communicate Using Chemical Signals PFC dendrite Axon from excitatory neuron excitatory spine
70 Neurons Communicate Using Chemical Signals PFC dendrite Axon from excitatory neuron excitatory spine
71 Neurons Communicate Using Chemical Signals PFC dendrite Axon from excitatory neuron excitatory spine If there are enough excitatory inputs, the axon fires and action potential
72 INHIBITORY NEURONS STOP CELL FIRING axon terminal
73 Neurons Communicate Using Chemical Signals Input from inhibitory neuron PFC dendrite spine
74 Neurons Communicate Using Chemical Signals Input from inhibitory neuron PFC dendrite spine
75 Neurons Communicate Using Chemical Signals Input from inhibitory neuron PFC dendrite spine
76 Neurons Communicate Using Chemical Signals Inhibitory: makes neuron stop firing Input from inhibitory neuron PFC dendrite spine
77 Neurons Communicate Using Chemical Signals Inhibitory: makes neuron stop firing Input from inhibitory neuron PFC dendrite Not the focus of today s talk spine
78 NEUROMODULATORS HAVE INDIRECT INFLUENCES
79 NEUROMODULATORS HAVE INDIRECT INFLUENCES e.g. norepinephrine, dopamine and other chemicals released based on our state of arousal
80 Neurons Communicate Using Chemical Signals PFC dendrite spine
81 Neurons Communicate Using Chemical Signals Neuromodulator PFC dendrite spine
82 Neurons Communicate Using Chemical Signals Neuromodulator Norepinephrine- A substance released when an interesting stimulus occurs, and according to our state of arousal PFC dendrite spine
83 Neurons Communicate Using Chemical Signals Neuromodulator Norepinephrine PFC dendrite spine
84 Neurons Communicate Using Chemical Signals Neuromodulator PFC dendrite Norepinephrine receptor α2a spine
85 Neurons Communicate Using Chemical Signals Neuromodulator PFC dendrite Ion channelan open pore α2a spine
86 Neurons Communicate Using Chemical Signals Neuromodulator PFC dendrite Ion channel open α2a spine
87 Neurons Communicate Using Chemical Signals Neuromodulator PFC dendrite Norepinephrine binds to receptor- Ion channel closes α2a spine
88 Neurons Communicate Using Chemical Signals Neuromodulator PFC dendrite Norepinephrine binds to receptor- Ion channel closed α2a spine
89 ELECTRON MICROSCOPY OF α2a RECEPTORS AND HCN ION CHANNELS ON THE SPINES (sp) OF PFC NEURONS
90 Summary: Networks maintain representations through recurrent excitation ; i.e. the cells excite each other to maintain firing even with no stimulation from the outside world. The neurons in the networks interact through synapses on dendritic spines. The spines in prefrontal cortex often contain receptors for neuromodulators such as norepinephrine, and contain ion channels that can alter the strength of input connections onto the spine. The chemical environment influences whether PFC cells can engage with correct networks, and disconnect from irrelevant inputs.
91 PFC network connections are very sensitive to their chemical environment
92
93 Goldilocks
94 Prefrontal Cortex
95
96 Just right Too little Too much
97 Just right Too little Too much
98 Just right Too little Too much Soup = Norepinephrine (NE) and dopamine (DA) These chemicals are released in the prefrontal cortex according to our state of arousal. Norepinephrine and dopamine are part of a family of chemicals called catecholamines
99 The Inverted U
100 The Prefrontal Cortex Requires A Proper Level of Catecholamines for Optimal Function
101 The Prefrontal Cortex Requires A Proper Level of Catecholamines for Optimal Function PFC Abilities
102 The Prefrontal Cortex Requires A Proper Level of Catecholamines for Optimal Function Focused Organized Responsible Distracted Disorganized Forgetful Disinhibited PFC Abilities
103 The Prefrontal Cortex Requires A Proper Level of Catecholamines for Optimal Function Focused Organized Responsible Distracted Disorganized Forgetful Disinhibited PFC Abilities levels of catecholamine release increase with arousal state
104 The Prefrontal Cortex Requires A Proper Level of Catecholamines for Optimal Function levels of catecholamine release increase with arousal state
105 The Prefrontal Cortex Requires A Proper Level of Catecholamines for Optimal Function Inadequate catecholamines fatigued bored levels of catecholamine release increase with arousal state
106 The Prefrontal Cortex Requires A Proper Level of Catecholamines for Optimal Function Moderate amounts of NE engage α2a receptors Moderate amounts of dopamine stimulate some D1 receptors alert interested levels of catecholamine release increase with arousal state
107 The Prefrontal Cortex Requires A Proper Level of Catecholamines for Optimal Function stressed Excessive norepinephrine engages α1, β1 receptors Excessive dopamine stimulation of too many D1 receptors levels of catecholamine release increase with arousal state
108 Chemical Cascades That Alter Network Firing
109 Chemical Cascades That Alter Network Firing NE α2a Moderate D1 Alert Interested OPTIMAL
110 Chemical Cascades That Alter Network Firing OPTIMAL PFC FUNCTION MODERATE LEVELS OF CATECHOLAMINES HCN closed HCN open STRENGTHEN NETWORKS BRINGING IN SIGNALS AC Gi α2a AC Gs D1/5 WEAKEN NETWORKS BRINGING IN NOISE NE α2a Moderate D1 NE DA Alert Interested OPTIMAL
111 OPTIMAL CATECHOLAMINE REGULATION NET NOREPINEPHRINE PFC dendrite NET APPROPRIATE INPUT α2a α2a increases signal spine
112 OPTIMAL CATECHOLAMINE REGULATION NET NOREPINEPHRINE PFC dendrite NET APPROPRIATE INPUT α2a α2a increases signal spine
113 OPTIMAL CATECHOLAMINE REGULATION NET NOREPINEPHRINE PFC dendrite NET α2a APPROPRIATE INPUT α2a increases signal spine
114 OPTIMAL CATECHOLAMINE REGULATION NET NOREPINEPHRINE PFC dendrite NET α2a APPROPRIATE INPUT α2a increases signal spine
115 OPTIMAL CATECHOLAMINE REGULATION NET NOREPINEPHRINE PFC dendrite NET α2a APPROPRIATE INPUT α2a increases signal spine
116 OPTIMAL CATECHOLAMINE REGULATION NET NOREPINEPHRINE PFC dendrite NET α2a APPROPRIATE INPUT α2a increases signal spine
117 OPTIMAL CATECHOLAMINE REGULATION DAT DOPAMINE NET NOREPINEPHRINE PFC dendrite D1 INAPPROPRIATE INPUT NET α2a D1 decreases noise glutamate APPROPRIATE INPUT α2a increases signal spine
118 OPTIMAL CATECHOLAMINE REGULATION DAT DOPAMINE NET NOREPINEPHRINE NET PFC dendrite D1 INAPPROPRIATE INPUT α2a D1 decreases noise glutamate APPROPRIATE INPUT α2a increases signal spine
119 OPTIMAL CATECHOLAMINE REGULATION DAT DOPAMINE NET NOREPINEPHRINE NET PFC dendrite D1 INAPPROPRIATE INPUT α2a D1 decreases noise glutamate APPROPRIATE INPUT α2a increases signal spine
120 OPTIMAL CATECHOLAMINE REGULATION DAT DOPAMINE NET NOREPINEPHRINE NET PFC dendrite D1 INAPPROPRIATE INPUT α2a D1 decreases noise glutamate APPROPRIATE INPUT α2a increases signal spine
121 OPTIMAL CATECHOLAMINE REGULATION DAT DOPAMINE NET NOREPINEPHRINE NET PFC dendrite D1 INAPPROPRIATE INPUT α2a D1 decreases noise glutamate APPROPRIATE INPUT α2a increases signal spine
122 OPTIMAL CATECHOLAMINE REGULATION DAT DOPAMINE NET NOREPINEPHRINE NET PFC dendrite D1 INAPPROPRIATE INPUT α2a D1 decreases noise glutamate APPROPRIATE INPUT α2a increases signal spine
123 ADHD
124 Chemical Cascades That Alter Network Firing OPTIMAL PFC FUNCTION MODERATE LEVELS OF CATECHOLAMINES HCN closed HCN open STRENGTHEN NETWORKS BRINGING IN SIGNALS AC Gi α2a AC Gs D1/5 WEAKEN NETWORKS BRINGING IN NOISE NE α2a Moderate D1 NET NE DA DAT Alert Interested
125 ADHD May Involve Inadequate Catecholamines OPTIMAL PFC FUNCTION GENETIC CHANGES IN ADHD HCN closed HCN open Weakened SIGNALS Strengthened NOISE AC AC Gi Gs α2a D1/5 NET NE dβh DA DAT ADHD Inadequate catecholamines
126 ADHD Medications Normalize Catecholamines in PFC OPTIMAL PFC FUNCTION GENETIC CHANGES IN ADHD HCN closed HCN open STRENGTHEN NETWORKS BRINGING IN SIGNALS guanfacine AC Gi α2a AC Gs D1/5 WEAKEN NETWORKS BRINGING IN NOISE ADHD + meds NET NE dβh DA DAT methylphenidate amphetamines atomoxetine methylphenidate amphetamines ADHD
127 OPTIMAL CATECHOLAMINE REGULATION DAT DOPAMINE NET NOREPINEPHRINE NET PFC dendrite D1 INAPPROPRIATE INPUT α2a D1 decreases noise glutamate APPROPRIATE INPUT α2a increases signal spine
128 GENETIC WEAKENING OF CATECHOLAMINES IN ADHD DAT DOPAMINE NET DBH NOREPINEPHRINE PFC dendrite D1 INAPPROPRIATE INPUT NET glutamate APPROPRIATE INPUT α2a spine
129 GENETIC WEAKENING OF CATECHOLAMINES IN ADHD DAT DOPAMINE NET DBH NOREPINEPHRINE PFC dendrite D1 INAPPROPRIATE INPUT NET glutamate APPROPRIATE INPUT α2a spine
130 GENETIC WEAKENING OF CATECHOLAMINES IN ADHD DAT NET DOPAMINE DBH NOREPINEPHRINE Alterations in DBH are associated with weak sustained attention and poor executive function in patients with ADHD (Bellgrove et al, 2005; Kieling et al, 2007) PFC dendrite D1 INAPPROPRIATE INPUT NET glutamate APPROPRIATE INPUT α2a spine
131 GENETIC WEAKENING OF CATECHOLAMINES IN ADHD DAT DOPAMINE NET DBH NOREPINEPHRINE PFC dendrite D1 INAPPROPRIATE INPUT NET glutamate APPROPRIATE INPUT α2a spine
132 ADHD TREATMENTS ENHANCE CATECHOLAMINES IN PFC NET methylphenidate amphetamine atomoxetine methylphenidate amphetamine DAT DOPAMINE DBH NOREPINEPHRINE PFC dendrite D1 INAPPROPRIATE INPUT NET guanfacine glutamate α2a APPROPRIATE INPUT spine
133
134 Stress Impairs Prefrontal Function stressed levels of catecholamine release
135 Brain Body Lungs β2 Stomach β3 on off on Heart β1 Turn off PFC during stress: α1, β1 Turn on during stress α1, β Epinephrine released into blood Norepinephrine released by sympathetic nervous system and throughout most of brain
136 Brain Body Reflexive Lungs β2 Stomach β3 on off on Heart β1 Reflective Turning off prefrontal cortical control of behavior during stress may have survival value, but may make us more vulnerable to neuropsychiatric illness
137 Brain Lungs β2 Stomach β3 on Body off on Heart β1 Reflective Uncontrollable stress Reflexive Even mild stress impairs prefrontal function, if we feel out of control. The prefrontal cortex is the brain region that assesses whether we are in control, and shuts off the stress response if it thinks we are.
138 Stress Impairs Prefrontal Function stressed NE α1, β1 Excessive D1 levels of catecholamine release
139 Stress Impairs Prefrontal Function IMPAIRED PFC FUNCTION EXCESSIVE LEVELS OF CATECHOLAMINES all HCN open AC DISCONNECTS ALL NETWORK CONNECTIONS Gs β1 or D1/5 NE DA stressed NE α1, β1 Excessive D1 levels of catecholamine release
140 Stress Impairs Prefrontal Function SUPPRESSES CELL FIRING IMPAIRED PFC FUNCTION EXCESSIVE LEVELS OF CATECHOLAMINES PKC DAG Ca 2+ IP3 PLC all HCN open AC DISCONNECTS ALL NETWORK CONNECTIONS α1 Gq NE Gs β1 or D1/5 DA stressed NE α1, β1 Excessive D1 levels of catecholamine release
141 Stress Impairs Prefrontal Function SUPPRESSES CELL FIRING IMPAIRED PFC FUNCTION EXCESSIVE LEVELS OF CATECHOLAMINES PKC DAG Ca 2+ IP3 PLC all HCN open AC DISCONNECTS ALL NETWORK CONNECTIONS α1 Gq NE Gs β1 or D1/5 DA stressed NE α1, β1 Excessive D1 It takes very high levels of NE to engage these receptors, and thus they seem to only kick in during stress levels of catecholamine release
142 Stress Impairs Prefrontal Function SUPPRESSES CELL FIRING IMPAIRED PFC FUNCTION EXCESSIVE LEVELS OF CATECHOLAMINES PKC DAG Ca 2+ IP3 PLC all HCN open AC DISCONNECTS ALL NETWORK CONNECTIONS α1 Gq NE Gs β1 or D1/5 DA stressed NE α1, β1 Excessive D1 levels of catecholamine release
143 Stress Impairs Prefrontal Function SUPPRESSES CELL FIRING IMPAIRED PFC FUNCTION EXCESSIVE LEVELS OF CATECHOLAMINES PKC DAG Ca 2+ IP3 PLC all HCN open AC DISCONNECTS ALL NETWORK CONNECTIONS α1 Gq NE Gs β1 or D1/5 DA stressed NE α1, β1 Excessive D1 levels of catecholamine release
144 IP3 PIP2 Ca 2+ DAG HCNopen SKopen PKC thought rational
145 EXCESSIVE CATECHOLAMINES (eg STRESS) DAT DOPAMINE NET NOREPINEPHRINE NET PFC dendrite D1 INAPPROPRIATE INPUT glutamate β1 APPROPRIATE INPUT D1 spine
146 EXCESSIVE CATECHOLAMINES (eg STRESS) DAT DOPAMINE NET NOREPINEPHRINE NET PFC dendrite D1 INAPPROPRIATE INPUT glutamate β1 APPROPRIATE INPUT D1 spine
147 EXCESSIVE CATECHOLAMINES (eg STRESS) DAT DOPAMINE NET NOREPINEPHRINE NET PFC dendrite D1 INAPPROPRIATE INPUT glutamate β1 APPROPRIATE INPUT D1 spine
148 EXCESSIVE CATECHOLAMINES (eg STRESS) DAT DOPAMINE NET α1 NOREPINEPHRINE NET PFC dendrite D1 INAPPROPRIATE INPUT glutamate APPROPRIATE INPUT β1 D1 spine
149 EXCESSIVE CATECHOLAMINES (eg STRESS) DAT DOPAMINE NET α1 NOREPINEPHRINE NET PFC dendrite D1 INAPPROPRIATE INPUT glutamate APPROPRIATE INPUT β1 D1 spine
150 EXCESSIVE CATECHOLAMINES (eg STRESS) NET α1 PKC Ca +2 DAT DOPAMINE NOREPINEPHRINE NET PFC dendrite D1 INAPPROPRIATE INPUT glutamate APPROPRIATE INPUT β1 D1 spine
151 EXCESSIVE CATECHOLAMINES (eg STRESS) NET α1 PKC Ca +2 DAT DOPAMINE NOREPINEPHRINE NET PFC dendrite D1 INAPPROPRIATE INPUT glutamate APPROPRIATE INPUT β1 D1 spine
152 EXCESSIVE CATECHOLAMINES (eg STRESS) NET α1 PKC Ca +2 DAT DOPAMINE NOREPINEPHRINE NET PFC dendrite D1 INAPPROPRIATE INPUT glutamate APPROPRIATE INPUT β1 Stop cell firing D1 spine
153 Stress Impairs Prefrontal Function IMPAIRED PFC FUNCTION EXCESSIVE LEVELS OF CATECHOLAMINES PKC Ca 2+ all HCN open DAG IP3 PLC Gq α1 NE AC Gs β1 or D1/5 DA stressed
154 Important Molecules Inside of Cells Provide Brakes On These Stress Pathways IMPAIRED PFC FUNCTION EXCESSIVE LEVELS OF CATECHOLAMINES PKC Ca 2+ all HCN open DAG IP3 DGKH=DAG Kinase DGKH PLC AC Gq Gs α1 β1 or D1/5 NE DA stressed
155 Molecular Brakes Altered in Mental Illness IMPAIRED PFC FUNCTION EXCESSIVE LEVELS OF CATECHOLAMINES PKC Ca 2+ all HCN open DAG DGKH IP3 PLC Gq α1 AC Gs β1 or D1/5 NE DA Bipolar disorder (mania)
156 Molecular Brakes Altered in Mental Illness IMPAIRED PFC FUNCTION EXCESSIVE LEVELS OF CATECHOLAMINES PKC Ca 2+ all HCN open DAG DGKH IP3 PLC Gq AC Gs Right prefrontal dysfunction in mania Blumberg et al α1 NE β1 or D1/5 DA Bipolar disorder (mania)
157 Molecular Brakes Altered in Mental Illness 0.2 Percent Signal Increase in rac BD Off Medication Healthy Controls BD On Lithium Lithium Depakote IMPAIRED PFC FUNCTION EXCESSIVE LEVELS OF CATECHOLAMINES PKC DAG DGKH Ca 2+ IP3 PLC Gq Gs all HCN open AC Normalized by medications that inhibits PKC signaling Blumberg et al α1 NE β1 or D1/5 DA Bipolar disorder (mania)
158 Molecular Brakes Altered in Mental Illness IMPAIRED PFC FUNCTION EXCESSIVE LEVELS OF CATECHOLAMINES PKC Ca 2+ all HCN open DAG IP3 DISC1=Disrupted In SChizophrenia PLC AC DISC1 Gq Gs α1 β1 or D1/5 NE DA Bipolar disorder (mania) Schizophrenia
159 Molecular Brakes Altered in Mental Illness IMPAIRED PFC FUNCTION EXCESSIVE LEVELS OF CATECHOLAMINES PKC Ca 2+ DAG IP3 PLC all HCN open AC DISC1 α1 NE Gq Gs β1 or D1/5 DA Bipolar disorder (mania) Schizophrenia
160 Molecular Brakes Altered in Mental Illness Could guanfacine treatment substitute for loss of DISC1 function? IMPAIRED PFC FUNCTION EXCESSIVE LEVELS OF CATECHOLAMINES PKC Ca 2+ DAG IP3 PLC all HCN open guanfacine AC DISC1 α1 NE Gq Gs β1 or D1/5 DA Bipolar disorder (mania) Schizophrenia
161 Molecular Brakes Altered in Mental Illness DISC1 is also needed for the normal development of the PFC IMPAIRED PFC FUNCTION EXCESSIVE LEVELS OF CATECHOLAMINES PKC Ca 2+ DAG IP3 PLC all HCN open AC DISC1 α1 NE Gq Gs β1 or D1/5 DA Bipolar disorder (mania) Schizophrenia
162 Lead Poisoning Mimics ADHD IMPAIRED PFC FUNCTION EXCESSIVE LEVELS OF CATECHOLAMINES PKC Ca 2+ all HCN open DAG IP3 PLC Gq α1 AC Gs β1 or D1/5 NE DA Lead poisoning
163 Lead Poisoning Mimics ADHD IMPAIRED PFC FUNCTION EXCESSIVE LEVELS OF CATECHOLAMINES Pb 2+ PKC Ca 2+ all HCN open DAG IP3 PLC Gq α1 AC Gs β1 or D1/5 NE DA Lead poisoning Pb 2+
164 Lead Poisoning Mimics ADHD IMPAIRED PFC FUNCTION EXCESSIVE LEVELS OF CATECHOLAMINES Pb 2+ PKC Ca 2+ all HCN open DAG IP3 PLC Gq α1 AC Gs β1 or D1/5 NE DA Wright et al, PLOS 2008 Lead poisoning Pb 2+ Lead poisoning is associated with criminal behavior and out of wedlock pregnancy. Even low levels cause impaired attention regulation.
165 Lead Poisoning Mimics ADHD Destruction to this area in early childhood (e.g. falling out a window, hit by a car) causes sociopathy IMPAIRED PFC FUNCTION EXCESSIVE LEVELS OF CATECHOLAMINES Pb 2+ PKC Ca 2+ all HCN open DAG IP3 PLC AC α1 NE Gq Gs β1 or D1/5 DA Cecil et al, PLOS 2008 Lead poisoning Pb 2+ Lead poisoning is associated with reduced PFC gray matter.
166 Increased PKC Signaling Decreases PFC Gray Matter PKC Pb 2+ Ca 2+ DAG IP3 PLC α1 Gq NE Lead poisoning Pb 2+
167 Increased PKC Signaling Decreases PFC Gray Matter actin MARCKS PKC Pb 2+ Ca 2+ DAG IP3 PLC α1 Gq NE Lead poisoning Pb 2+
168 Increased PKC Signaling Decreases PFC Gray Matter actin MARCKS PKC Actin bundles hold the spine in place Actin is anchored to the membrane by MARCKS Pb 2+ Ca 2+ DAG IP3 PLC α1 Gq NE Lead poisoning Pb 2+
169 Increased PKC Signaling Decreases PFC Gray Matter actin MARCKS PKC alters MARCKS so it lets go from the membrane PKC Pb 2+ Ca 2+ DAG IP3 PLC α1 Gq NE Lead poisoning Pb 2+
170 Increased PKC Signaling Decreases PFC Gray Matter pmarcks PKC Pb 2+ Ca 2+ DAG IP3 PLC α1 Gq NE Lead poisoning Pb 2+
171 Increased PKC Signaling Decreases PFC Gray Matter pmarcks PKC Pb 2+ Ca 2+ DAG IP3 PLC α1 Gq NE Lead poisoning Pb 2+
172 Increased PKC Signaling Decreases PFC Gray Matter pmarcks PKC Pb 2+ Ca 2+ DAG IP3 PLC α1 Gq NE Lead poisoning Pb 2+
173 Increased PKC Signaling Decreases PFC Gray Matter pmarcks PKC Pb 2+ Ca 2+ DAG IP3 PLC α1 Gq NE Lead poisoning Pb 2+
174 Increased PKC Signaling Decreases PFC Gray Matter pmarcks PKC Pb 2+ Ca 2+ DAG IP3 PLC α1 Gq NE Lead poisoning Pb 2+
175 Increased PKC Signaling Decreases PFC Gray Matter pmarcks PKC Pb 2+ Ca 2+ DAG IP3 PLC Spine collapses Gq α1 NE Lead poisoning Pb 2+
176 Increased PKC Signaling Decreases PFC Gray Matter disruption of actin pmarcks CHEL PKC Ca +2 PIP 2 DAG Gq IP3 phospholipase C α 1
177 Loss of PFC Activity/Gray Matter In Conditions that Resemble ADHD ADHD Mania Lead Poisoning
178 Medications That Inhibit PKC Protect PFC Gray Matter In Bipolar DIsorder Bipolar Patients Blumberg et al. Biol Psychiatry 2006 Medications= Lithium, Depakote Ventral Prefrontal Cortex
179 Medications That Inhibit PKC Protect PFC Gray Matter In Bipolar DIsorder Bipolar Patients Might these medications be helpful in treating children with lead poisoning as well, especially if chelation is unable to remove all the lead from their systems? Blumberg et al. Biol Psychiatry 2006 Medications= Lithium, Depakote Ventral Prefrontal Cortex
180 SUMMARY: Prefrontal Dysfunction Resembles ADHD A normal child when stressed Genetic mutations that weaken brakes on stress pathways e.g. DAG kinase (bipolar disorder) DISC1 (schizophrenia) Lead poisoning
181 SUMMARY: Prefrontal Dysfunction Resembles ADHD A normal child when tired Genetic mutations that reduce catecholamine levels in PFC A normal child when stressed Genetic mutations that weaken brakes on stress pathways e.g. DAG kinase (bipolar disorder) DISC1 (schizophrenia) Lead poisoning
182 SUMMARY: Prefrontal Dysfunction Resembles ADHD A normal child when tired Genetic mutations that reduce catecholamine levels in PFC Head injury to PFC Genetic mutations that slow or impair the development of the PFC or its connections A normal child when stressed Genetic mutations that weaken brakes on stress pathways e.g. DAG kinase (bipolar disorder) DISC1 (schizophrenia) Lead poisoning
183 SUMMARY: Prefrontal Dysfunction Resembles ADHD A normal child when tired Genetic mutations that reduce catecholamine levels in PFC Head injury to PFC Genetic mutations that slow or impair the development of the PFC or its connections A normal child when stressed Genetic mutations that weaken brakes on stress pathways e.g. DAG kinase (bipolar disorder) DISC1 (schizophrenia) Lead poisoning True ADHD?
184 SUMMARY: Prefrontal Dysfunction Resembles ADHD Important to distinguish the true cause of ADHD-like behaviors, in order to plan the correct treatment A normal child when tired Genetic mutations that reduce catecholamine levels in PFC Head injury to PFC Genetic mutations that slow or impair the development of the PFC or its connections A normal child when stressed Genetic mutations that weaken brakes on stress pathways e.g. DAG kinase (bipolar disorder) DISC1 (schizophrenia) Lead poisoning True ADHD?
185 The future: A more rational approach to neuropsychiatry
186 Acknowledgements
187 Acknowledgements NIMH NIA NARSAD Dr. Min Wang Dr. Brian Ramos Dr. Constantinos Paspalas Dr. Susheel Vijayraghavan Dr. Shari Birnbaum Dr. Craig Berridge Dr. Arthur Simen Dr. Alvaro Duque Avis Brennan Hains Nao Gamo
Chapter 17. Nervous System Nervous systems receive sensory input, interpret it, and send out appropriate commands. !
Chapter 17 Sensory receptor Sensory input Integration Nervous System Motor output Brain and spinal cord Effector cells Peripheral nervous system (PNS) Central nervous system (CNS) 28.1 Nervous systems
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